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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Apoetm1Unc
targeted mutation 1, University of North Carolina
MGI:1857129
Summary 164 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Apoetm1Unc/Apoetm1Unc B6.129P2-Apoetm1Unc MGI:3758858
hm2
Apoetm1Unc/Apoetm1Unc B6.129P2-Apoetm1Unc/J MGI:2384131
hm3
Apoetm1Unc/Apoetm1Unc B6.Cg-Apoetm1Unc Faslpr MGI:3799495
hm4
Apoetm1Unc/Apoetm1Unc either: B6.129P2-Apoetm1Unc/J or (involves: 129P2/OlaHsd * C57BL/6J * ICR) MGI:3717197
hm5
Apoetm1Unc/Apoetm1Unc involves: 129P2/OlaHsd MGI:3718006
hm6
Apoetm1Unc/Apoetm1Unc involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:3764959
hm7
Apoetm1Unc/Apoetm1Unc involves: 129P2/OlaHsd * C57BL/6 MGI:3714936
hm8
Apoetm1Unc/Apoetm1Unc involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:4358709
hm9
Apoetm1Unc/Apoetm1Unc involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:3822450
hm10
Apoetm1Unc/Apoetm1Unc Not Specified MGI:5449935
ht11
Apoetm1Unc/Apoe+ involves: 129P2/OlaHsd * C57BL/6 MGI:3836194
ht12
Apoetm1Unc/Apoe+ Not Specified MGI:5449957
ht13
Apoeshl/Apoetm1Unc involves: 129P2/OlaHsd * KOR MGI:3716843
cn14
Apoetm1Unc/Apoetm1Unc
Gja5tm1Mchn/Gja5tm1Mchn
Tg(TIE2-lacZ)182Sato/0
involves: 129P2/OlaHsd * BALB/c * C57BL/6 MGI:4818410
cn15
Apoetm1Unc/Apoetm1Unc
Klf15tm2Jain/Klf15tm2Jain
Tg(Tagln-cre)1Jjl/0
involves: 129P2/OlaHsd * FVB/N MGI:5552967
cx16
Apoetm1Unc/Apoetm1Unc
Cdkn1atm1Tyj/Cdkn1atm1Tyj
B6.129-Apoetm1Unc Cdkn1atm1Tyj MGI:4420802
cx17
Apoetm1Unc/Apoetm1Unc
Cx3cl1tm1Sgs/Cx3cl1tm1Sgs
B6.129-Apoetm1Unc Cx3cl1tm1Sgs MGI:3527869
cx18
Apoetm1Unc/Apoetm1Unc
Cx3cr1tm1Zm/Cx3cr1tm1Zm
B6.129-Apoetm1Unc Cx3cr1tm1Zm MGI:3618277
cx19
Apoetm1Unc/Apoetm1Unc
Cx3cr1tm1Zm/Cx3cr1+
B6.129-Apoetm1Unc Cx3cr1tm1Zm MGI:3618279
cx20
Apoetm1Unc/Apoetm1Unc
Ifngtm1Ts/Ifngtm1Ts
B6.129-Apoetm1Unc Ifngtm1Ts MGI:4938323
cx21
Apoetm1Unc/Apoetm1Unc
Pecam1Gt(OST16303)Lex/Pecam1Gt(OST16303)Lex
B6.129-Apoetm1Unc Pecam1Gt(OST16303)Lex MGI:3822293
cx22
Apoetm1Unc/Apoetm1Unc
Cxcl10tm1Adl/Cxcl10tm1Adl
B6.129-Cxcl10tm1Adl Apoetm1Unc MGI:4938324
cx23
Apoetm1Unc/Apoetm1Unc
Thbdtm1.1(THBD)Sltz/Thbdtm1.1(THBD)Sltz
B6.129(FVB)-Thbdtm1.1(THBD)Sltz Apoetm1Unc MGI:5462232
cx24
Apoetm1Unc/Apoetm1Unc
Hsd11b1tm1Lex/Hsd11b1tm1Lex
B6.129-Hsd11b1tm1Lex Apoetm1Unc MGI:5502603
cx25
Apoetm1Unc/Apoetm1Unc
Il1r1tm1Imx/Il1r1tm1Imx
B6.129-Il1r1tm1Imx Apoetm1Unc MGI:4939466
cx26
Apoetm1Unc/Apoetm1Unc
Nceh1tm1Ishi/Nceh1tm1Ishi
B6.129-Nceh1tm1Ishi Apoetm1Unc MGI:4359427
cx27
Apoetm1Unc/Apoetm1Unc
Nos3tm1Plh/Nos3tm1Plh
B6.129-Nos3tm1Plh Apoetm1Unc MGI:4367467
cx28
Apoetm1Unc/Apoetm1Unc
Cd44tm1Mak/Cd44+
B6.129P2-Cd44tm1Mak Apoetm1Unc MGI:4942389
cx29
Apoetm1Unc/Apoetm1Unc
Cd44tm1Mak/Cd44tm1Mak
B6.129P2-Cd44tm1Mak Apoetm1Unc MGI:4942387
cx30
Apoetm1Unc/Apoetm1Unc
Nos3tm1Unc/Nos3tm1Unc
B6.129P2-Nos3tm1Unc Apoetm1Unc MGI:3794764
cx31
Apoetm1Unc/Apoetm1Unc
Serpine1tm1Mlg/Serpine1tm1Mlg
B6.129-Serpine1tm1Mlg Apoetm1Unc MGI:3811066
cx32
Apoetm1Unc/Apoetm1Unc
Ccr2tm1Ifc/Ccr2tm1Ifc
B6.Cg-Apoetm1Unc Ccr2tm1Ifc MGI:4833679
cx33
Apoetm1Unc/Apoetm1Unc
Ccr2tm1Ifc/Ccr2tm1Ifc
Cx3cl1tm1Lira/Cx3cl1tm1Lira
B6.Cg-Apoetm1Unc Cx3cl1tm1Lira Ccr2tm1Ifc MGI:4833678
cx34
Apoetm1Unc/Apoetm1Unc
Faslpr/Faslpr
B6.Cg-Apoetm1Unc Faslpr MGI:3800213
cx35
Apoetm1Unc/Apoetm1Unc
Pik3cgtm1Dwu/Pik3cgtm1Dwu
B6.Cg-Apoetm1Unc Pik3cgtm1Dwu MGI:4358191
cx36
Apoetm1Unc/Apoetm1Unc
Tg(CMV-Serpine1)1Dgi/0
B6.Cg-Apoetm1Unc Tg(CMV-Serpine1)1Dgi MGI:3810982
cx37
Apoetm1Unc/Apoetm1Unc
Tg(EIF1AX-Aldh2*E487K)101Oht/Tg(EIF1AX-Aldh2*E487K)101Oht
B6.Cg-Apoetm1Unc Tg(EIF1AX-Aldh2*E487K)101Oht MGI:5699095
cx38
Apoetm1Unc/Apoetm1Unc
Tg(GFAP-APOE_i3)37Hol/0
B6.Cg-Apoetm1Unc Tg(GFAP-APOE_i3)37Hol MGI:3784381
cx39
Apoetm1Unc/Apoetm1Unc
Tg(GFAP-APOE_i4)22Hol/0
B6.Cg-Apoetm1Unc Tg(GFAP-APOE_i4)22Hol MGI:3784306
cx40
Apoetm1Unc/Apoetm1Unc
Tg(GFAP-APOE_i4)#Hol/0
B6.Cg-Apoetm1Unc Tg(GFAP-APOE_i4)#Hol MGI:3784380
cx41
Apoetm1Unc/Apoetm1Unc
Arhgef26tm1.1Kbur/Arhgef26tm1.1Kbur
B6.Cg-Arhgef26tm1.1Kbur Apoetm1Unc MGI:5500052
cx42
Apoetm1Unc/Apoetm1Unc
Crptm1Hjf/Crptm1Hjf
B6.Cg-Crptm1Hjf Apoetm1Unc MGI:4947400
cx43
Apoetm1Unc/Apoetm1Unc
Fabp4tm1Brsp/Fabp4tm1Brsp
Fabp5tm1Hota/Fabp5tm1Hota
B6.Cg-Fabp4tm1Brsp Fabp5tm1Hota Apoetm1Unc MGI:3815438
cx44
Apoetm1Unc/Apoetm1Unc
Faslgld/Faslgld
B6.Cg-Faslgld Apoetm1Unc MGI:5514345
cx45
Apoetm1Unc/Apoetm1Unc
Tg(GFAP-APOE_i3)37Hol/0
B6.Cg-Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/J MGI:3784303
cx46
Apoetm1Unc/Apoetm1Unc
Tg(GFAP-APOE_i4)1Hol/0
B6.Cg-Tg(GFAP-APOE_i4)1Hol Apoetm1Unc/J MGI:3784302
cx47
Apoetm1Unc/Apoetm1Unc
Glg1Gt(RST092)Byg/Glg1+
B6J.129P2-Apoetm1Unc Glg1Gt(RST092)Byg MGI:5699561
cx48
Apoetm1Unc/Apoetm1Unc
Msr1tm1Csk/Msr1tm1Csk
either: (involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6J * ICR) or (involves: 129P2/OlaHsd * 129X1/SvJ * 129/Sv * ICR) MGI:2177115
cx49
Apoetm1Unc/Apoetm1Unc
Hptm1Alev/Hptm1Alev
involves: 129 MGI:3790694
cx50
Apoetm1Unc/Apoetm1Unc
Egr1tm1Jmi/Egr1tm1Jmi
involves: 129 * C57BL/6 MGI:4821395
cx51
Apoetm1Unc/Apoetm1Unc
Lpltm1Sem/Lpltm1Sem
involves: 129P2/OlaHsd MGI:4354296
cx52
Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/Tg(APPV717F)109Ili
involves: 129P2/OlaHsd MGI:3721542
cx53
Apoetm1Unc/Apoetm1Unc
Cd36tm1Mfe/Cd36tm1Mfe
involves: 129P2/OlaHsd * 129S1/Sv * C57BL/6 MGI:4888254
cx54
Apoetm1Unc/Apoetm1Unc
Clutm1Jakh/Clutm1Jakh
Tg(APPV717F)109Ili/Tg(APPV717F)109Ili
involves: 129P2/OlaHsd * 129S2/SvPas MGI:3721541
cx55
Apoetm1Unc/Apoetm1Unc
Ncf1tm1Shl/Ncf1tm1Shl
involves: 129P2/OlaHsd * 129S2/SvPas MGI:4438110
cx56
Apoetm1Unc/Apoetm1Unc
Scarb1tm1Kri/Scarb1tm1Kri
involves: 129P2/OlaHsd * 129S2/SvPas * BALB/c * C57BL/6 MGI:5558016
cx57
Apoetm1Unc/Apoetm1Unc
Itgb3tm1Hyn/Itgb3tm1Hyn
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:4439279
cx58
Apoetm1Unc/Apoetm1Unc
Fut4tm1Jbl/Fut4tm1Jbl
Fut7tm1Jbl/Fut7tm1Jbl
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:3652962
cx59
Apoetm1Unc/Apoetm1Unc
Scarb1tm1Kri/Scarb1tm1Kri
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:3799448
cx60
Apoetm1Unc/Apoetm1Unc
Ccr1tm1Gao/Ccr1tm1Gao
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5317889
cx61
Apobec1tm1Chan/Apobec1tm1Chan
Apoetm1Unc/Apoetm1Unc
involves: 129P2/OlaHsd * 129S4/SvJae MGI:3850552
cx62
Apoetm1Unc/Apoetm1Unc
Ttpatm1Far/Ttpa+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:3653676
cx63
Apoetm1Unc/Apoetm1Unc
Ttpatm1Far/Ttpatm1Far
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:3653653
cx64
Apoetm1Unc/Apoetm1Unc
Timp1tm1Pds/Y
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:3652791
cx65
Apoetm1Unc/Apoetm1Unc
Ccr2tm1Ifc/Ccr2tm1Ifc
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:4831158
cx66
Apoetm1Unc/Apoetm1Unc
Ccr2tm1Ifc/Ccr2+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:4831159
cx67
Apoetm1Unc/Apoetm3(APOE_i4)Yhg
Tg(PDGFB-APPSwInd)20Lms/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2 MGI:5427502
cx68
Apoetm1Unc/Apoetm2(APOE_i3)Yhg
Tg(PDGFB-APPSwInd)20Lms/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2 MGI:5427501
cx69
Apoetm1Unc/Apoetm1Unc
Soat1tm1Far/Soat1tm1Far
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J MGI:3761832
cx70
Apoetm1Unc/Apoetm1Unc
Soat2tm1Far/Soat2tm1Far
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J MGI:3762636
cx71
Angptl3tm1Lex/Angptl3tm1Lex
Apoetm1Unc/Apoetm1Unc
involves: 129P2/OlaHsd * 129S5/SvEvBrd * C57BL/6 MGI:3849583
cx72
Apoetm1Unc/Apoetm1Unc
Mmp9tm1Tvu/Mmp9tm1Tvu
involves: 129P2/OlaHsd * 129S6/SvEvTac MGI:4367614
cx73
Apoetm1Unc/Apoetm1Unc
Spp1tm1Blh/Spp1tm1Blh
involves: 129P2/OlaHsd * 129S6/SvEvTac * Black Swiss * C57BL/6J MGI:4361696
cx74
Apoetm1Unc/Apoetm1Unc
Spp1tm1Blh/Spp1+
involves: 129P2/OlaHsd * 129S6/SvEvTac * Black Swiss * C57BL/6J MGI:4361697
cx75
Apoetm1Unc/Apoetm1Unc
Cyp19a1tm1Esi/Cyp19a1tm1Esi
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 MGI:5428435
cx76
Apoetm1Unc/Apoetm1Unc
Dp(17Nfkbil1-Olfr91)1Cogr/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6J MGI:5451045
cx77
Apoetm1Unc/Apoetm1Unc
Lipgtm1Tq/Lipgtm1Tq
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6J MGI:3785086
cx78
Apoetm1Unc/Apoetm1Unc
Ldlrtm1Her/Ldlrtm1Her
involves: 129P2/OlaHsd * 129S7/SvEvBrd MGI:4367224
cx79
Apoetm1Unc/Apoetm1Unc
Spp1tm1Rit/Spp1+
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:4361864
cx80
Soat1tm1Ishi/Soat1tm1Ishi
Apoetm1Unc/Apoetm1Unc
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:3582202
cx81
Apobec1tm1Ishi/Apobec1tm1Ishi
Apoetm1Unc/Apoetm1Unc
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:3710350
cx82
Apoetm1Unc/Apoetm1Unc
Nos2tm1Mrl/Nos2tm1Mrl
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:4837860
cx83
Apoetm1Unc/Apoetm1Unc
Spp1tm1Rit/Spp1tm1Rit
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6 MGI:4361863
cx84
Apoetm1Unc/Apoetm1Unc
Ldlrtm1Her/Ldlrtm1Her
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J MGI:3789482
cx85
Apoetm1Unc/Apoetm1Unc
Rag2tm1Fwa/Rag2tm1Fwa
involves: 129P2/OlaHsd * 129S/SvEv MGI:3789198
cx86
Apoetm1Unc/Apoetm1Unc
Rag2tm1Fwa/Rag2+
involves: 129P2/OlaHsd * 129S/SvEv MGI:3789200
cx87
Apoetm1Unc/Apoetm1Unc
Il1rntm1Dih/Il1rntm1Dih
involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6 MGI:3789134
cx88
Apoetm1Unc/Apoetm1Unc
Klf15tm1Jain/Klf15tm1Jain
involves: 129P2/OlaHsd * 129X1/SvJ MGI:5552968
cx89
Apoetm1Unc/Apoetm1Unc
Pon1tm1Lus/Pon1tm1Lus
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6J MGI:2654938
cx90
Apoetm1Unc/Apoetm1Unc
Npc1m1N/Npc1m1N
involves: 129P2/OlaHsd * BALB/c MGI:3785902
cx91
Apoetm1Unc/Apoetm1Unc
Csf1op/Csf1op
involves: 129P2/OlaHsd * C3HeB/Fe * C57BL/6 MGI:3836254
cx92
Apoetm1Unc/Apoetm1Unc
Ath29C57BL/6J/?
involves: 129P2/OlaHsd * C3H/HeJ * C57BL/6J MGI:3766466
cx93
Apoetm1Unc/Apoetm1Unc
Ptgdrtm1Dgen/Ptgdrtm1Dgen
involves: 129P2/OlaHsd * C57BL/6 MGI:5473362
cx94
Apoetm1Unc/Apoetm1Unc
Ccr5tm1Kuz/Ccr5tm1Kuz
involves: 129P2/OlaHsd * C57BL/6 MGI:5317842
cx95
Apoetm1Unc/Apoetm1Unc
Ccr5tm1Blck/Ccr5tm1Blck
involves: 129P2/OlaHsd * C57BL/6 MGI:5317846
cx96
Apoetm1Unc/Apoetm1Unc
Il10tm1Cgn/Il10tm1Cgn
involves: 129P2/OlaHsd * C57BL/6 MGI:4460235
cx97
Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/0
involves: 129P2/OlaHsd * C57BL/6 MGI:3784385
cx98
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APP*751)10Cord/0
involves: 129P2/OlaHsd * C57BL/6 MGI:3784391
cx99
Apoetm1Unc/Apoetm1Unc
Tlr4tm1Aki/Tlr4tm1Aki
involves: 129P2/OlaHsd * C57BL/6 MGI:3588777
cx100
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APP*751)10Cord/0
Tg(GFAP-APOE_i3)37Hol/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3784390
cx101
Apoetm1Unc/Apoetm1Unc
Serpind1tm1Moto/Serpind1+
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3713848
cx102
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APP*751)10Cord/0
Tg(GFAP-APOE_i4)1Hol/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3784389
cx103
Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/0
Tg(GFAP-APOE_i3)37Hol/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3784384
cx104
Apoetm1Unc/Apoetm1Unc
Tg(Prnp-Abca1)EHol/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3801012
cx105
Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/0
Tg(GFAP-APOE_i4)#Hol/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3784383
cx106
Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/0
Tg(GFAP-APOE_i2)14Hol/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3784387
cx107
Apoetm1Unc/Apoetm1Unc
Lcattm1Hgc/Lcattm1Hgc
involves: 129P2/OlaHsd * C57BL/6 * DBA MGI:4358706
cx108
Apoetm1Unc/Apoetm1Unc
Tg(CAG-IL1RN)2Cga/?
involves: 129P2/OlaHsd * C57BL/6 * DBA/1 * FVB MGI:3789132
cx109
Apoetm1Unc/Apoetm1Unc
Tg(CAG-IL1RN)1Cga/?
involves: 129P2/OlaHsd * C57BL/6 * DBA/1 * FVB MGI:3789130
cx110
Abca1tm1Jdm/Abca1tm1Jdm
Abcg1tm1Dgen/Abcg1tm1Dgen
Apoetm1Unc/Apoetm1Unc
involves: 129P2/OlaHsd * C57BL/6 * DBA * DBA/1LacJ MGI:5451015
cx111
Apoetm1Unc/Apoetm1Unc
Tg(NOS3)3Crom/0
involves: 129P2/OlaHsd * C57BL/6 * FVB MGI:2653579
cx112
Apoetm1Unc/Apoetm1Unc
Tg(NOS3)2Crom/0
involves: 129P2/OlaHsd * C57BL/6 * FVB MGI:2653578
cx113
Apoetm1Unc/Apoe+
Tg(APPV717I)1130Kha/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:3722317
cx114
Apoetm1Unc/Apoetm1Unc
Tg(Cyp21a1-Apoe)619Fet/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:3822449
cx115
Apoetm1Unc/Apoetm1Unc
Tg(Cyp21a1-Apoe)614Fet/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:3822447
cx116
Apoetm1Unc/Apoetm1Unc
Tg(APPV717I)1130Kha/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N MGI:3722316
cx117
Apoetm1Unc/Apoetm1Unc
Nfe2l2tm1Mym/Nfe2l2tm1Mym
involves: 129P2/OlaHsd * C57BL/6J MGI:4420430
cx118
Apoetm1Unc/Apoetm1Unc
Tg(APOC1)1Bres/0
involves: 129P2/OlaHsd * C57BL/6J * CBA/J MGI:2653531
cx119
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APOE_i3)1Rabr/0
involves: 129P2/OlaHsd * C57BL/6J * ICR MGI:3717196
cx120
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APOE_i4)1Rabr/0
involves: 129P2/OlaHsd * C57BL/6J * ICR MGI:3717195
cx121
Ay/a
Apoetm1Unc/Apoetm1Unc
involves: 129P2/OlaHsd * C57BL/6J * KK/TaJcl MGI:5297860
cx122
Ay/a
Apoetm1Unc/Apoetm1Unc
Ccr2tm1Mae/Ccr2tm1Mae
involves: 129P2/OlaHsd * C57BL/6J * KK/TaJcl MGI:5297861
cx123
Apoetm1Unc/Apoetm1Unc
Tg(MSR1-Plau)1Ddi/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3690213
cx124
Apoetm1Unc/Apoetm1Unc
Leprdb/Leprdb
involves: 129P2/OlaHsd * C57BLKS/J MGI:3775795
cx125
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APOE_i4)1Rabr/0
involves: 129P2/OlaHsd * ICR MGI:3718008
cx126
Apoetm1Unc/Apoetm1Unc
Tg(Eno2-APOE_i3)1Rabr/0
involves: 129P2/OlaHsd * ICR MGI:3718007
cx127
Apoetm1Unc/Apoetm1Unc
Tnfrsf11btm1Eac/Tnfrsf11btm1Eac
involves: 129S4/SvJaeSor * C57BL/6 MGI:3852641
cx128
Apoetm1Unc/Apoetm1Unc
Pla2g15tm1Ytan/Pla2g15tm1Ytan
involves: 129S/SvEv * B6.129P2-Apoetm1Unc/J MGI:3576623
cx129
Apoetm1Unc/Apoetm1Unc
Cst3tm1Karl/Cst3tm1Karl
involves: 129S/SvEv * C57BL/6 MGI:3621887
cx130
Apoetm1Unc/Apoetm1Unc
Cav1tm1Mls/Cav1tm1Mls
involves: 129/Sv * 129P2/OlaHsd * C57BL/6J * SJL MGI:4418046
cx131
Apoetm1Unc/Apoetm1Unc
Lgals3tm1Poi/Lgals3tm1Poi
involves: 129/Sv * C57BL/6 * SJL MGI:3789127
cx132
Albq4A/J/Albq4C57BL/6J
Apoetm1Unc/Apoetm1Unc
involves: A/J * C57BL/6J MGI:3794640
cx133
Albq4A/J/Albq4A/J
Apoetm1Unc/Apoetm1Unc
involves: A/J * C57BL/6J MGI:3794639
cx134
Apoetm1Unc/Apoetm1Unc
Nhdlq12C3H/HeJ/Nhdlq12C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3769560
cx135
Apoetm1Unc/Apoetm1Unc
Nhdlq11C3H/HeJ/Nhdlq11C3H/HeJ
involves: C3H/HeJ * C57BL/6J MGI:3769557
cx136
Apoetm1Unc/Apoetm1Unc
Nhdlq11C3H/HeJ/Nhdlq11C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3769556
cx137
Apoetm1Unc/Apoetm1Unc
Trigq4C3H/HeJ/Trigq4C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3769550
cx138
Apoetm1Unc/Apoetm1Unc
Trigq4C3H/HeJ/Trigq4C3H/HeJ
involves: C3H/HeJ * C57BL/6J MGI:3769549
cx139
Apoetm1Unc/Apoetm1Unc
Hdlq91C3H/HeJ/?
involves: C3H/HeJ * C57BL/6J MGI:3769548
cx140
Apoetm1Unc/Apoetm1Unc
Hdlq19C57BL/6J/Hdlq19C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3769547
cx141
Apoetm1Unc/Apoetm1Unc
Ath29C57BL/6J/Ath29C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3819481
cx142
Apoetm1Unc/Apoetm1Unc
Hdlq86C3H/HeJ/Hdlq86C3H/HeJ
involves: C3H/HeJ * C57BL/6J MGI:3769545
cx143
Apoetm1Unc/Apoetm1Unc
Hdl5C57BL/6J/Hdl5C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3769543
cx144
Apoetm1Unc/Apoetm1Unc
Cath1C3H/HeJ/Cath1C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3769542
cx145
Apoetm1Unc/Apoetm1Unc
Cath1C57BL/6J/Cath1C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3769541
cx146
Apoetm1Unc/Apoetm1Unc
Gofm4C3H/HeJ/?
involves: C3H/HeJ * C57BL/6J MGI:3707039
cx147
Apoetm1Unc/Apoetm1Unc
Gofm3C57BL/6J/?
involves: C3H/HeJ * C57BL/6J MGI:3707037
cx148
Apoetm1Unc/Apoetm1Unc
Gofm2C3H/HeJ/?
involves: C3H/HeJ * C57BL/6J MGI:3707036
cx149
Apoetm1Unc/Apoetm1Unc
Gofm2C57BL/6J/?
involves: C3H/HeJ * C57BL/6J MGI:3707035
cx150
Apoetm1Unc/Apoetm1Unc
Gofm1C57BL/6J/?
involves: C3H/HeJ * C57BL/6J MGI:3707034
cx151
Apoetm1Unc/Apoetm1Unc
Athsq3C57BL/6J/Athsq3C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:5613592
cx152
Apoetm1Unc/Apoetm1Unc
Hdlq86C3H/HeJ/?
involves: C3H/HeJ * C57BL/6J MGI:3769546
cx153
Apoetm1Unc/Apoetm1Unc
Tnfsf4Ath1-C57BL/6J/Tnfsf4Ath1-C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3819480
cx154
Apoetm1Unc/Apoetm1Unc
Athsq3C3H/HeJ/Athsq3C3H/HeJ
involves: C3H/HeJ * C57BL/6J MGI:3819478
cx155
Apoetm1Unc/Apoetm1Unc
Ath33C3H/HeJ/Ath33C3H/HeJ
involves: C3H/HeJ * C57BL/6J MGI:3819477
cx156
Apoetm1Unc/Apoetm1Unc
Ath32C57BL/6J/Ath32C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3819476
cx157
Apoetm1Unc/Apoetm1Unc
Ath31C57BL/6J/Ath31C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3819475
cx158
Apoetm1Unc/Apoetm1Unc
Ath30C57BL/6J/Ath30C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3819474
cx159
Apoetm1Unc/Apoetm1Unc
Trigq3C3H/HeJ/?
involves: C3H/HeJ * C57BL/6J MGI:3769569
cx160
Apoetm1Unc/Apoetm1Unc
Trigq3C3H/HeJ/Trigq3C3H/HeJ
involves: C3H/HeJ * C57BL/6J MGI:3769568
cx161
Apoetm1Unc/Apoetm1Unc
Pnhdlc6C3H/HeJ/?
involves: C3H/HeJ * C57BL/6J MGI:3769566
cx162
Apoetm1Unc/Apoetm1Unc
Pnhdlc1C57BL/6J/Pnhdlc1C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3769564
cx163
Apoetm1Unc/Apoetm1Unc
Nhdlq12C57BL/6J/Nhdlq12C57BL/6J
involves: C3H/HeJ * C57BL/6J MGI:3769561
cx164
Apoetm1Unc/Apoetm1Unc
Faslpr/Faslpr
MRL.Cg-Apoetm1Unc Faslpr MGI:3799494


Genotype
MGI:3758858
hm1
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
B6.129P2-Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• mice maintained on a high fat diet and infected with Leishmania major generate more IL-4 and IL-5 producing CD4+ T cells compared to wild-type mice (J:125366)
• mice maintained on a high fat diet and infected with Leishmania major generate more IL-4 and IL-5 producing CD4+ T cells compared to wild-type mice (J:125366)
• the immune response of mice fed a high fat diet to Leishmania major infection is skewed towards a Th2-type response (J:125366)
• in an adoptive transfer experiment, the proliferation of Tg(TcrLCMV)2Aox CD45.2+ cell in mice fed a high fat diet and receiving then immunized with GP61-80 peptide with CpG is reduced compared to in wild-type mice similarly treated (J:125366)
• the immune response of mice fed a high fat diet to Leishmania major infection is skewed towards a Th2-type response (J:125366)
• in an adoptive transfer experiment, the proliferation of Tg(TcrLCMV)2Aox CD45.2+ cell in mice fed a high fat diet and receiving then immunized with GP61-80 peptide with CpG is reduced compared to in wild-type mice similarly treated (J:125366)
• dendrictic cells mount reduced IL-12p40 and TNF-alpha responses to stimulation with zymosan, poly(I:C), LPS, imiquimod, and a combination of anti-CD40 antibodies and CpG compared to wild-type mice but similar to wild-type mice fed a high fat diet (J:125366)
• in mice fed a high fat diet, dendritic cell production of IL-12p40, IL-6 and TNF-alpha after 35 to 40 weeks, but not after 6 to 10 weeks, is severely impaired compared to wild-type cells in response to CpG/anti-CD-40 stimulation (J:125366)
• CD8alpha-, but not CD8alpha+, dendritic cells are defective in their ability to produce IL-12p40 (J:125366)
• dendritic cells from mice on a high fat diet are severely impaired in their ability to produce Il-12p40, -12p70, -6, and TNF-alpha compared to dendritic cells from wild-type mice on a high fat diet (J:125366)
• however, CD8alpha+ dendritic cells produce normal amounts of Il-12p70 and -12p40 (J:125366)
• mice fed a high fat diet and co-stimulated with CpG or LPS have fewer IL-12p40-producing CD8alpha- dendritic cells (4.6+/-1.1%) than wild-type mice fed a high fat diet (15.3+/-2.4%) (J:125366)
• however, the immune responses of bone marrow derived dendritic cells from mice fed a high fat diet or splenic dendritic cells from mice fed a regular diet are normal (J:125366)
• dendrictic cells mount reduced IL-12p40 and TNF-alpha responses to stimulation with zymosan, poly(I:C), LPS, imiquimod, and a combination of anti-CD40 antibodies and CpG compared to wild-type mice but similar to wild-type mice fed a high fat diet (J:125366)
• in mice fed a high fat diet, dendritic cell production of IL-12p40, IL-6 and TNF-alpha after 35 to 40 weeks, but not after 6 to 10 weeks, is severely impaired compared to wild-type cells in response to CpG/anti-CD-40 stimulation (J:125366)
• CD8alpha-, but not CD8alpha+, dendritic cells are defective in their ability to produce IL-12p40 (J:125366)
• dendritic cells from mice on a high fat diet are severely impaired in their ability to produce Il-12p40, -12p70, -6, and TNF-alpha compared to dendritic cells from wild-type mice on a high fat diet (J:125366)
• however, CD8alpha+ dendritic cells produce normal amounts of Il-12p70 and -12p40 (J:125366)
• mice fed a high fat diet and co-stimulated with CpG or LPS have fewer IL-12p40-producing CD8alpha- dendritic cells (4.6+/-1.1%) than wild-type mice fed a high fat diet (15.3+/-2.4%) (J:125366)
• however, the immune responses of bone marrow derived dendritic cells from mice fed a high fat diet or splenic dendritic cells from mice fed a regular diet are normal (J:125366)
• mice maintained on a high fat diet and infected with Leishmania major produce more IL-4 and IL-5 producing CD4+ T cells compared to wild-type mice (J:125366)
• the immune response of mice fed a high fat diet to Leishmania major infection is skewed towards a Th2-type response (J:125366)
• mice maintained on a high fat diet or regular chow and infected with Leishmania major exhibit an increased swelling and parasitic burden at the site of infection (footpad) (J:125366)
• mice maintained on a high fat diet and infected with Leishmania major produce more IL-4 and IL-5 producing CD4+ T cells compared to wild-type mice (J:125366)
• the immune response of mice fed a high fat diet to Leishmania major infection is skewed towards a Th2-type response (J:125366)
• mice maintained on a high fat diet or regular chow and infected with Leishmania major exhibit an increased swelling and parasitic burden at the site of infection (footpad) (J:125366)

homeostasis/metabolism
• plasma leptin levels are low at both 6 and 18 months (J:60585)
• plasma leptin levels are low at both 6 and 18 months (J:60585)
• mice have increased levels of circulating oxidized lipids compared to wild-type mice (J:125366)
• mice have increased levels of circulating oxidized lipids compared to wild-type mice (J:125366)
• mice develop severe cholesterolemia when receiving a high fat diet from 6 to 30 weeks (elevated levels are detected at 6, 15, and 30 weeks) (J:61287)
• mice develop severe cholesterolemia when receiving a high fat diet from 6 to 30 weeks (elevated levels are detected at 6, 15, and 30 weeks) (J:61287)

behavior/neurological
• increased water intake at 18 months (J:60585)
• increased water intake at 18 months (J:60585)
• increased food intake at 12 and 18 months but not earlier (J:60585)
• increased food intake at 12 and 18 months but not earlier (J:60585)
• at 6 months as measured in an elevated plus maze (J:60585)
• at 6 months as measured in an elevated plus maze (J:60585)
• mice consume food slower in a new environment than Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc and wild-type mice (J:71062)
• mice require more time to habituate to a novel environment compared to wild-type mice (J:71062)
• mice are less reluctant than wild-type mice to move into an open area (J:71062)
• mice consume food slower in a new environment than Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc and wild-type mice (J:71062)
• mice require more time to habituate to a novel environment compared to wild-type mice (J:71062)
• mice are less reluctant than wild-type mice to move into an open area (J:71062)
• reduced exploratory behavior in an open field test by 12 months although normal earlier (J:60585)
• exploratory behavior remains constant over several days whereas controls show higher initial exploratory behavior which drops off quickly (J:60585)
• reduced exploratory behavior in an open field test by 12 months although normal earlier (J:60585)
• exploratory behavior remains constant over several days whereas controls show higher initial exploratory behavior which drops off quickly (J:60585)
• at 14 to 17 months of age, mice perform better than Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc and wild-type mice in a rotating holeboard test (J:71062)
• at 14 to 17 months of age, mice perform better than Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc and wild-type mice in a rotating holeboard test (J:71062)
• mice spend more time than Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc in the center of an open field (J:71062)
• mice spend more time than Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc in the center of an open field (J:71062)
• 41% increase in foot withdrawal latency from painful thermal stimuli (J:106368)
• 100% slower tail withdrawal latency (J:106368)
• 41% increase in foot withdrawal latency from painful thermal stimuli (J:106368)
• 100% slower tail withdrawal latency (J:106368)
• after-discharge duration is significantly prolonged by the sixth trial (J:118390)
• delayed rekindling after 3-4 weeks (J:118390)
• after-discharge duration is significantly prolonged by the sixth trial (J:118390)
• delayed rekindling after 3-4 weeks (J:118390)

hematopoietic system
• mice maintained on a high fat diet and infected with Leishmania major generate more IL-4 and IL-5 producing CD4+ T cells compared to wild-type mice (J:125366)
• mice maintained on a high fat diet and infected with Leishmania major generate more IL-4 and IL-5 producing CD4+ T cells compared to wild-type mice (J:125366)

nervous system
• after-discharge duration is significantly prolonged by the sixth trial (J:118390)
• delayed rekindling after 3-4 weeks (J:118390)
• after-discharge duration is significantly prolonged by the sixth trial (J:118390)
• delayed rekindling after 3-4 weeks (J:118390)
• restraint stress at 6 months results in disproportionately low ACTH levels as compared to plasma corticosterone levels (J:60585)
• restraint stress at 6 months results in disproportionately low ACTH levels as compared to plasma corticosterone levels (J:60585)
• very little Schwann cell cytoplasm (J:106368)
• blurring of lipid membrane border between axons and Schwann cells (J:106368)
• very little Schwann cell cytoplasm (J:106368)
• blurring of lipid membrane border between axons and Schwann cells (J:106368)
• synaptophysin levels are somewhat more reduced than in controls after entorhinal cortex lesion (J:118390)
• synaptophysin levels are somewhat more reduced than in controls after entorhinal cortex lesion (J:118390)
• cross-section of unmyelinated axons is irregular (J:106368)
• very little Schwann cell cytoplasm (J:106368)
• blurring of lipid membrane border between axons and Schwann cells (J:106368)
• reduced number of unmyelinated axons (J:106368)
• ratio of unmyelinated to myelinated axons is reduced (J:106368)
• cross-section of unmyelinated axons is irregular (J:106368)
• very little Schwann cell cytoplasm (J:106368)
• blurring of lipid membrane border between axons and Schwann cells (J:106368)
• reduced number of unmyelinated axons (J:106368)
• ratio of unmyelinated to myelinated axons is reduced (J:106368)

endocrine/exocrine glands
• increased lipid droplets seen at six months (J:60585)
• increased lipid droplets seen at six months (J:60585)
• increased lipid droplets seen at six months (J:60585)
• increased lipid droplets seen at six months (J:60585)
• fter 10 min of restraint stress plasma levels are elevated at six months but not at three months (J:60585)
• elevated adrenal levels at six months but not earlier (J:60585)
• fter 10 min of restraint stress plasma levels are elevated at six months but not at three months (J:60585)
• elevated adrenal levels at six months but not earlier (J:60585)
• restraint stress at 6 months results in disproportionately low ACTH levels as compared to plasma corticosterone levels (J:60585)
• restraint stress at 6 months results in disproportionately low ACTH levels as compared to plasma corticosterone levels (J:60585)

adipose tissue
• decreased interscapular brown fat at 18 but not at 6 months (J:60585)
• decreased interscapular brown fat at 18 but not at 6 months (J:60585)
• epididymal white fat reduced at both 6 and 18 months (J:60585)
• epididymal white fat reduced at both 6 and 18 months (J:60585)

cardiovascular system
• cellular composition of lesions is similar among Serpine1-deficient or transgenic, Apoe-deficient genotypes, or Apoe-deficient only mice; at early time points, a greater foam cell content is observed, with more prominent cholesterol clefts and necrotic areas evident with increasing age (J:61287)
• cellular composition of lesions is similar among Serpine1-deficient or transgenic, Apoe-deficient genotypes, or Apoe-deficient only mice; at early time points, a greater foam cell content is observed, with more prominent cholesterol clefts and necrotic areas evident with increasing age (J:61287)

integument
• 41% increase in foot withdrawal latency from painful thermal stimuli (J:106368)
• 100% slower tail withdrawal latency (J:106368)
• 41% increase in foot withdrawal latency from painful thermal stimuli (J:106368)
• 100% slower tail withdrawal latency (J:106368)




Genotype
MGI:2384131
hm2
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
B6.129P2-Apoetm1Unc/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 35% dead by 18 months (J:73202)
• 35% dead by 18 months (J:73202)

cardiovascular system
• endothelial nitric oxide synthase (eNOS) in mutant aortic wall is distinctly reduced (J:101576)
• endothelial nitric oxide synthase (eNOS) in mutant aortic wall is distinctly reduced (J:101576)
• Cx43 distribution at cell-cell junction shows significant disruption (J:142083)
• Cx43 distribution at cell-cell junction shows significant disruption (J:142083)
• arterioles of the vascular pole show a "foamy" degeneration of smooth muscle cells (J:125978)
• arterioles of the vascular pole show a "foamy" degeneration of smooth muscle cells (J:125978)
• homozygotes fed an atherosclerotic diet develop atherosclerotic alterations in the spiral modiolar artery (SMA) (J:101576)
• in contrast, no such changes are detected in the SMA of homozygotes fed a normal diet (J:101576)
• homozygotes fed an atherosclerotic diet develop atherosclerotic alterations in the spiral modiolar artery (SMA) (J:101576)
• in contrast, no such changes are detected in the SMA of homozygotes fed a normal diet (J:101576)
• homozygotes exhibit a 13% increase in aortic pulse-wave velocity (PWV) relative to wild-type mice (428 14.5 cm/s vs 379 10.1 cm/s), indicating increased arterial stiffness and reduced vascular elasticity (J:108154)
• homozygotes exhibit a 13% increase in aortic pulse-wave velocity (PWV) relative to wild-type mice (428 14.5 cm/s vs 379 10.1 cm/s), indicating increased arterial stiffness and reduced vascular elasticity (J:108154)
• 23% of luminal surface in the aortic arch and thoracic aorta is covered by plaques at 4 months of age (J:60364)
• 61% covered by plaques at 13 months of age (J:60364)
• thickened intima, foam cell accumulation and thin collagen cap (J:60364)
• focal fragmentation of elastic laminae (J:60364)
• 23% of luminal surface in the aortic arch and thoracic aorta is covered by plaques at 4 months of age (J:60364)
• 61% covered by plaques at 13 months of age (J:60364)
• thickened intima, foam cell accumulation and thin collagen cap (J:60364)
• focal fragmentation of elastic laminae (J:60364)
• advanced atherosclerotic lesions; massive atheromas with abundant cholesterol crystals, neutral lipids, and diminished extracellular matrix in arotic roots and coronary arteries (J:73202)
• advanced atherosclerotic lesions; massive atheromas with abundant cholesterol crystals, neutral lipids, and diminished extracellular matrix in arotic roots and coronary arteries (J:73202)
• regular exercise does not reduce atherosclerotic lesion formation in homozygotes, as shown by a comparable % oil red-O staining of whole aortas from sedentary and exercised mutant mice (J:97385)
• regular exercise does not reduce atherosclerotic lesion formation in homozygotes, as shown by a comparable % oil red-O staining of whole aortas from sedentary and exercised mutant mice (J:97385)
• at 24 weeks of age, homozygotes fed a normal diet (but not similarly-fed C57BL/6J control mice) show obvious atherosclerotic lesions in the aortic sinus and ascending aorta (J:101576)
• the number of atherosclerotic lesions in aortic sinus and ascending aorta is significantly increased in homozygotes fed an atherosclerotic diet vs a normal diet (J:101576)
• plaques in the luminal surface of the aorta are significantly larger in atherosclerotic diet homozygotes than in normal diet homozygotes (J:101576)
• at 24 weeks of age, homozygotes fed a normal diet (but not similarly-fed C57BL/6J control mice) show obvious atherosclerotic lesions in the aortic sinus and ascending aorta (J:101576)
• the number of atherosclerotic lesions in aortic sinus and ascending aorta is significantly increased in homozygotes fed an atherosclerotic diet vs a normal diet (J:101576)
• plaques in the luminal surface of the aorta are significantly larger in atherosclerotic diet homozygotes than in normal diet homozygotes (J:101576)
• intimal lesions are observed in atherosclerotic aortas in mutants (J:105736)
• intimal lesions are observed in atherosclerotic aortas in mutants (J:105736)
• at 13 months, homozygotes display atherosclerotic lesions extending from the carotid arteries, heart, and aorta down to the renal arteries and the iliac bifurcation (J:108154)
• lesions are most severe in the proximal aorta and at the bifurcation of carotid arteries; the proximal carotid arteries are relatively free of lesions (J:108154)
• at 13 months, homozygotes display atherosclerotic lesions extending from the carotid arteries, heart, and aorta down to the renal arteries and the iliac bifurcation (J:108154)
• lesions are most severe in the proximal aorta and at the bifurcation of carotid arteries; the proximal carotid arteries are relatively free of lesions (J:108154)
• major lesions are observed on lesser curvature of aortic arch in males and females with minor lesions found at branches of aortic arch (J:142083)
• lesions comprise around 14-16% of total aortic arch area in male and female mutants (J:142083)
• aortic lesions are observed in aortic sinus at level of aortic valve leaflets; lesions are about 27% of total aortal area (J:142083)
• major lesions are observed on lesser curvature of aortic arch in males and females with minor lesions found at branches of aortic arch (J:142083)
• lesions comprise around 14-16% of total aortic arch area in male and female mutants (J:142083)
• aortic lesions are observed in aortic sinus at level of aortic valve leaflets; lesions are about 27% of total aortal area (J:142083)
• on a high fat, high cholesterol diet, mutants exhibit moderate to severe aortic and carotid atherosclerosis (J:43846)
• on a high fat, high cholesterol diet, mutants exhibit moderate to severe aortic and carotid atherosclerosis (J:43846)
• severity of atherosclerosis is 2-fold and 99-fold higher in atherosclerotic diet homozygotes than in normal diet homozygotes and C57BL/6J control mice, respectively (J:101576)
• severity of atherosclerosis is 2-fold and 99-fold higher in atherosclerotic diet homozygotes than in normal diet homozygotes and C57BL/6J control mice, respectively (J:101576)
• at times mesangiolysis is associated with ballooning dilatation ("microaneurysm") of adjacent glomerular capillaries (J:125978)
• at times mesangiolysis is associated with ballooning dilatation ("microaneurysm") of adjacent glomerular capillaries (J:125978)
• lipid droplets filling glomerular capillary lumina at 36 weeks in about 50% of mice (J:125978)
• such thrombus-like structures commonly dsiplay a laminated appearance with adjacent foam cells in the mesangium (J:125978)
• lipid droplets filling glomerular capillary lumina at 36 weeks in about 50% of mice (J:125978)
• such thrombus-like structures commonly dsiplay a laminated appearance with adjacent foam cells in the mesangium (J:125978)
• at times mesangiolysis is associated with ballooning dilatation ("microaneurysm") of adjacent glomerular capillaries (J:125978)
• at times mesangiolysis is associated with ballooning dilatation ("microaneurysm") of adjacent glomerular capillaries (J:125978)
• vascular stenosis is significantly increased in homozygotes fed an atherosclerotic diet vs a normal diet (J:101576)
• vascular stenosis is significantly increased in homozygotes fed an atherosclerotic diet vs a normal diet (J:101576)
• lumen stenosis of the spiral modiolar artery in the cochlea is exacerbated by an atherosclerotic diet relative to a normal diet (J:101576)
• lumen stenosis of the spiral modiolar artery in the cochlea is exacerbated by an atherosclerotic diet relative to a normal diet (J:101576)
• at 13 months, homozygotes show a 23% increase in heart weight relative to wild-type mice (186 7.1 vs. 151 2.5 mg) (J:108154)
• at 13 months, homozygotes show a 23% increase in heart weight relative to wild-type mice (186 7.1 vs. 151 2.5 mg) (J:108154)
• at 13 months, homozygotes show a 59% increase in heart weight-to-body weight ratio relative to wild-type mice (J:108154)
• at 13 months, homozygotes show a 59% increase in heart weight-to-body weight ratio relative to wild-type mice (J:108154)
• anesthetized homozygotes show significantly increased transaortic blood velocities relative to wild-type mice with peak aortic velocity at 133.4 7.8 cm/s vs 89.2 5.8 cm/s, and mean aortic velocity at 35.9 2.7 vs 22.0 1.6 cm/s, respectively (J:108154)
• in addition, anesthetized homozygotes show significantly increased transmitral blood velocities relative to wild-type mice with peak mitral velocities at 92 7.2 cm/s vs 47.2 5.3 cm/s, and mean mitral velocities at 20.6 1.7 vs 11.4 1.3 cm/s, respectively (J:108154)
• no significant differences in heart rate, peak aortic acceleration or ejection time are observed in the conscious or anesthetized state, when normalized to body weight (J:108154)
• however, homozygotes show alterations in aortic arch acceleration suggestive of increased peripheral wave reflections (J:108154)
• anesthetized homozygotes show significantly increased transaortic blood velocities relative to wild-type mice with peak aortic velocity at 133.4 7.8 cm/s vs 89.2 5.8 cm/s, and mean aortic velocity at 35.9 2.7 vs 22.0 1.6 cm/s, respectively (J:108154)
• in addition, anesthetized homozygotes show significantly increased transmitral blood velocities relative to wild-type mice with peak mitral velocities at 92 7.2 cm/s vs 47.2 5.3 cm/s, and mean mitral velocities at 20.6 1.7 vs 11.4 1.3 cm/s, respectively (J:108154)
• no significant differences in heart rate, peak aortic acceleration or ejection time are observed in the conscious or anesthetized state, when normalized to body weight (J:108154)
• however, homozygotes show alterations in aortic arch acceleration suggestive of increased peripheral wave reflections (J:108154)
• under anesthesia, homozygotes exhibit elevated flow velocities suggesting elevated cardiac output (J:108154)
• under anesthesia, homozygotes exhibit elevated flow velocities suggesting elevated cardiac output (J:108154)
• under anesthesia, homozygotes appear to exhibit significantly increased stroke volume (J:108154)
• under anesthesia, homozygotes appear to exhibit significantly increased stroke volume (J:108154)
• under anesthesia, homozygotes appear to exhibit significantly reduced peripheral vascular resistance and compliance in the presence of normal blood pressures (J:108154)
• under anesthesia, homozygotes appear to exhibit significantly reduced peripheral vascular resistance and compliance in the presence of normal blood pressures (J:108154)
• pulse wave velocity is insignificantly elevated at 4 months (J:60364)
• pulse wave velocity significantly elevated at 13 months (J:60364)
• pulse wave velocity is insignificantly elevated at 4 months (J:60364)
• pulse wave velocity significantly elevated at 13 months (J:60364)
• impaired blood-brain barrier and blood-nerve barrier as indicated by extensive extravasation of serum proteins into sciatic nerve, spinal cord and cerebellum and occasional extravasation into cortex and subcortex (J:69455)
• impaired blood-brain barrier and blood-nerve barrier as indicated by extensive extravasation of serum proteins into sciatic nerve, spinal cord and cerebellum and occasional extravasation into cortex and subcortex (J:69455)
• homozygotes fed a normal or atherosclerotic diet show severely impaired endothelium-dependent relaxation to acetylcholine in aortic rings relative to age-matched C57BL/6J control mice (J:101576)
• homozygotes fed a normal or atherosclerotic diet show severely impaired endothelium-dependent relaxation to acetylcholine in aortic rings relative to age-matched C57BL/6J control mice (J:101576)
• aortae show macrophage and T cell extravasation within atherosclerotic lesions (J:91058)
• aortae show macrophage and T cell extravasation within atherosclerotic lesions (J:91058)

muscle
• homozygotes fed a normal or atherosclerotic diet show severely impaired endothelium-dependent relaxation to acetylcholine in aortic rings relative to age-matched C57BL/6J control mice (J:101576)
• homozygotes fed a normal or atherosclerotic diet show severely impaired endothelium-dependent relaxation to acetylcholine in aortic rings relative to age-matched C57BL/6J control mice (J:101576)
• relaxation response to acetylcholine in blood vessels is significantly attenuated at 13 months of age (J:60364)
• maximal response to acetylcholine is considerably reduced (J:60364)
• relaxation response to acetylcholine in blood vessels is significantly attenuated at 13 months of age (J:60364)
• maximal response to acetylcholine is considerably reduced (J:60364)

homeostasis/metabolism
• lipid droplets filling glomerular capillary lumina at 36 weeks in about 50% of mice (J:125978)
• such thrombus-like structures commonly dsiplay a laminated appearance with adjacent foam cells in the mesangium (J:125978)
• lipid droplets filling glomerular capillary lumina at 36 weeks in about 50% of mice (J:125978)
• such thrombus-like structures commonly dsiplay a laminated appearance with adjacent foam cells in the mesangium (J:125978)
• decrease in plasma total homocysteine levels (J:73202)
• decrease in plasma total homocysteine levels (J:73202)
• decreased HDL/total cholesterol ratio (J:73202)
• decreased HDL/LDL ratio (J:73202)
• decreased HDL/total cholesterol ratio (J:73202)
• decreased HDL/LDL ratio (J:73202)
• increasing with age; 4-fold increase in plasma total cholesterol levels in 10-12 week old mutants and 13-fold increase at 29 weeks (J:73202)
• increasing with age; 4-fold increase in plasma total cholesterol levels in 10-12 week old mutants and 13-fold increase at 29 weeks (J:73202)
• exercise (15 or 60 min/day swim) causes no significant changes in total cholesterol levels among homozygotes or wild-type mice relative to sedentary, genotype-matched controls (J:97385)
• exercise (15 or 60 min/day swim) causes no significant changes in total cholesterol levels among homozygotes or wild-type mice relative to sedentary, genotype-matched controls (J:97385)
• on a normal diet, homozygotes display significantly increased plasma total cholesterol (TC) levels relative to C57BL/6J control mice (J:101576)
• on an atherosclerotic diet, homozygotes show a further significant increase in plasma TC levels relative to homozygotes on a normal diet (J:101576)
• on a normal diet, homozygotes display significantly increased plasma total cholesterol (TC) levels relative to C57BL/6J control mice (J:101576)
• on an atherosclerotic diet, homozygotes show a further significant increase in plasma TC levels relative to homozygotes on a normal diet (J:101576)
• total serum cholesterol 70 fold higher than controls on a normal diet (J:104609)
• total serum cholesterol 20 fold higher than controls on high fat diet where controls show 4 fold increase over normal diet (J:104609)
• total serum cholesterol 70 fold higher than controls on a normal diet (J:104609)
• total serum cholesterol 20 fold higher than controls on high fat diet where controls show 4 fold increase over normal diet (J:104609)
• 5 fold increase in total cholesterol at 24 and 36 weeks (J:125978)
• 5 fold increase in total cholesterol at 24 and 36 weeks (J:125978)
• significantly increased relative to wild-type controls at 24 weeks of age; levels in mutants after induction of chronic graft versus host disease (cGVH) to induce systemic lupus erythematosus (SLE) are equivalent to the Apoe-null mice (J:133606)
• significantly increased relative to wild-type controls at 24 weeks of age; levels in mutants after induction of chronic graft versus host disease (cGVH) to induce systemic lupus erythematosus (SLE) are equivalent to the Apoe-null mice (J:133606)
• on a normal diet, homozygotes display significantly increased plasma LDL cholesterol levels relative to C57BL/6J control mice (J:101576)
• on an atherosclerotic diet, homozygotes show a further significant increase in plasma LDL levels relative to homozygotes on a normal diet (J:101576)
• on a normal diet, homozygotes display significantly increased plasma LDL cholesterol levels relative to C57BL/6J control mice (J:101576)
• on an atherosclerotic diet, homozygotes show a further significant increase in plasma LDL levels relative to homozygotes on a normal diet (J:101576)
• on a normal diet, homozygotes display significantly increased plasma VLDL cholesterol levels relative to C57BL/6J control mice (J:101576)
• on an atherosclerotic diet, homozygotes show a further significant increase in plasma VLDL cholesterol levels relative to homozygotes on a normal diet (J:101576)
• on a normal diet, homozygotes display significantly increased plasma VLDL cholesterol levels relative to C57BL/6J control mice (J:101576)
• on an atherosclerotic diet, homozygotes show a further significant increase in plasma VLDL cholesterol levels relative to homozygotes on a normal diet (J:101576)
• 2-fold increase in plasma triglyceride levels in 10-12 week old mutants (J:73202)
• 2-fold increase in plasma triglyceride levels in 10-12 week old mutants (J:73202)
• on a normal diet, homozygotes display significantly increased plasma triglyceride levels relative to C57BL/6J control mice (J:101576)
• on an atherosclerotic diet, homozygotes show a further significant increase in plasma triglyceride levels relative to homozygotes on a normal diet (J:101576)
• on a normal diet, homozygotes display significantly increased plasma triglyceride levels relative to C57BL/6J control mice (J:101576)
• on an atherosclerotic diet, homozygotes show a further significant increase in plasma triglyceride levels relative to homozygotes on a normal diet (J:101576)
• homozygotes develop hyperlipidemia; however, HDL cholesterol levels, body weight and blood glucose remain unchanged relative to C57BL/6J control mice on a normal diet, with no further differences noted on an atheroscletoric diet (J:101576)
• homozygotes develop hyperlipidemia; however, HDL cholesterol levels, body weight and blood glucose remain unchanged relative to C57BL/6J control mice on a normal diet, with no further differences noted on an atheroscletoric diet (J:101576)
• 1 of 11 aged mice on a normal diet develops cerebral xanthoma (J:43846)
• 1 of 11 aged mice on a normal diet develops cerebral xanthoma (J:43846)
• eruptive xanthomas on shoulder and back areas with lipids and extracellular matix as the predominant components (J:73202)
• eruptive xanthomas on shoulder and back areas with lipids and extracellular matix as the predominant components (J:73202)
• activity of cholesterol synthesis enzyme HMG-CoA reductase is reduced up to 60% in aging mice compared to 30% in wild-type aging mice (J:73202)
• activity of cholesterol synthesis enzyme HMG-CoA reductase is reduced up to 60% in aging mice compared to 30% in wild-type aging mice (J:73202)

growth/size/body
• at 13 months, homozygotes show a 22% reduction in body weight relative to wild-type mice (34.5 0.9 vs. 44.5 1.1 g) (J:108154)
• at 13 months, homozygotes show a 22% reduction in body weight relative to wild-type mice (34.5 0.9 vs. 44.5 1.1 g) (J:108154)
• nose to rump length less than controls at both 1 and 3 months (J:136630)
• nose to rump length less than controls at both 1 and 3 months (J:136630)
• body weight was less than controls at 3 months but identical at 8 months (J:136630)
• body weight was less than controls at 3 months but identical at 8 months (J:136630)

hematopoietic system
• at 13 months, awake, unanesthetized homozygotes display slightly but significantly reduced hematocrits ( 11%) relative to wild-type mice at 41.7 1.1% vs 46.6 0.4%; in contrast, systolic blood pressures remain unaffected (140 7.6 mmHg vs 136 7.4 mmHg) (J:108154)
• at 13 months, awake, unanesthetized homozygotes display slightly but significantly reduced hematocrits ( 11%) relative to wild-type mice at 41.7 1.1% vs 46.6 0.4%; in contrast, systolic blood pressures remain unaffected (140 7.6 mmHg vs 136 7.4 mmHg) (J:108154)
• decreased relative to controls (J:133606)
• decreased relative to controls (J:133606)
• with induction of SLE by cGVH, levels are slightly decreased compared to wild-type (J:133606)
• with induction of SLE by cGVH, levels are slightly decreased compared to wild-type (J:133606)
• newly formed B cells are significantly increased compared to wild-type (J:133606)
• newly formed B cells are significantly increased compared to wild-type (J:133606)
• increased 2-fold compared to wild-type (J:133606)
• increased 2-fold compared to wild-type (J:133606)
• increased numbers of cytokine producing T cells (J:47027)
• increased numbers of cytokine producing T cells (J:47027)
• clusters of CD4+ cells found in fatty streak lesions (J:47027)
• ratio of Th2 to Th1 cells is increased from 4.4 to 11.4 on a normal diet and up to 20.9 on a high cholesterol diet (J:47027)
• clusters of CD4+ cells found in fatty streak lesions (J:47027)
• ratio of Th2 to Th1 cells is increased from 4.4 to 11.4 on a normal diet and up to 20.9 on a high cholesterol diet (J:47027)
• increased spleen weight while the thymus weight remains normal (J:61564)
• increased spleen weight while the thymus weight remains normal (J:61564)
• spleen cells display polyclonal B cell activation, with increased expression of MHC II, Fas, and CD86 and lower expression of CD21, CD22, and CD23 (J:133606)
• spleen cells display polyclonal B cell activation, with increased expression of MHC II, Fas, and CD86 and lower expression of CD21, CD22, and CD23 (J:133606)
• mutants with cGVH-induced SLE show greatly increased levels compared to wild-type controls or untreated mutants (J:133606)
• mutants with cGVH-induced SLE show greatly increased levels compared to wild-type controls or untreated mutants (J:133606)
• IgM response to tetanus toxoid is significantly increased as compared to controls (J:61564)
• IgM response to tetanus toxoid is significantly increased as compared to controls (J:61564)

cellular
• regular exercise fails to reduce endogenous oxidant load and mitochondrial damage in hypercholesterolemic mutant mice (J:97385)
• in contrast, regular exercise results in reduced mitochondrial damage and oxidant load and increased SOD2 and adenine nucleotide translocator activities in normocholesterolemic control mice (J:97385)
• regular exercise fails to reduce endogenous oxidant load and mitochondrial damage in hypercholesterolemic mutant mice (J:97385)
• in contrast, regular exercise results in reduced mitochondrial damage and oxidant load and increased SOD2 and adenine nucleotide translocator activities in normocholesterolemic control mice (J:97385)

hearing/vestibular/ear
• endothelial nitric oxide synthase (eNOS) in mutant cochlea is distinctly reduced (J:101576)
• endothelial nitric oxide synthase (eNOS) in mutant cochlea is distinctly reduced (J:101576)
• on an atherosclerotic diet, homozygotes display a sclerosed and atrophic basilar membrane (J:101576)
• on an atherosclerotic diet, homozygotes display a sclerosed and atrophic basilar membrane (J:101576)
• at 24 weeks, homozygotes fed a normal diet show almost complete loss of IHCs in the basal turn and some IHC loss in the middle turn (J:101576)
• IHC loss at the base turn is exacerbated by an atherosclerotic diet (J:101576)
• at 24 weeks, homozygotes fed a normal diet show almost complete loss of IHCs in the basal turn and some IHC loss in the middle turn (J:101576)
• IHC loss at the base turn is exacerbated by an atherosclerotic diet (J:101576)
• at 24 weeks, homozygotes fed a normal diet show almost complete loss of OHCs in the basal turn and some OHC loss in the middle turn (J:101576)
• OHC loss at the base turn is exacerbated by an atherosclerotic diet (J:101576)
• at 24 weeks, homozygotes fed a normal diet show almost complete loss of OHCs in the basal turn and some OHC loss in the middle turn (J:101576)
• OHC loss at the base turn is exacerbated by an atherosclerotic diet (J:101576)
• at 24 weeks, homozygotes fed a normal diet show significant degeneration of the organ of Corti in the basal turn while the middle turn is relatively normal (J:101576)
• degeneration of the organ of Corti is excerbated by an atherosclerotic diet, with complete loss noted in the basal turn in some animals (J:101576)
• at 24 weeks, homozygotes fed a normal diet show significant degeneration of the organ of Corti in the basal turn while the middle turn is relatively normal (J:101576)
• degeneration of the organ of Corti is excerbated by an atherosclerotic diet, with complete loss noted in the basal turn in some animals (J:101576)
• on an atherosclerotic diet, homozygotes display a sclerosed and atrophic stria vascularis (J:101576)
• on an atherosclerotic diet, homozygotes display a sclerosed and atrophic stria vascularis (J:101576)
• on an atherosclerotic diet, homozygotes display a sclerosed and atrophic tectorial membrane (J:101576)
• on an atherosclerotic diet, homozygotes display a sclerosed and atrophic tectorial membrane (J:101576)
• at 10 weeks, homozygotes fed a normal diet display higher ABR thresholds than C57BL/6J control mice at all test frequencies, with more hearing loss noted at 32 kHz; by 24 weeks, further hearing loss is detected at all test stimuli levels (J:101576)
• homozygotes fed an atherosclerotic diet show higher ABR thresholds than homozygotes fed a normal diet (J:101576)
• at 10 weeks, homozygotes fed a normal diet display higher ABR thresholds than C57BL/6J control mice at all test frequencies, with more hearing loss noted at 32 kHz; by 24 weeks, further hearing loss is detected at all test stimuli levels (J:101576)
• homozygotes fed an atherosclerotic diet show higher ABR thresholds than homozygotes fed a normal diet (J:101576)
• homozygotes fed a normal diet display hearing loss esp. at high frequencies as compared with C57BL/6J control mice (J:101576)
• a high positive correlation between ABR thresholds at 16 and 8 kHz, or click and atherosclerotic lesions, and atherosclerotic plaque area of the aorta, and plasma total choelsterol levels is observed in both normal diet and high-fat diet homozygotes (J:101576)
• homozygotes fed a normal diet display hearing loss esp. at high frequencies as compared with C57BL/6J control mice (J:101576)
• a high positive correlation between ABR thresholds at 16 and 8 kHz, or click and atherosclerotic lesions, and atherosclerotic plaque area of the aorta, and plasma total choelsterol levels is observed in both normal diet and high-fat diet homozygotes (J:101576)

nervous system
• impaired blood-brain barrier and blood-nerve barrier as indicated by extensive extravasation of serum proteins into sciatic nerve, spinal cord and cerebellum and occasional extravasation into cortex and subcortex (J:69455)
• impaired blood-brain barrier and blood-nerve barrier as indicated by extensive extravasation of serum proteins into sciatic nerve, spinal cord and cerebellum and occasional extravasation into cortex and subcortex (J:69455)
• at 24 weeks, homozygotes fed a normal diet show almost complete loss of IHCs in the basal turn and some IHC loss in the middle turn (J:101576)
• IHC loss at the base turn is exacerbated by an atherosclerotic diet (J:101576)
• at 24 weeks, homozygotes fed a normal diet show almost complete loss of IHCs in the basal turn and some IHC loss in the middle turn (J:101576)
• IHC loss at the base turn is exacerbated by an atherosclerotic diet (J:101576)
• at 24 weeks, homozygotes fed a normal diet show almost complete loss of OHCs in the basal turn and some OHC loss in the middle turn (J:101576)
• OHC loss at the base turn is exacerbated by an atherosclerotic diet (J:101576)
• at 24 weeks, homozygotes fed a normal diet show almost complete loss of OHCs in the basal turn and some OHC loss in the middle turn (J:101576)
• OHC loss at the base turn is exacerbated by an atherosclerotic diet (J:101576)
• at 24 weeks, homozygotes fed a normal diet show a reduced number of spiral ganglion cells in the basal turn of the cochlea (J:101576)
• loss of ganglion cells is excerbated by an atherosclerotic diet (J:101576)
• at 24 weeks, homozygotes fed a normal diet show a reduced number of spiral ganglion cells in the basal turn of the cochlea (J:101576)
• loss of ganglion cells is excerbated by an atherosclerotic diet (J:101576)

immune system
• decreased relative to controls (J:133606)
• decreased relative to controls (J:133606)
• with induction of SLE by cGVH, levels are slightly decreased compared to wild-type (J:133606)
• with induction of SLE by cGVH, levels are slightly decreased compared to wild-type (J:133606)
• newly formed B cells are significantly increased compared to wild-type (J:133606)
• newly formed B cells are significantly increased compared to wild-type (J:133606)
• increased 2-fold compared to wild-type (J:133606)
• increased 2-fold compared to wild-type (J:133606)
• increased numbers of cytokine producing T cells (J:47027)
• increased numbers of cytokine producing T cells (J:47027)
• clusters of CD4+ cells found in fatty streak lesions (J:47027)
• ratio of Th2 to Th1 cells is increased from 4.4 to 11.4 on a normal diet and up to 20.9 on a high cholesterol diet (J:47027)
• clusters of CD4+ cells found in fatty streak lesions (J:47027)
• ratio of Th2 to Th1 cells is increased from 4.4 to 11.4 on a normal diet and up to 20.9 on a high cholesterol diet (J:47027)
• increased spleen weight while the thymus weight remains normal (J:61564)
• increased spleen weight while the thymus weight remains normal (J:61564)
• aortae show macrophage and T cell extravasation within atherosclerotic lesions (J:91058)
• aortae show macrophage and T cell extravasation within atherosclerotic lesions (J:91058)
• spleen cells display polyclonal B cell activation, with increased expression of MHC II, Fas, and CD86 and lower expression of CD21, CD22, and CD23 (J:133606)
• spleen cells display polyclonal B cell activation, with increased expression of MHC II, Fas, and CD86 and lower expression of CD21, CD22, and CD23 (J:133606)
• decreased antigen specific delayed hypersensitivity response (J:61564)
• decreased antigen specific delayed hypersensitivity response (J:61564)
• mutants with cGVH-induced SLE show greatly increased levels compared to wild-type controls or untreated mutants (J:133606)
• mutants with cGVH-induced SLE show greatly increased levels compared to wild-type controls or untreated mutants (J:133606)
• IgM response to tetanus toxoid is significantly increased as compared to controls (J:61564)
• IgM response to tetanus toxoid is significantly increased as compared to controls (J:61564)
• production is reduced when fed a high cholesterol diet (J:47027)
• production is reduced when fed a high cholesterol diet (J:47027)
• after induction of cGVH-SLE, IgG and IgM anti-oxidized LDL and anti-cardiolipin antibodies are increased compared to wild-type or Apoe-null controls (J:133606)
• after induction of cGVH-SLE, IgG and IgM anti-oxidized LDL and anti-cardiolipin antibodies are increased compared to wild-type or Apoe-null controls (J:133606)
• after induction of cGVH-SLE, mice display greatly increased levels of anti-chromatin antibodies compared to wild-type controls or non-cGVH mutants (J:133606)
• after induction of cGVH-SLE, mice display greatly increased levels of anti-chromatin antibodies compared to wild-type controls or non-cGVH mutants (J:133606)
• after induction of cGVH-SLE, mice display greatly increased levels compared to wild-type controls or non-cGVH-SLE mutants (J:133606)
• after induction of cGVH-SLE, mice display greatly increased levels compared to wild-type controls or non-cGVH-SLE mutants (J:133606)

behavior/neurological
• elevated thigmotaxis in Morris maze tests (J:120203)
• elevated thigmotaxis in Morris maze tests (J:120203)
• longer latency to find the platform in Morris maze tests (J:120203)
• slow to acquire a preference for the target quadrant and the magnitude of the preference is always less than controls (J:120203)
• longer latency to find the platform in Morris maze tests (J:120203)
• slow to acquire a preference for the target quadrant and the magnitude of the preference is always less than controls (J:120203)

renal/urinary system
• arterioles of the vascular pole show a "foamy" degeneration of smooth muscle cells (J:125978)
• arterioles of the vascular pole show a "foamy" degeneration of smooth muscle cells (J:125978)
• at times mesangiolysis is associated with ballooning dilatation ("microaneurysm") of adjacent glomerular capillaries (J:125978)
• at times mesangiolysis is associated with ballooning dilatation ("microaneurysm") of adjacent glomerular capillaries (J:125978)
• increased glomerular tuft area (J:125978)
• glomerular cell numbers are increased (J:125978)
• increased glomerular tuft area (J:125978)
• glomerular cell numbers are increased (J:125978)
• at times mesangiolysis is associated with ballooning dilatation ("microaneurysm") of adjacent glomerular capillaries (J:125978)
• at times mesangiolysis is associated with ballooning dilatation ("microaneurysm") of adjacent glomerular capillaries (J:125978)
• lipid droplets filling glomerular capillary lumina at 36 weeks in about 50% of mice (J:125978)
• such thrombus-like structures commonly dsiplay a laminated appearance with adjacent foam cells in the mesangium (J:125978)
• lipid droplets filling glomerular capillary lumina at 36 weeks in about 50% of mice (J:125978)
• such thrombus-like structures commonly dsiplay a laminated appearance with adjacent foam cells in the mesangium (J:125978)
• progressive increase in glomerular matrix, already evident at 24 weeks, associated with accumulation of laminin and collagen IV (J:125978)
• progressive increase in glomerular matrix, already evident at 24 weeks, associated with accumulation of laminin and collagen IV (J:125978)
• loss of mesangial matrix sometimes at 36 weeks but never at 24 weeks or in controls (J:125978)
• loss of mesangial matrix sometimes at 36 weeks but never at 24 weeks or in controls (J:125978)
• glomerular foam cells in the mesangium, capillary lumina and within the glomerular stalk close to the vascular pole (J:125978)
• lipid deposits in arteriolar walls in the vascular poles (J:125978)
• lipid droplets filling glomerular capillary lumina at 36 weeks in about 50% of mice (J:125978)
• glomerular foam cells in the mesangium, capillary lumina and within the glomerular stalk close to the vascular pole (J:125978)
• lipid deposits in arteriolar walls in the vascular poles (J:125978)
• lipid droplets filling glomerular capillary lumina at 36 weeks in about 50% of mice (J:125978)

liver/biliary system
• no significant change in serum alanine transaminase with high fat diet as is seen in controls (marker for liver damage) (J:104609)
• hepatic uptake of LDL is increased two fold (J:104609)
• no significant change in serum alanine transaminase with high fat diet as is seen in controls (marker for liver damage) (J:104609)
• hepatic uptake of LDL is increased two fold (J:104609)

vision/eye
• perinuclear vacuolation on a high cholesterol diet (J:70245)
• perinuclear vacuolation on a high cholesterol diet (J:70245)
• cell numbers reduced (J:70245)
• cell numbers reduced (J:70245)
• cell numbers reduced (J:70245)
• cell numbers reduced (J:70245)
• implicit times increased for a and b waves of dark adapted electroretinogram (J:70245)
• wave amplitudes attenuated for a and b waves of dark adapted electroretinogram (J:70245)
• implicit times increased for a and b waves of dark adapted electroretinogram (J:70245)
• wave amplitudes attenuated for a and b waves of dark adapted electroretinogram (J:70245)

taste/olfaction
• preference for plain water over 0.1% iso-amyl alcohol moderate compared to the strong preference shown by controls (J:89344)
• slower than control to find buried food pellet although found pellets visually more rapidly (J:89344)
• latency to taste vanillin-cued quinine significantly increased only at day 5 (J:89344)
• preference for plain water over 0.1% iso-amyl alcohol moderate compared to the strong preference shown by controls (J:89344)
• slower than control to find buried food pellet although found pellets visually more rapidly (J:89344)
• latency to taste vanillin-cued quinine significantly increased only at day 5 (J:89344)

skeleton
• higher bone mineralization density in vertebral bodies (J:111209)
• increased bone volume to tissue volume ratio (J:111209)
• higher bone mineralization density in vertebral bodies (J:111209)
• increased bone volume to tissue volume ratio (J:111209)
• in vertebral bodies and tibia (J:111209)
• in vertebral bodies and tibia (J:111209)
• increased number of trabeculae (J:111209)
• increased number of trabeculae (J:111209)
• increased rate of bone formation (J:111209)
• increased rate of bone formation (J:111209)

respiratory system
• fewer but larger alveoli at 3 months of age (J:136630)
• less surface area to volume (J:136630)
• fewer but larger alveoli at 3 months of age (J:136630)
• less surface area to volume (J:136630)
• percent increase in hysteresivity with age greater than in controls (J:136630)
• percent increase in hysteresivity with age greater than in controls (J:136630)
• lung volume similar to controls at 3 months but 2.5 fold greater at 8 months of age (J:136630)
• lung volume similar to controls at 3 months but 2.5 fold greater at 8 months of age (J:136630)
• resistance to airflow greater than controls at 3 months but not at 8 months of age (J:136630)
• resistance to airflow greater than controls at 3 months but not at 8 months of age (J:136630)
• dynamic and static compliance greater than controls at 8 months of age (J:136630)
• dynamic and static compliance greater than controls at 8 months of age (J:136630)

integument
• progressive skin lesions, mainly seen as eruptive xanthomas on shoulder and back areas with lipids and extracellular matix as the predominant components (J:73202)
• progressive skin lesions, mainly seen as eruptive xanthomas on shoulder and back areas with lipids and extracellular matix as the predominant components (J:73202)




Genotype
MGI:3799495
hm3
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
B6.Cg-Apoetm1Unc Faslpr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• mice display greatly increased levels compared to wild-type controls or Apoe-null mice (J:133606)
• mice display greatly increased levels compared to wild-type controls or Apoe-null mice (J:133606)
• mice display greatly increased levels compared to wild-type controls or Apoe-null mice (J:133606)
• mice display greatly increased levels compared to wild-type controls or Apoe-null mice (J:133606)
• mice display greatly increased levels compared to wild-type controls or Apoe-null mice (J:133606)
• mice display greatly increased levels compared to wild-type controls or Apoe-null mice (J:133606)

homeostasis/metabolism
• significantly increased relative to wild-type controls or Fas-single mutants at 24 weeks of age; levels are higher than that of B6.129P2-Apoetm1Unc (J:133606)
• significantly increased relative to wild-type controls or Fas-single mutants at 24 weeks of age; levels are higher than that of B6.129P2-Apoetm1Unc (J:133606)

cardiovascular system
• modest increase in total area of lipid deposits in aorta compared to Apoe-null mice (J:133606)
• modest increase in total area of lipid deposits in aorta compared to Apoe-null mice (J:133606)

hematopoietic system
• mice display greatly increased levels compared to wild-type controls or Apoe-null mice (J:133606)
• mice display greatly increased levels compared to wild-type controls or Apoe-null mice (J:133606)




Genotype
MGI:3717197
hm4
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
either: B6.129P2-Apoetm1Unc/J or (involves: 129P2/OlaHsd * C57BL/6J * ICR)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• no alterations in passive avoidance learning are observed; coordination levels measured in rotorod tests are similar to wild-type (J:100975)
• no alterations in passive avoidance learning are observed; coordination levels measured in rotorod tests are similar to wild-type (J:100975)
• 6-month old female mice show subtle learning impairment in water maze task compared to transgenic mutants; 6-month old males show significantly decreased learning ability in the Morris water maze test (J:100975)
• 6-month old female mice show subtle learning impairment in water maze task compared to transgenic mutants; 6-month old males show significantly decreased learning ability in the Morris water maze test (J:100975)
• mice have fewer rearing events and shorter rearing times than wild-type controls (J:100975)
• mice have fewer rearing events and shorter rearing times than wild-type controls (J:100975)

nervous system
N
• upon 18 mg/kg kainic acid injection, significant loss of neocortical synaptophysin-positive presynaptic terminals and disruption of hippocampal axons are observed, similar to wild-type (J:55835)
• mice show significant loss of synaptophysin-positive presynaptic terminals and neuronal dendrites of the neocortex and hippocampus with age (7-9 months compared to 3-4 months), similar to wild-type (J:55835)
• upon 18 mg/kg kainic acid injection, significant loss of neocortical synaptophysin-positive presynaptic terminals and disruption of hippocampal axons are observed, similar to wild-type (J:55835)
• mice show significant loss of synaptophysin-positive presynaptic terminals and neuronal dendrites of the neocortex and hippocampus with age (7-9 months compared to 3-4 months), similar to wild-type (J:55835)
• mice exhibit age-dependent loss of synaptophysin-reactive terminals and microtubule-associated protein 2-positive neuronal dendrites in the neocortex and hippocampus, similar to wild-type (J:100975)
• mice exhibit age-dependent loss of synaptophysin-reactive terminals and microtubule-associated protein 2-positive neuronal dendrites in the neocortex and hippocampus, similar to wild-type (J:100975)




Genotype
MGI:3718006
hm5
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• in the elevated-plus maze, mice show increased anxiety with reduced time and distance moved in the open arms; mice have significantly lower number of open-arm entries than wild-type (J:101973)
• effect is age-dependent; phenotype is present in older mice, but not in young 2-4 month-old mice (J:101973)
• in the elevated-plus maze, mice show increased anxiety with reduced time and distance moved in the open arms; mice have significantly lower number of open-arm entries than wild-type (J:101973)
• effect is age-dependent; phenotype is present in older mice, but not in young 2-4 month-old mice (J:101973)
• response is higher in mice at 6 months of age compared to wild-type (J:101973)
• response is higher in mice at 6 months of age compared to wild-type (J:101973)

homeostasis/metabolism
• all males have higher plasma concentrations than wild-type after behavioral testing (J:101973)
• all males have higher plasma concentrations than wild-type after behavioral testing (J:101973)
• circulating VLDL/LDL cholesterol levels are increased compared to in Apobec1tm1Chan homozygotes and wild-type mice (J:48202)
• circulating VLDL/LDL cholesterol levels are increased compared to in Apobec1tm1Chan homozygotes and wild-type mice (J:48202)
• when fed a chow or Western-type diet for 2 weeks, mice exhibit increased serum cholesterol compared with Apobec1tm1Chan homozygotes and wild-type mice (J:48202)
• when fed a chow or Western-type diet for 2 weeks, mice exhibit increased serum cholesterol compared with Apobec1tm1Chan homozygotes and wild-type mice (J:48202)
• compared to in Tg(Eno2-APP751)10Cord Apoetm1Unc/Apoetm1Unc mice (J:133156)
• compared to in Tg(Eno2-APP751)10Cord Apoetm1Unc/Apoetm1Unc mice (J:133156)

nervous system
• compared to in Tg(Eno2-APP751)10Cord Apoetm1Unc/Apoetm1Unc mice (J:133156)
• compared to in Tg(Eno2-APP751)10Cord Apoetm1Unc/Apoetm1Unc mice (J:133156)
• mutants have lower levels of MAP 2-positive neuronal dendrites than wild-type; at 3 months, levels are similar in mutants and controls (J:101973)
• mutants have lower levels of MAP 2-positive neuronal dendrites than wild-type; at 3 months, levels are similar in mutants and controls (J:101973)

cardiovascular system
• atherosclerotic lesions begin to form in the left common carotid by 2 weeks after partial ligation of the left common carotid (J:154332)
• atherosclerotic lesion development is well advanced by 4-6 weeks after partial ligation of the left common carotid (J:154332)
• atherosclerotic lesions begin to form in the left common carotid by 2 weeks after partial ligation of the left common carotid (J:154332)
• atherosclerotic lesion development is well advanced by 4-6 weeks after partial ligation of the left common carotid (J:154332)
• bone marrow transplanted into Apoa1tm1Unc homozygotes confer susceptibility to atherosclerosis (J:107390)
• bone marrow transplanted into Apoa1tm1Unc homozygotes confer susceptibility to atherosclerosis (J:107390)
• impaired vasodilation induced by sodium nitroprusside 7 days after partial ligation of the left common carotid (J:154332)
• impaired vasodilation induced by sodium nitroprusside 7 days after partial ligation of the left common carotid (J:154332)

muscle
• impaired vasodilation induced by sodium nitroprusside 7 days after partial ligation of the left common carotid (J:154332)
• impaired vasodilation induced by sodium nitroprusside 7 days after partial ligation of the left common carotid (J:154332)




Genotype
MGI:3764959
hm6
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Morphology of aortic lesions in Apoetm1Unc/Apoetm1Unc and Apoetm1Unc/Apoetm1Unc Ttpatm1Far/Ttpatm1Far mice

cardiovascular system
• most severe in the aortic arch region (J:66419)
• most severe in the aortic arch region (J:66419)




Genotype
MGI:3714936
hm7
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• fatty streaks with foam cells are found in the proximal aorta of 3-8 month old mice fed normal chow (J:16573)
• the foam cells are often adjacent to valve attachment sites and can form multi-layers (J:16573)
• lesions get bigger with age and near total occlusion at the entrance of a coronary artery can be observed at 8 months of age (J:16573)
• fatty streaks with foam cells are found in the proximal aorta of 3-8 month old mice fed normal chow (J:16573)
• the foam cells are often adjacent to valve attachment sites and can form multi-layers (J:16573)
• lesions get bigger with age and near total occlusion at the entrance of a coronary artery can be observed at 8 months of age (J:16573)
• 75% of mice develop lesions in the aortic arch with most females and some males having calcification within the lesions (J:40136)
• aortic cartilaginous metaplasia is noted in the most severely affected mice (J:40136)
• 75% of mice develop lesions in the aortic arch with most females and some males having calcification within the lesions (J:40136)
• aortic cartilaginous metaplasia is noted in the most severely affected mice (J:40136)
• greater than in wild-type (J:80689)
• greater than in wild-type (J:80689)

homeostasis/metabolism
• mean HDL levels (33 mg/dl) are 45% of that found in controls (J:16573)
• mean HDL levels (33 mg/dl) are 45% of that found in controls (J:16573)
• mean total cholesterol levels are elevated about 5-fold over wild-type to 434 mg/dl (J:16573)
• mean total cholesterol levels are elevated about 5-fold over wild-type to 434 mg/dl (J:16573)
• total cholesterol levels are about 4-fold higher than controls with a mean of 379 mg/dl (J:40136)
• total cholesterol levels are about 4-fold higher than controls with a mean of 379 mg/dl (J:40136)
• relative to wild-type (J:80689)
• relative to wild-type (J:80689)
• mice have elevated levels of LDL in the blood (J:16573)
• mice have elevated levels of LDL in the blood (J:16573)
• the majority of lipoprotein particles in the blood are in the VLDL size range (J:16573)
• the majority of lipoprotein particles in the blood are in the VLDL size range (J:16573)
• circulating triglyceride levels are 123 mg/dl compared to 73 mg/dl in controls (J:16573)
• circulating triglyceride levels are 123 mg/dl compared to 73 mg/dl in controls (J:16573)
• relative to wild-type (J:80689)
• relative to wild-type (J:80689)
• relative to wild-type (J:80689)
• relative to wild-type (J:80689)
• amount of PGE2 in aortas is 4X higher than in controls (J:125376)
• PGE2 level doubles on a high fat diet (J:125376)
• amount of PGE2 in aortas is 4X higher than in controls (J:125376)
• PGE2 level doubles on a high fat diet (J:125376)

nervous system
• elevated cholesterol in the exofacial leaflet of the synaptic plasma membrane but not so high as for Ldlr deficient mice (J:43043)
• cholesterol levels in the cytofacial leaflet are reduced (J:43043)
• elevated cholesterol in the exofacial leaflet of the synaptic plasma membrane but not so high as for Ldlr deficient mice (J:43043)
• cholesterol levels in the cytofacial leaflet are reduced (J:43043)
• astrocytes secrete less phospholipids or free cholesterol compared to wild-type astrocytes (J:58019)
• astrocytes secrete less phospholipids or free cholesterol compared to wild-type astrocytes (J:58019)

immune system
• isolated small foci of mononuclear cells are present in lung after 6 weeks of high-fat feeding (J:83615)
• isolated small foci of mononuclear cells are present in lung after 6 weeks of high-fat feeding (J:83615)

respiratory system
• isolated small foci of mononuclear cells are present in lung after 6 weeks of high-fat feeding (J:83615)
• isolated small foci of mononuclear cells are present in lung after 6 weeks of high-fat feeding (J:83615)

Mouse Models of Human Disease
OMIM ID Ref(s)
Apolipoprotein E; APOE 107741 J:16573




Genotype
MGI:4358709
hm8
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• increase in APOB-48 (J:75567)
• increase in APOB-48 (J:75567)
• the HDL phospholipid fraction is enriched in 16:0 and 18:0 species and contains less 20:4 and 22:6 species compared to Ldlrtm1Her single mutants (J:75567)
• the HDL phospholipid fraction is enriched in 16:0 and 18:0 species and contains less 20:4 and 22:6 species compared to Ldlrtm1Her single mutants (J:75567)
• increase in the APOB lipoprotein cholesterol level compared to wild-type controls (J:75567)
• there is a 2.3 fold increase in the ratio of saturated + monounsaturated/polyunsaturated cholesterol ester fatty acid species compared to Ldlrtm1Her single mutants (J:75567)
• the ratio of saturated + monounsaturated/polyunsaturated cholesterol ester fatty acid species in the LDL fraction is significantly increased compared to Ldlrtm1Her single mutants (J:75567)
• increase in the APOB lipoprotein cholesterol level compared to wild-type controls (J:75567)
• there is a 2.3 fold increase in the ratio of saturated + monounsaturated/polyunsaturated cholesterol ester fatty acid species compared to Ldlrtm1Her single mutants (J:75567)
• the ratio of saturated + monounsaturated/polyunsaturated cholesterol ester fatty acid species in the LDL fraction is significantly increased compared to Ldlrtm1Her single mutants (J:75567)
• about a 50% decrease in HDL compared to controls (J:75567)
• about a 50% decrease in HDL compared to controls (J:75567)
• increased total cholesterol and esterfied cholesterol levels in the plasma (J:75567)
• increased total cholesterol and esterfied cholesterol levels in the plasma (J:75567)




Genotype
MGI:3822450
hm9
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• lesions are observed in aortas of nontransgenic mice (J:130658)
• lesions are observed in aortas of nontransgenic mice (J:130658)




Genotype
MGI:5449935
hm10
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Data Sources
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
WTSI (J:175295)
WTSI (J:175295)
WTSI (J:175295)
WTSI (J:175295)

hematopoietic system
WTSI (J:175295)
WTSI (J:175295)

homeostasis/metabolism
WTSI (J:175295)
WTSI (J:175295)
WTSI (J:175295)
WTSI (J:175295)
EuPh (J:165965)
EuPh (J:165965)
WTSI (J:175295)
WTSI (J:175295)
WTSI (J:175295)
WTSI (J:175295)
EuPh (J:165965)
EuPh (J:165965)
WTSI (J:175295)
WTSI (J:175295)
EuPh (J:165965)
EuPh (J:165965)
WTSI (J:175295)
WTSI (J:175295)

immune system

growth/size/body
WTSI (J:175295)
WTSI (J:175295)
WTSI (J:175295)
WTSI (J:175295)




Genotype
MGI:3836194
ht11
Allelic
Composition
Apoetm1Unc/Apoe+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• circulating triglyceride levels are 39% higher than in wild-type controls (J:16573)
• circulating triglyceride levels are 39% higher than in wild-type controls (J:16573)




Genotype
MGI:5449957
ht12
Allelic
Composition
Apoetm1Unc/Apoe+
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Data Sources
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
WTSI (J:175295)
WTSI (J:175295)

immune system




Genotype
MGI:3716843
ht13
Allelic
Composition
Apoeshl/Apoetm1Unc
Genetic
Background
involves: 129P2/OlaHsd * KOR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoeshl mutation (1 available); any Apoe mutation (64 available)
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• in all mice (J:54051)
• in all mice (J:54051)
• in all mice (J:54051)
• in all mice (J:54051)




Genotype
MGI:4818410
cn14
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Gja5tm1Mchn/Gja5tm1Mchn
Tg(TIE2-lacZ)182Sato/0
Genetic
Background
involves: 129P2/OlaHsd * BALB/c * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Gja5tm1Mchn mutation (0 available); any Gja5 mutation (5 available)
Tg(TIE2-lacZ)182Sato mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• mice exhibit normal mean arterial pressure, heart rate, and endothelium-dependent vasomotor responses to KCl and norepinephrine (J:162224)
• mice exhibit normal mean arterial pressure, heart rate, and endothelium-dependent vasomotor responses to KCl and norepinephrine (J:162224)
• whether fed a high-fat or standard diet, mice exhibit increased lipid staining in the thoracoabdominal aortas compared with Apoetm1Unc homozygotes (J:162224)
• whether fed a high-fat or standard diet, mice exhibit accelerated atherosclerosis compared with Apoetm1Unc homozygotes (J:162224)
• whether fed a high-fat or standard diet, mice exhibit increased lipid staining in the thoracoabdominal aortas compared with Apoetm1Unc homozygotes (J:162224)
• whether fed a high-fat or standard diet, mice exhibit accelerated atherosclerosis compared with Apoetm1Unc homozygotes (J:162224)

immune system
• LPS-treated mice exhibit increased inflammatory cell recruitment, mostly neutrophils, into the alveolar spaces compared with similarly treated Apoetm1Unc homozygotes (J:162224)
• LPS-treated mice exhibit increased inflammatory cell recruitment, mostly neutrophils, into the alveolar spaces compared with similarly treated Apoetm1Unc homozygotes (J:162224)
• LPS-treated mice exhibit increased inflammatory cell recruitment, mostly neutrophils, into the alveolar spaces compared with similarly treated Apoetm1Unc homozygotes (J:162224)
• LPS-treated mice exhibit increased inflammatory cell recruitment, mostly neutrophils, into the alveolar spaces compared with similarly treated Apoetm1Unc homozygotes (J:162224)

respiratory system
• LPS-treated mice exhibit increased inflammatory cell recruitment, mostly neutrophils, into the alveolar spaces compared with similarly treated Apoetm1Unc homozygotes (J:162224)
• LPS-treated mice exhibit increased inflammatory cell recruitment, mostly neutrophils, into the alveolar spaces compared with similarly treated Apoetm1Unc homozygotes (J:162224)

hematopoietic system
• LPS-treated mice exhibit increased inflammatory cell recruitment, mostly neutrophils, into the alveolar spaces compared with similarly treated Apoetm1Unc homozygotes (J:162224)
• LPS-treated mice exhibit increased inflammatory cell recruitment, mostly neutrophils, into the alveolar spaces compared with similarly treated Apoetm1Unc homozygotes (J:162224)




Genotype
MGI:5552967
cn15
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Klf15tm2Jain/Klf15tm2Jain
Tg(Tagln-cre)1Jjl/0
Genetic
Background
involves: 129P2/OlaHsd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Klf15tm2Jain mutation (0 available); any Klf15 mutation (1 available)
Tg(Tagln-cre)1Jjl mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
N
• mice fed a high fat diet exhibit the same circulating levels of cholesterol and triglycerides as in Apoetm1Unc homozygotes (J:203920)
• mice fed a high fat diet exhibit the same circulating levels of cholesterol and triglycerides as in Apoetm1Unc homozygotes (J:203920)

immune system
• increased macrophage in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes (J:203920)
• increased macrophage in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes (J:203920)
• increased macrophage in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes (J:203920)
• increased macrophage in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes (J:203920)

cardiovascular system
• in mice fed a high fat diet compared with Apoetm1Unc homozygotes (J:203920)
• in mice fed a high fat diet compared with Apoetm1Unc homozygotes (J:203920)
• decreased vascular smooth muscle cells in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes (J:203920)
• decreased vascular smooth muscle cells in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes (J:203920)
• increased macrophage in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes (J:203920)
• increased macrophage in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes (J:203920)

muscle
• decreased vascular smooth muscle cells in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes (J:203920)
• decreased vascular smooth muscle cells in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes (J:203920)

hematopoietic system
• increased macrophage in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes (J:203920)
• increased macrophage in the aortic wall and atherosclerotic lesions of mice fed a high fat diet with Apoetm1Unc homozygotes (J:203920)




Genotype
MGI:4420802
cx16
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cdkn1atm1Tyj/Cdkn1atm1Tyj
Genetic
Background
B6.129-Apoetm1Unc Cdkn1atm1Tyj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Cdkn1atm1Tyj mutation (3 available); any Cdkn1a mutation (45 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• angiotensin II-treated mice exhibit less of an increase in mortality compared with similarly treated Apoetm1Unc homozygotes (J:125247)
• angiotensin II-treated mice exhibit less of an increase in mortality compared with similarly treated Apoetm1Unc homozygotes (J:125247)

cardiovascular system
• angiotensin II-treated mice exhibit a smaller increase in plaque area, plaque grade, aortic aneurysms, atheroma, and mortality but an increase in proliferation of vascular smooth muscle cells compared with similarly treated Apoetm1Unc homozygotes (J:125247)
• angiotensin II-treated mice exhibit a smaller increase in plaque area, plaque grade, aortic aneurysms, atheroma, and mortality but an increase in proliferation of vascular smooth muscle cells compared with similarly treated Apoetm1Unc homozygotes (J:125247)
• treatment with angiotensin II induces less vascular smooth muscle cell senescence and more proliferation compared to in similarly treated Apoetm1Unc homozygotes (J:125247)
• treatment with angiotensin II induces less vascular smooth muscle cell senescence and more proliferation compared to in similarly treated Apoetm1Unc homozygotes (J:125247)

homeostasis/metabolism
• angiotensin II-treated mice exhibit a smaller increase in plaque area, plaque grade, aortic aneurysms, atheroma, and mortality but an increase in proliferation and decrease in senescence of vascular smooth muscle cells compared with similarly treated Apoetm1Unc homozygotes (J:125247)
• angiotensin II-treated mice exhibit a smaller increase in plaque area, plaque grade, aortic aneurysms, atheroma, and mortality but an increase in proliferation and decrease in senescence of vascular smooth muscle cells compared with similarly treated Apoetm1Unc homozygotes (J:125247)

cellular
• treatment with angiotensin II induces less vascular smooth muscle cell senescence compared to in similarly treated Apoetm1Unc homozygotes (J:125247)
• treatment with angiotensin II induces less vascular smooth muscle cell senescence compared to in similarly treated Apoetm1Unc homozygotes (J:125247)

muscle
• treatment with angiotensin II induces less vascular smooth muscle cell senescence and more proliferation compared to in similarly treated Apoetm1Unc homozygotes (J:125247)
• treatment with angiotensin II induces less vascular smooth muscle cell senescence and more proliferation compared to in similarly treated Apoetm1Unc homozygotes (J:125247)




Genotype
MGI:3527869
cx17
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cx3cl1tm1Sgs/Cx3cl1tm1Sgs
Genetic
Background
B6.129-Apoetm1Unc Cx3cl1tm1Sgs
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Cx3cl1tm1Sgs mutation (0 available); any Cx3cl1 mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• brachiocephalic artery lesion area is reduced by about 85% at 200 um and 400 um but not at 600 um from its branching site into the carotid and subclavian arteries in female double homozygotes compared to Apoe single homozygotes (J:95279)
• in male double homozygotes brachiocephalic artery lesion area is reduced by 82% at 200 um, 58% at 400 um, and 59% at 600 um (J:95279)
• aortic root lesion area is reduced by about 30% in double homozygous females at 12 weeks of age but not in males at 12 weeks or in either sex at 16 weeks (J:95279)
• lesions are less advanced than in Apoe single homozygotes and are composed almost entirely of foam cells (J:95279)
• brachiocephalic artery lesion area is reduced by about 85% at 200 um and 400 um but not at 600 um from its branching site into the carotid and subclavian arteries in female double homozygotes compared to Apoe single homozygotes (J:95279)
• in male double homozygotes brachiocephalic artery lesion area is reduced by 82% at 200 um, 58% at 400 um, and 59% at 600 um (J:95279)
• aortic root lesion area is reduced by about 30% in double homozygous females at 12 weeks of age but not in males at 12 weeks or in either sex at 16 weeks (J:95279)
• lesions are less advanced than in Apoe single homozygotes and are composed almost entirely of foam cells (J:95279)

immune system
• atherosclerotic lesions are composed almost entirely of foam cells (J:95279)
• atherosclerotic lesions are composed almost entirely of foam cells (J:95279)
• macrophage accumulation is reduced by 80% in the brachiocephalic artery at 200 um from its branching site into the carotid and subclavian arteries (J:95279)
• macrophage accumulation is reduced by 80% in the brachiocephalic artery at 200 um from its branching site into the carotid and subclavian arteries (J:95279)

hematopoietic system
• atherosclerotic lesions are composed almost entirely of foam cells (J:95279)
• atherosclerotic lesions are composed almost entirely of foam cells (J:95279)
• macrophage accumulation is reduced by 80% in the brachiocephalic artery at 200 um from its branching site into the carotid and subclavian arteries (J:95279)
• macrophage accumulation is reduced by 80% in the brachiocephalic artery at 200 um from its branching site into the carotid and subclavian arteries (J:95279)

cellular
• atherosclerotic lesions are composed almost entirely of foam cells (J:95279)
• atherosclerotic lesions are composed almost entirely of foam cells (J:95279)
• macrophage accumulation is reduced by 80% in the brachiocephalic artery at 200 um from its branching site into the carotid and subclavian arteries (J:95279)
• macrophage accumulation is reduced by 80% in the brachiocephalic artery at 200 um from its branching site into the carotid and subclavian arteries (J:95279)




Genotype
MGI:3618277
cx18
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cx3cr1tm1Zm/Cx3cr1tm1Zm
Genetic
Background
B6.129-Apoetm1Unc Cx3cr1tm1Zm
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Cx3cr1tm1Zm mutation (1 available); any Cx3cr1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• lesion area in the aorta and aortic sinus is decreased by about 50% compared to mice homozygous for the Apoe allele only; however the accumulation of smooth muscle cells and collagen within the plaque is similar to wild-type (J:103047)
• a 50% reduction is seen in the aortic sinus area containing monocyte-macrophage markers (J:103047)
• lesion area in the aorta and aortic sinus is decreased by about 50% compared to mice homozygous for the Apoe allele only; however the accumulation of smooth muscle cells and collagen within the plaque is similar to wild-type (J:103047)
• a 50% reduction is seen in the aortic sinus area containing monocyte-macrophage markers (J:103047)




Genotype
MGI:3618279
cx19
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cx3cr1tm1Zm/Cx3cr1+
Genetic
Background
B6.129-Apoetm1Unc Cx3cr1tm1Zm
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Cx3cr1tm1Zm mutation (1 available); any Cx3cr1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• lesion area in the thoracic aorta is decreased by about 50% compared to mice homozygous for the Apoe allele only (J:103047)
• lesion area in the thoracic aorta is decreased by about 50% compared to mice homozygous for the Apoe allele only (J:103047)




Genotype
MGI:4938323
cx20
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ifngtm1Ts/Ifngtm1Ts
Genetic
Background
B6.129-Apoetm1Unc Ifngtm1Ts
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Ifngtm1Ts mutation (14 available); any Ifng mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• about 50% of mice infused with angiotensin-II die within 2 to 10 days due to rupture of the abdominal aorta compared to 0 deaths of mutant mice wild-type for Ifng (J:166204)
• about 50% of mice infused with angiotensin-II die within 2 to 10 days due to rupture of the abdominal aorta compared to 0 deaths of mutant mice wild-type for Ifng (J:166204)

cardiovascular system
• about 50% of mice infused with 1000 ng/kg*min angiotensin-II die within 2 to 10 days due to rupture of the abdominal aorta compared to 0 deaths of mutant mice wild-type for Ifng (J:166204)
• increase in the incidence of abdominal aorta aneurysyms in in mice infused with 500 ng/kg*min angiotensin-II compared to mutant mice wild-type for Ifng (J:166204)
• about 50% of mice infused with 1000 ng/kg*min angiotensin-II die within 2 to 10 days due to rupture of the abdominal aorta compared to 0 deaths of mutant mice wild-type for Ifng (J:166204)
• increase in the incidence of abdominal aorta aneurysyms in in mice infused with 500 ng/kg*min angiotensin-II compared to mutant mice wild-type for Ifng (J:166204)
• increase in the suprarenal aortic diameter in mice infused with 500 ng/kg*min angiotensin-II compared to mutant mice wild-type for Ifng (J:166204)
• increase in the suprarenal aortic diameter in mice infused with 500 ng/kg*min angiotensin-II compared to mutant mice wild-type for Ifng (J:166204)

growth/size/body
• compared to mutant mice wild-type for Ifng (J:166204)
• compared to mutant mice wild-type for Ifng (J:166204)




Genotype
MGI:3822293
cx21
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Pecam1Gt(OST16303)Lex/Pecam1Gt(OST16303)Lex
Genetic
Background
B6.129-Apoetm1Unc Pecam1Gt(OST16303)Lex
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Pecam1Gt(OST16303)Lex mutation (1 available); any Pecam1 mutation (228 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• Cx43 distribution at cell-cell junction shows less disruption than in single Apoe-deficient mice (J:142083)
• Cx43 distribution at cell-cell junction shows less disruption than in single Apoe-deficient mice (J:142083)
• major lesions are observed on lesser curvature of aortic arch in males and females with minor lesions found at branches of aortic arch (J:142083)
• lesions comprise around 14-16% of total aortic arch area in male and female mutants (J:142083)
• aortic lesions are observed in aortic sinus at level of aortic valve leaflets; lesions are about 27% of total aortal area (J:142083)
• major lesions are observed on lesser curvature of aortic arch in males and females with minor lesions found at branches of aortic arch (J:142083)
• lesions comprise around 14-16% of total aortic arch area in male and female mutants (J:142083)
• aortic lesions are observed in aortic sinus at level of aortic valve leaflets; lesions are about 27% of total aortal area (J:142083)

homeostasis/metabolism
N
• cholesterol levels of double mutants on a Western or normal chow diet are not significantly different from diet-matched Apoe-null animals (J:142083)
• cholesterol levels of double mutants on a Western or normal chow diet are not significantly different from diet-matched Apoe-null animals (J:142083)




Genotype
MGI:4938324
cx22
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cxcl10tm1Adl/Cxcl10tm1Adl
Genetic
Background
B6.129-Cxcl10tm1Adl Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Cxcl10tm1Adl mutation (2 available); any Cxcl10 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• increased incidence of death due to ruptured abdominal aorta aneurysyms following angiotensin-II infusion compared to mutant mice wild-type for Cxcl10 (J:166204)
• increased incidence of death due to ruptured abdominal aorta aneurysyms following angiotensin-II infusion compared to mutant mice wild-type for Cxcl10 (J:166204)

cardiovascular system
• display more severe morphological changes following angiotensin-II infusion compared to mutant mice wild-type for Cxcl10 (J:166204)
• display more severe morphological changes following angiotensin-II infusion compared to mutant mice wild-type for Cxcl10 (J:166204)
• increase in the suprarenal aortic diameter and suprarenal/thoracic to infrarenal aortic area ratiosin mice infused with angiotensin-II compared to mutant mice wild-type for Cxcl10 (J:166204)
• increase in the suprarenal aortic diameter and suprarenal/thoracic to infrarenal aortic area ratiosin mice infused with angiotensin-II compared to mutant mice wild-type for Cxcl10 (J:166204)
• large aneurysms with spiral dissections are seen following angiotensin-II infusion (J:166204)
• increase in the incidence of grade III aneurysms following angiotensin-II infusion compared to mutant mice wild-type for Cxcl10 (J:166204)
• decrease in CD4+ T cell accumulation in angiotensin-II induced aneurysms (J:166204)
• large aneurysms with spiral dissections are seen following angiotensin-II infusion (J:166204)
• increase in the incidence of grade III aneurysms following angiotensin-II infusion compared to mutant mice wild-type for Cxcl10 (J:166204)
• decrease in CD4+ T cell accumulation in angiotensin-II induced aneurysms (J:166204)
• increased incidence of death due to ruptured abdominal aorta aneurysyms following angiotensin-II infusion compared to mutant mice wild-type for Cxcl10 (J:166204)
• increased incidence of death due to ruptured abdominal aorta aneurysyms following angiotensin-II infusion compared to mutant mice wild-type for Cxcl10 (J:166204)
• seen following angiotensin-II infusion (J:166204)
• seen following angiotensin-II infusion (J:166204)
• decrease in lesion size in the angiotensin-II induced model compared to mutant mice wild-type for Cxcl10 (J:166204)
• decrease in lesion size in the angiotensin-II induced model compared to mutant mice wild-type for Cxcl10 (J:166204)
• seen following angiotensin-II infusion (J:166204)
• seen following angiotensin-II infusion (J:166204)

immune system
• decrease in macrophage accumulation in the arterial wall in angiotensin-II treated mice (J:166204)
• decrease in macrophage accumulation in the arterial wall in angiotensin-II treated mice (J:166204)
• decrease in CD4+ T cell accumulation in angiotensin-II induced aneurysms (J:166204)
• decrease in CD4+ T cell accumulation in angiotensin-II induced aneurysms (J:166204)

hematopoietic system
• decrease in macrophage accumulation in the arterial wall in angiotensin-II treated mice (J:166204)
• decrease in macrophage accumulation in the arterial wall in angiotensin-II treated mice (J:166204)
• decrease in CD4+ T cell accumulation in angiotensin-II induced aneurysms (J:166204)
• decrease in CD4+ T cell accumulation in angiotensin-II induced aneurysms (J:166204)

cellular
• decrease in macrophage accumulation in the arterial wall in angiotensin-II treated mice (J:166204)
• decrease in macrophage accumulation in the arterial wall in angiotensin-II treated mice (J:166204)




Genotype
MGI:5462232
cx23
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Thbdtm1.1(THBD)Sltz/Thbdtm1.1(THBD)Sltz
Genetic
Background
B6.129(FVB)-Thbdtm1.1(THBD)Sltz Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Thbdtm1.1(THBD)Sltz mutation (0 available); any Thbd mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
N
• mice fed a high fat diet exhibit the same increase in total cholesterol, atherosclerotic lesion area and time to occlusion of the carotid artery following photochemical injury as Apoetm1Unc homozygotes (J:191461)
• mice fed a high fat diet exhibit the same increase in total cholesterol, atherosclerotic lesion area and time to occlusion of the carotid artery following photochemical injury as Apoetm1Unc homozygotes (J:191461)
• mice fed a high fat diet exhibit decreased amount of circulating activated protein C compared with Apoetm1Unc homozygotes (J:191461)
• mice fed a high fat diet exhibit decreased amount of circulating activated protein C compared with Apoetm1Unc homozygotes (J:191461)




Genotype
MGI:5502603
cx24
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Hsd11b1tm1Lex/Hsd11b1tm1Lex
Genetic
Background
B6.129-Hsd11b1tm1Lex Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Hsd11b1tm1Lex mutation (1 available); any Hsd11b1 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Decreased aortic root atherosclerosis susceptibility in Apoetm1Unc/Apoetm1Unc Hsd11b1tm1Lex/Hsd11b1tm1Lex mice

immune system
N
• mice fed a high fat diet and subjected to intraperitoneal thioglycollate challenge exhibit normal inflammatory cell migration (J:199430)
• mice fed a high fat diet and subjected to intraperitoneal thioglycollate challenge exhibit normal inflammatory cell migration (J:199430)
• foam cells from mice fed a high fat diet exhibit reduced cholesterol content compared with control cells (J:199430)
• foam cells from mice fed a high fat diet exhibit reduced cholesterol content compared with control cells (J:199430)
• in atherosclerotic lesions of mice fed a high fat diet (J:199430)
• in atherosclerotic lesions of mice fed a high fat diet (J:199430)
• peritoneal foam cells treated with oxidized LDL exhibit reduced secretion of G-CSF, KC, MCP-1 and TNFalpha compared with control cells (J:199430)
• peritoneal foam cells treated with oxidized LDL exhibit reduced secretion of G-CSF, KC, MCP-1 and TNFalpha compared with control cells (J:199430)
• in peritoneal foam cells treated with oxidized LDL (J:199430)
• in peritoneal foam cells treated with oxidized LDL (J:199430)

homeostasis/metabolism
• in mice fed a high fat diet as in Apoetm1Unc homozygotes (J:199430)
• in mice fed a high fat diet as in Apoetm1Unc homozygotes (J:199430)
• decreased total, 7-ketocholesterol and 7beta-hydroxycholesterol levels in the aorta of mice fed a high fat diet compared with similarly treated Apoetm1Unc homozygotes (J:199430)
• foam cells from mice fed a high fat diet exhibit reduced cholesterol content compared with control cells (J:199430)
• decreased total, 7-ketocholesterol and 7beta-hydroxycholesterol levels in the aorta of mice fed a high fat diet compared with similarly treated Apoetm1Unc homozygotes (J:199430)
• foam cells from mice fed a high fat diet exhibit reduced cholesterol content compared with control cells (J:199430)

cardiovascular system
N
• mice fed a high fat diet exhibit normal blood pressure (J:199430)
• mice fed a high fat diet exhibit normal blood pressure (J:199430)
• decreased total, 7-ketocholesterol and 7beta-hydroxycholesterol levels in the aorta of mice fed a high fat diet compared with similarly treated Apoetm1Unc homozygotes (J:199430)
• foam cells from mice fed a high fat diet exhibit reduced cholesterol content compared with control cells (J:199430)
• decreased total, 7-ketocholesterol and 7beta-hydroxycholesterol levels in the aorta of mice fed a high fat diet compared with similarly treated Apoetm1Unc homozygotes (J:199430)
• foam cells from mice fed a high fat diet exhibit reduced cholesterol content compared with control cells (J:199430)

behavior/neurological
N
• mice fed a high fat diet exhibit normal behavior (J:199430)
• mice fed a high fat diet exhibit normal behavior (J:199430)

growth/size/body
N
• mice fed a high fat diet exhibit normal weight gain (J:199430)
• mice fed a high fat diet exhibit normal weight gain (J:199430)

hematopoietic system
• foam cells from mice fed a high fat diet exhibit reduced cholesterol content compared with control cells (J:199430)
• foam cells from mice fed a high fat diet exhibit reduced cholesterol content compared with control cells (J:199430)
• in atherosclerotic lesions of mice fed a high fat diet (J:199430)
• in atherosclerotic lesions of mice fed a high fat diet (J:199430)
• bone marrow-derived stem cells transferred into Apoetm1Unc recipient fed a high fat diet results in decreased atherosclerosis in whole thoracic aorta and descending aorta (J:199430)
• bone marrow-derived stem cells transferred into Apoetm1Unc recipient fed a high fat diet results in decreased atherosclerosis in whole thoracic aorta and descending aorta (J:199430)

cellular
• foam cells from mice fed a high fat diet exhibit reduced cholesterol content compared with control cells (J:199430)
• foam cells from mice fed a high fat diet exhibit reduced cholesterol content compared with control cells (J:199430)




Genotype
MGI:4939466
cx25
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Il1r1tm1Imx/Il1r1tm1Imx
Genetic
Background
B6.129-Il1r1tm1Imx Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Il1r1tm1Imx mutation (4 available); any Il1r1 mutation (9 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• when fed a Western diet with high cholate, but not when fed standard chow or a Western diet (J:148173)
• mice receiving Apoetm1Unc bone marrow develop 1.9-fold smaller lesions compared with similarly treated Apoetm1Unc homozygotes (J:148173)
• when fed a Western diet with high cholate, but not when fed standard chow or a Western diet (J:148173)
• mice receiving Apoetm1Unc bone marrow develop 1.9-fold smaller lesions compared with similarly treated Apoetm1Unc homozygotes (J:148173)
• when fed either a Western diet with high cholate, mice exhibit a greater active pressure-diameter response compared with similarly treated Apoetm1Unc homozygotes (J:148173)
• when fed either a Western diet with high cholate, mice exhibit a greater active pressure-diameter response compared with similarly treated Apoetm1Unc homozygotes (J:148173)
• when fed either a Western diet with high cholate, mice exhibit greater constriction in response to sensitivity to L-NAME treatment compared with similarly treated Apoetm1Unc homozygotes (J:148173)
• when fed either a Western diet with high cholate, mice exhibit greater constriction in response to sensitivity to L-NAME treatment compared with similarly treated Apoetm1Unc homozygotes (J:148173)
• when fed either a Western diet or a Western diet with high cholate, mice exhibit greater vasodilator sensitivity to acetyl choline compared with similarly treated Apoetm1Unc homozygotes (J:148173)
• when fed either a Western diet or a Western diet with high cholate, mice exhibit greater vasodilator sensitivity to acetyl choline compared with similarly treated Apoetm1Unc homozygotes (J:148173)
• when fed either a Western diet or a Western diet with high cholate compared with similarly treated Apoetm1Unc homozygotes (J:148173)
• when fed either a Western diet or a Western diet with high cholate compared with similarly treated Apoetm1Unc homozygotes (J:148173)

homeostasis/metabolism
• when fed either a Western diet compared with similarly treated Apoetm1Unc homozygotes (J:148173)
• when fed either a Western diet compared with similarly treated Apoetm1Unc homozygotes (J:148173)

immune system
• when fed either a Western diet compared with similarly treated Apoetm1Unc homozygotes (J:148173)
• when fed either a Western diet compared with similarly treated Apoetm1Unc homozygotes (J:148173)

muscle
• when fed either a Western diet with high cholate, mice exhibit greater constriction in response to sensitivity to L-NAME treatment compared with similarly treated Apoetm1Unc homozygotes (J:148173)
• when fed either a Western diet with high cholate, mice exhibit greater constriction in response to sensitivity to L-NAME treatment compared with similarly treated Apoetm1Unc homozygotes (J:148173)
• when fed either a Western diet or a Western diet with high cholate, mice exhibit greater vasodilator sensitivity to acetyl choline compared with similarly treated Apoetm1Unc homozygotes (J:148173)
• when fed either a Western diet or a Western diet with high cholate, mice exhibit greater vasodilator sensitivity to acetyl choline compared with similarly treated Apoetm1Unc homozygotes (J:148173)




Genotype
MGI:4359427
cx26
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Nceh1tm1Ishi/Nceh1tm1Ishi
Genetic
Background
B6.129-Nceh1tm1Ishi Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Nceh1tm1Ishi mutation (0 available); any Nceh1 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• free cholesterol levels are increased 1.5-fold and 1.3-fold for males and females, respectively, compared to in Apoetm1Unc homozygotes (J:152385)
• cholesterol esters are increased 2-fold and 1.3-fold in males and females, respectively, compared to in Apoetm1Unc homozygotes (J:152385)
• free cholesterol levels are increased 1.5-fold and 1.3-fold for males and females, respectively, compared to in Apoetm1Unc homozygotes (J:152385)
• cholesterol esters are increased 2-fold and 1.3-fold in males and females, respectively, compared to in Apoetm1Unc homozygotes (J:152385)

cardiovascular system
• atherosclerotic lesions are increased compared to in Apoetm1Unc homozygotes (2.2-fold for males and 2.3-fold in females at 17 weeks, 1.7-fold in males and 2.4-fold for females at 21 weeks) (J:152385)
• atherosclerotic lesions are increased compared to in Apoetm1Unc homozygotes (2.2-fold for males and 2.3-fold in females at 17 weeks, 1.7-fold in males and 2.4-fold for females at 21 weeks) (J:152385)




Genotype
MGI:4367467
cx27
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Nos3tm1Plh/Nos3tm1Plh
Genetic
Background
B6.129-Nos3tm1Plh Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Nos3tm1Plh mutation (1 available); any Nos3 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• 3 of 12 mice fed a Western type diet for 16 weeks developed atherosclerotic suprarenal abdominal aortic aneurysms that are not seen in Apoe single mutants (J:103306)
• 3 of 12 mice fed a Western type diet for 16 weeks developed atherosclerotic suprarenal abdominal aortic aneurysms that are not seen in Apoe single mutants (J:103306)
• 2 of 12 mice fed a Western type diet for 16 weeks developed acute Stanford type B aortic dissections that are not seen in Apoe single mutants (J:103306)
• 2 of 12 mice fed a Western type diet for 16 weeks developed acute Stanford type B aortic dissections that are not seen in Apoe single mutants (J:103306)
• increase in lesion area relative to Apoe single mutants when fed a Western type diet (J:103306)
• unlike in Apoe single mutants no difference in lesion area is seen at 4 months of age in double mutants fed a Western type diet (J:103306)
• all mice show distal coronary arteriosclerosis associated with perivascular and endomyocardial fibrosis and endomyocardial scars consistent with nontransmural infarction (J:103306)
• increase in lesion area relative to Apoe single mutants when fed a Western type diet (J:103306)
• unlike in Apoe single mutants no difference in lesion area is seen at 4 months of age in double mutants fed a Western type diet (J:103306)
• all mice show distal coronary arteriosclerosis associated with perivascular and endomyocardial fibrosis and endomyocardial scars consistent with nontransmural infarction (J:103306)
• thickening of the interventricular septum is seen in double mutants fed a Western type diet for 16 weeks (J:103306)
• thickening of the interventricular septum is seen in double mutants fed a Western type diet for 16 weeks (J:103306)
• 2 of 10 mice fed a Western type diet for 16 weeks displayed massive dilation of the left ventricle (J:103306)
• 2 of 10 mice fed a Western type diet for 16 weeks displayed massive dilation of the left ventricle (J:103306)
• thickening of the posterior wall is seen in double mutants fed a Western type diet for 16 weeks (J:103306)
• thickening of the posterior wall is seen in double mutants fed a Western type diet for 16 weeks (J:103306)
• all mice show distal coronary arteriosclerosis associated with perivascular and endomyocardial fibrosis and endomyocardial scars consistent with nontransmural infarction (J:103306)
• all mice show distal coronary arteriosclerosis associated with perivascular and endomyocardial fibrosis and endomyocardial scars consistent with nontransmural infarction (J:103306)
• decrease in fractional shortening in double mutants fed a Western type diet for 16 weeks (J:103306)
• decrease in fractional shortening in double mutants fed a Western type diet for 16 weeks (J:103306)
• increased relative to wild-type controls and Apoe single mutants but similar to Nos3 single mutants (J:103306)
• increased relative to wild-type controls and Apoe single mutants but similar to Nos3 single mutants (J:103306)

muscle
• decrease in fractional shortening in double mutants fed a Western type diet for 16 weeks (J:103306)
• decrease in fractional shortening in double mutants fed a Western type diet for 16 weeks (J:103306)




Genotype
MGI:4942389
cx28
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cd44tm1Mak/Cd44+
Genetic
Background
B6.129P2-Cd44tm1Mak Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Cd44tm1Mak mutation (1 available); any Cd44 mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• reduced lesion area in the thoracic abdominal aorta (J:72315)
• normal plasma cholesterol levels (J:72315)
• reduced lesion area in the thoracic abdominal aorta (J:72315)
• normal plasma cholesterol levels (J:72315)




Genotype
MGI:4942387
cx29
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Cd44tm1Mak/Cd44tm1Mak
Genetic
Background
B6.129P2-Cd44tm1Mak Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Cd44tm1Mak mutation (1 available); any Cd44 mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• reduced lesion area in the aortic root and thoracic abdominal aorta in a gene dosage-dependent manner (J:72315)
• normal plasma cholesterol levels (J:72315)
• reduced lesion area in the aortic root and thoracic abdominal aorta in a gene dosage-dependent manner (J:72315)
• normal plasma cholesterol levels (J:72315)




Genotype
MGI:3794764
cx30
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Nos3tm1Unc/Nos3tm1Unc
Genetic
Background
B6.129P2-Nos3tm1Unc Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Nos3tm1Unc mutation (6 available); any Nos3 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• microaneurysmal dilations in 20% of males (J:60670)
• sometimes involving coronary arteries (J:60670)
• microaneurysmal dilations in 20% of males (J:60670)
• sometimes involving coronary arteries (J:60670)
• plaques larger at 4 months than in Apoe homozygotes, by 182% for males and 165% for females (J:60670)
• plaques larger at 4 months than in Apoe homozygotes, by 182% for males and 165% for females (J:60670)
• plaques in descending aorta in 90% of males as opposed to 20% of Apoe males (J:60670)
• plaques in descending aorta in 90% of males as opposed to 20% of Apoe males (J:60670)
• about 20mm higher than in Apoe homozygotes (J:60670)
• about 20mm higher than in Apoe homozygotes (J:60670)

renal/urinary system
• 15% of glomeruli with large lipid deposits in foam cells filling the glomeruli (J:60670)
• glomerular injury progresses to dystrophic calcification and glomerular loss (J:60670)
• 15% of glomeruli with large lipid deposits in foam cells filling the glomeruli (J:60670)
• glomerular injury progresses to dystrophic calcification and glomerular loss (J:60670)
• 15% lower than in Apoe homozygotes (J:60670)
• 15% lower than in Apoe homozygotes (J:60670)

homeostasis/metabolism
• 66% higher than controls (J:60670)
• 66% higher than controls (J:60670)




Genotype
MGI:3811066
cx31
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Serpine1tm1Mlg/Serpine1tm1Mlg
Genetic
Background
B6.129-Serpine1tm1Mlg Apoetm1Unc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Serpine1tm1Mlg mutation (4 available); any Serpine1 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• when fed a high fat Western diet for 6-30 weeks, mice develop atherosclerotic aortic lesions of the intimal and medial areas; incidence and severity are similar for Serpine1-deficient or transgenic Apoe-deficient genotypes (J:61287)
• lesions are somewhat larger than those observed on the Ldlr-deficient background (J:61287)
• cellular composition of lesions is similar among Serpine-deficient or transgenic, Apoe-deficient genotypes, or Apoe-deficient only mice; at early time points, a greater foam cell content is observed, with more prominent cholesterol clefts and necrotic areas evident with increasing age (J:61287)
• fibrin deposition is not significantly different among Serpine-deficient or transgenic, Apoe-deficient genotypes, or Apoe-deficient only mice (J:61287)
• when fed a high fat Western diet for 6-30 weeks, mice develop atherosclerotic aortic lesions of the intimal and medial areas; incidence and severity are similar for Serpine1-deficient or transgenic Apoe-deficient genotypes (J:61287)
• lesions are somewhat larger than those observed on the Ldlr-deficient background (J:61287)
• cellular composition of lesions is similar among Serpine-deficient or transgenic, Apoe-deficient genotypes, or Apoe-deficient only mice; at early time points, a greater foam cell content is observed, with more prominent cholesterol clefts and necrotic areas evident with increasing age (J:61287)
• fibrin deposition is not significantly different among Serpine-deficient or transgenic, Apoe-deficient genotypes, or Apoe-deficient only mice (J:61287)

homeostasis/metabolism
• mice develop severe cholesterolemia when receiving a high fat diet from 6 to 30 weeks (elevated levels are detected at 6, 15, and 30 weeks) (J:61287)
• mice develop severe cholesterolemia when receiving a high fat diet from 6 to 30 weeks (elevated levels are detected at 6, 15, and 30 weeks) (J:61287)




Genotype
MGI:4833679
cx32
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ccr2tm1Ifc/Ccr2tm1Ifc
Genetic
Background
B6.Cg-Apoetm1Unc Ccr2tm1Ifc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Ccr2tm1Ifc mutation (1 available); any Ccr2 mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mice fed a high fat diet exhibit decreased lesion size and macrophage accumulation compared to in Apoetm1Unc homozygotes (J:153310)
• mice fed a high fat diet exhibit decreased lesion size and macrophage accumulation compared to in Apoetm1Unc homozygotes (J:153310)

hematopoietic system
• mice fed a high fat diet exhibit decreased circulating monocyte numbers compared to in Apoetm1Unc homozygotes (J:153310)
• mice fed a high fat diet exhibit decreased circulating monocyte numbers compared to in Apoetm1Unc homozygotes (J:153310)

immune system
• mice fed a high fat diet exhibit decreased circulating monocyte numbers compared to in Apoetm1Unc homozygotes (J:153310)
• mice fed a high fat diet exhibit decreased circulating monocyte numbers compared to in Apoetm1Unc homozygotes (J:153310)




Genotype
MGI:4833678
cx33
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Ccr2tm1Ifc/Ccr2tm1Ifc
Cx3cl1tm1Lira/Cx3cl1tm1Lira
Genetic
Background
B6.Cg-Apoetm1Unc Cx3cl1tm1Lira Ccr2tm1Ifc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Ccr2tm1Ifc mutation (1 available); any Ccr2 mutation (6 available)
Cx3cl1tm1Lira mutation (0 available); any Cx3cl1 mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mice fed a high fat diet exhibit decreased lesion size and macrophage accumulation compared to in Apoetm1Unc homozygotes and Apoetm1Unc Ccr2tm1Ifc homozygotes (J:153310)
• mice fed a high fat diet exhibit decreased lesion size and macrophage accumulation compared to in Apoetm1Unc homozygotes and Apoetm1Unc Ccr2tm1Ifc homozygotes (J:153310)

hematopoietic system
• mice fed a high fat diet exhibit decreased circulating monocyte numbers compared to in Apoetm1Unc homozygotes (J:153310)
• however, levels are the same as in Apoetm1Unc Ccr2tm1Ifc homozygotes (J:153310)
• mice fed a high fat diet exhibit decreased circulating monocyte numbers compared to in Apoetm1Unc homozygotes (J:153310)
• however, levels are the same as in Apoetm1Unc Ccr2tm1Ifc homozygotes (J:153310)

immune system
• mice fed a high fat diet exhibit decreased circulating monocyte numbers compared to in Apoetm1Unc homozygotes (J:153310)
• however, levels are the same as in Apoetm1Unc Ccr2tm1Ifc homozygotes (J:153310)
• mice fed a high fat diet exhibit decreased circulating monocyte numbers compared to in Apoetm1Unc homozygotes (J:153310)
• however, levels are the same as in Apoetm1Unc Ccr2tm1Ifc homozygotes (J:153310)




Genotype
MGI:3800213
cx34
Allelic
Composition
Apoetm1Unc/Apoetm1Unc
Faslpr/Faslpr
Genetic
Background
B6.Cg-Apoetm1Unc Faslpr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Faslpr mutation (24 available); any Fas mutation (47 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• at 5 months, there are no significant differences in most leukocyte subsets (NK-cells, monocytes/macrophages, and neutrophils) compared to controls (J:121671)
• at 5 months, there are no significant differences in most leukocyte subsets (NK-cells, monocytes/macrophages, and neutrophils) compared to controls (J:121671)
• numbers of circulating cells are significantly reduced (J:121671)
• numbers of circulating cells are significantly reduced (J:121671)
• numbers of circulating cells are significantly reduced comparted to Apoe-wt, Fas-homozygous mice at 5 months (J:121671)
• numbers of circulating cells are significantly reduced comparted to Apoe-wt, Fas-homozygous mice at 5 months (J:121671)
• significantly enlarged compared to Apoe-null, Fas-heterozygous mice or Apoe-wt, Fas-homozygous mice at 5 months (J:121671)
• significantly enlarged compared to Apoe-null, Fas-heterozygous mice or Apoe-wt, Fas-homozygous mice at 5 months (J:121671)
• serum levels of IgG are significantly higher than in Apoe-null and Apoe-null, Fas-heterozygous mice at 6 weeks and at 5 months (J:121671)
• serum levels of IgG are significantly higher than in Apoe-null and Apoe-null, Fas-heterozygous mice at 6 weeks and at 5 months (J:121671)

immune system
• numbers of circulating cells are significantly reduced (J:121671)
• numbers of circulating cells are significantly reduced (J:121671)
• numbers of circulating cells are significantly reduced comparted to Apoe-wt, Fas-homozygous mice at 5 months (J:121671)
• numbers of circulating cells are significantly reduced comparted to Apoe-wt, Fas-homozygous mice at 5 months (J:121671)
• significantly enlarged compared to Apoe-null, Fas-heterozygous mice or Apoe-wt, Fas-homozygous mice at 5 months (J:121671)
• significantly enlarged compared to Apoe-null, Fas-heterozygous mice or Apoe-wt, Fas-homozygous mice at 5 months (J:121671)
• serum levels of IgG are significantly higher than in Apoe-null and Apoe-null, Fas-heterozygous mice at 6 weeks and at 5 months (J:121671)
• serum levels of IgG are significantly higher than in Apoe-null and Apoe-null, Fas-heterozygous mice at 6 weeks and at 5 months (J:121671)
• serum antibodies against oxidized phospholipid (OxPL) are decreased compared to Apoe-wt, Fas-homozygous and Apoe-null, Fas-wt controls (J:121671)
• serum antibodies against oxidized phospholipid (OxPL) are decreased compared to Apoe-wt, Fas-homozygous and Apoe-null, Fas-wt controls (J:121671)
• levels of IgG anti-cardiolipin antibodies are increased at 5 months relative to controls (J:121671)
• levels of IgG anti-POVPC and anti-PGPC autoantibodies are significantly higher than in controls at 5 months; IgM anti-POVPC levels are increased also (J:121671)
• levels of IgG anti-cardiolipin antibodies are increased at 5 months relative to controls (J:121671)
• levels of IgG anti-POVPC and anti-PGPC autoantibodies are significantly higher than in controls at 5 months; IgM anti-POVPC levels are increased also (J:121671)
• serum levels of IgG anti-dsDNA antibodies are significantly higher than in Apoe-null, Fas-wt controls and Apoe-null, Fas-heterozygous mice at 6 weeks and at 5 months (J:121671)
• serum levels of IgG anti-dsDNA antibodies are significantly higher than in Apoe-null, Fas-wt controls and Apoe-null, Fas-heterozygous mice at 6 weeks and at 5 months (J:121671)
• renal damage is observed, with IgG and C3 deposits present in the mesangium and peripheral capillary loops (J:121671)
• renal damage is observed, with IgG and C3 deposits present in the mesangium and peripheral capillary loops (J:121671)

renal/urinary system