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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(CAG-cre/Esr1*)5Amc
transgene insertion 5, Andrew P McMahon
MGI:2182767
Summary 152 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Apptm1.1Tlyp/Apptm1.1Tlyp
Tg(CAG-cre/Esr1*)5Amc/?
B6.Cg-Apptm1.1Tlyp Tg(CAG-cre/Esr1*)5Amc MGI:6114982
cn2
Gt(ROSA)26Sortm7(Pik3ca*,EGFP)Rsky/Gt(ROSA)26Sor+
Tg(CAG-cre/Esr1*)5Amc/0
B6.Cg-Gt(ROSA)26Sortm7(Pik3ca*,EGFP)Rsky Tg(CAG-cre/Esr1*)5Amc MGI:6197269
cn3
Rtn4rtm2.1Stmr/Rtn4rtm2.2Stmr
Tg(CAG-cre/Esr1*)5Amc/0
B6.Cg-Rtn4rtm2.1Stmr/Rtn4rtm2.2Stmr Tg(CAG-cre/Esr1*)5Amc0 MGI:5510953
cn4
Camk2atm1.1Yelg/Camk2atm1.1Yelg
Tg(CAG-cre/Esr1*)5Amc/0
B6J.Cg-Camk2atm1.1Yelg Tg(CAG-cre/Esr1*)5Amc MGI:5795687
cn5
Npc1m1N/Npc1tm1.1Apl
Tg(CAG-cre/Esr1*)5Amc/0
B6J.Cg-Npc1m1N/Npc1tm1.1Apl Tg(CAG-cre/Esr1*)5Amc MGI:5925342
cn6
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm7(SMO*/YFP)Amc
Tg(CAG-cre/Esr1*)5Amc/0
chimera involves: 129S4/SvJae * 129X1/SvJ * C57BL/6 * CBA * Swiss Webster MGI:4839957
cn7
Gnl3tm2.1Rylt/Gnl3tm2.1Rylt
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129 * 129S2/SvPas * C57BL/6 * CBA MGI:5523423
cn8
Gnl3tm2.1Rylt/Gnl3tm2.1Rylt
Trp53tm1Tyj/Trp53tm1Tyj
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129 * 129S2/SvPas * C57BL/6 * CBA MGI:5523425
cn9
Avpr2tm2.1Jwe/Y
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129 * C57BL/6 MGI:7282305
cn10
Pdpntm2.1Mlkn/Pdpntm2.1Mlkn
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129 * C57BL/6 MGI:5824831
cn11
Tbx3tm3.1Moon/Tbx3tm3.1Moon
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129 * C57BL/6 MGI:5538607
cn12
Hap1tm2Xjl/Hap1tm2Xjl
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129 * C57BL/6 * CBA MGI:5691394
cn13
Seh1ltm1Lzha/Seh1ltm1Lzha
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129 * C57BL/6 * CBA MGI:6712827
cn14
Dicer1tm1Bdh/Dicer1tm1Bdh
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129 * C57BL/6 * CBA MGI:6449234
cn15
Pax3tm1.1Sjc/Pax3tm1.1Sjc
Pax7tm1.2Fan/Pax7tm1.2Fan
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129 * C57BL/6 * CBA * SJL MGI:4353177
cn16
Tardbptm1.1Pcw/Tardbptm1.1Pcw
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129 * C57BL/6 * CBA * SJL MGI:4834592
cn17
Sox4tm1Vlf/Sox4tm1Vlf
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129 * C57BL/6 * CBA * SJL MGI:3773016
cn18
Cdk1tm2.1Kald/Cdk1tm2.1Kald
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129 * C57BL/6 * CBA * SJL MGI:5318110
cn19
Tardbptm1.1Pcw/Tardbp+
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129 * C57BL/6 * CBA * SJL MGI:4834589
cn20
Celf4tm1.1Frk/Celf4tm1.1Frk
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129 * C57BL/6J MGI:6194636
cn21
Tg(CAG-cre/Esr1*)5Amc/0
Ube3atm1Yelg/Ube3a+
involves: 129P2/OlaHsd * 129S2/SvPasCrl * C57BL/6J MGI:5704117
cn22
Lhx2tm1Monu/Lhx2tm1Monu
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CBA MGI:4453348
cn23
Lhx2tm1Monu/Lhx2tm1Dra
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CBA MGI:4453346
cn24
Supv3l1tm2.1Jkl/Supv3l1tm2.2Jkl
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * FVB/N MGI:3833891
cn25
St14tm2Bug/St14tm3Bug
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * Black Swiss * C57BL/6 * CBA MGI:4361221
cn26
Supv3l1tm2Jkl/Supv3l1tm2Jkl
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129P2/OlaHsd * C57BL/6 MGI:3833890
cn27
Mcattm1.1Ssmi/Mcattm1.1Ssmi
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * CBA MGI:5466536
cn28
Mecp2tm2Bird/Mecp2+
Tg(CAG-cre/Esr1*)5Amc/?
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3712287
cn29
Mecp2tm2Bird/Y
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:3832684
cn30
Nrg1tm3Cbm/Nrg1tm3Cbm
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:5524264
cn31
Recktm1Ito/Recktm1.1Noda
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:4830343
cn32
Ppp2r1atm1.1Wltr/Ppp2r1atm1.2Wltr
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/Sv * 129S4/SvJaeSor * C57BL/6 * CBA * FVB/NCrl MGI:5287435
cn33
Dohhtm1.1Sbal/Dohhtm1.1Sbal
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/Sv * 129X1/SvJ * BALB/cJ MGI:5903288
cn34
Inpp5etm1.1Ssch/Inpp5etm1.2Ssch
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:4360189
cn35
Bub1tm1Ssta/Bub1tm1Ssta
Tg(CAG-cre/Esr1*)5Amc/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:3767641
cn36
Edn2tm1.1Nat/Edn2tm1.1Nat
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:4438398
cn37
Sdhdtm1Jlob/Sdhdtm2Jlob
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:5438129
cn38
Dscamtm1Pfu/Dscamtm1Pfu
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:5305034
cn39
Bub1tm1Ssta/Bub1tm1.1Ssta
Tg(CAG-cre/Esr1*)5Amc/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA MGI:3767640
cn40
Kcnq1ot1tm2.1Ckan/Kcnq1ot1+
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA * SD7 MGI:5431829
cn41
Numa1tm1.1Dwc/Numa1tm1.1Dwc
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA * SJL MGI:3838126
cn42
Htttm1Mem/Htttm6Mem
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA * Swiss Webster MGI:7266814
cn43
Six3tm2Gco/Six3tm2.1Gco
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/Sv * C57BL/6 * CBA MGI:3693848
cn44
Gdnftm1Bbd/Gdnftm1Jlob
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/Sv * C57BL/6 * CBA MGI:3809283
cn45
Glstm2.1Sray/Gls+
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/Sv * C57BL/6 * CBA MGI:5784520
cn46
Wnt5atm1.1Tpy/Wnt5atm1.1Tpy
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/Sv * C57BL/6 * CBA MGI:5440734
cn47
Pnkptm1.1Pmc/Pnkptm1.1Pmc
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/Sv * C57BL/6 * CBA MGI:5795834
cn48
Rapgef2tm1.1Hous/Rapgef2tm1.1Hous
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/Sv * C57BL/6 * CBA MGI:4839181
cn49
Ate1tm1Avar/Ate1tm2.1Avar
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/Sv * C57BL/6 * CBA MGI:4415303
cn50
Kmt5atm1.1Dare/Kmt5atm1.2Dare
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/Sv * C57BL/6 * CBA * SJL MGI:3842509
cn51
Mecomtm1Aspe/Mecomtm2.1Aspe
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/SvImJ * C57BL/6 * C57BL/6J * CBA MGI:5301413
cn52
Mecomtm2.1Aspe/Mecomtm2.1Aspe
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/SvImJ * C57BL/6 * CBA MGI:5301414
cn53
Cxadrtm1.1Ics/Cxadrtm1.1Ics
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S2/SvPas * C57BL/6 * C57BL/6J * CBA MGI:5086257
cn54
Atrtm2Bal/Atrtm2Bal
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S2/SvPas * C57BL/6 * CBA MGI:5316225
cn55
Ccnd1tm1Wbg/Ccnd1tm5.1Pisc
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S2/SvPas * C57BL/6 * CBA MGI:5468350
cn56
Syngap1tm2Geno/Syngap1+
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S2/SvPas * C57BL/6 * CBA MGI:5469879
cn57
Alkbh4tm1Geno/Alkbh4tm1Geno
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S2/SvPas * C57BL/6 * CBA MGI:5549958
cn58
Ccnd1tm1Wbg/Ccnd1tm5.1Pisc
Tg(CAG-cre/Esr1*)5Amc/0
Tg(MMTV-Erbb2)NK1Mul/0
involves: 129S2/SvPas * C57BL/6 * CBA * FVB/N MGI:5468352
cn59
Esco2tm1.1Ge/Esco2tm1.1Ge
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S2/SvPas * C57BL/6 * CBA * SJL MGI:5308067
cn60
Kdm6atm1Cdcn/Y
Tg(CAG-cre/Esr1*)5Amc/0
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6J * CBA * FVB/N MGI:6192377
cn61
Cdc73tm1Btt/Cdc73tm1Btt
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:3795455
cn62
Trpm7tm1Clph/Trpm7tm1Clph
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:6220878
cn63
Lhx2tm1.1Lcar/Lhx2tm1Dra
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:4453345
cn64
Lhx2tm1.1Lcar/Lhx2tm1.1Lcar
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:4453347
cn65
Pomctm2Low/Pomctm2Low
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:5473527
cn66
Nrltm1Jcco/Nrltm1Jcco
Rhotm1Jlem/Rhotm1Jlem
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:5490597
cn67
Mmp14tm1Hbh/Mmp14tm1.1Khol
Mmp15tm1Kohl/Mmp15tm1Kohl
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 * CBA MGI:4868430
cn68
Pappatm1Lex/Pappatm1Lex
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S5/SvEvBrd * C57BL/6 * CBA MGI:5523415
cn69
Kdm5atm1Kael/Kdm5atm1Kael
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S6/SvEvTac * C57BL/6 * CBA MGI:5296661
cn70
Ewsr1tm2(FLI1*)Sblee/Ewsr1+
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S6/SvEvTac * C57BL/6 * CBA MGI:4429149
cn71
Tg(CAG-cre/Esr1*)5Amc/0
Wee1tm1Cxd/Wee1tm1Cxd
involves: 129S6/SvEvTac * C57BL/6 * CBA MGI:5707476
cn72
Ccn2tm2Mae/Ccn2+
Tg(CAG-cre/Esr1*)5Amc/?
involves: 129S6/SvEvTac * C57BL/6 * CBA MGI:4838161
cn73
Ewsr1tm1Sblee/Ewsr1+
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S6/SvEvTac * C57BL/6 * CBA MGI:4429150
cn74
Ptpn11tm6Bgn/Ptpn11+
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S6/SvEvTac * C57BL/6 * CBA MGI:3845013
cn75
Gaktm2Legr/Gaktm2Legr
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S6/SvEvTac * C57BL/6 * CBA MGI:5305780
cn76
Tg(CAG-cre/Esr1*)5Amc/0
Tgfbr2tm1.2Hlm/Tgfbr2tm1.2Hlm
involves: 129S6/SvEvTac * C57BL/6 * CBA MGI:5688888
cn77
Egln1tm1Kael/Egln1tm1Kael
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S6/SvEvTac * C57BL/6 * CBA MGI:3793292
cn78
Sav1tm1.1Rjo/Sav1tm1.1Rjo
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S6/SvEvTac * C57BL/6 * CBA * CD-1 * SJL MGI:4430543
cn79
Mdm4tm3Glo/Mdm4tm3.1Glo
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S6/SvEvTac * C57BL/6 * CBA * FVB/N MGI:5142305
cn80
Hdac3tm1Swh/Hdac3tm1.1Swh
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S6/SvEvTac * C57BL/6 * CBA * FVB/N MGI:3795942
cn81
Ift20tm1.1Gjp/Ift20tm1.2Gjp
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6J * CBA MGI:6383666
cn82
Myogtm3Whk/Myogtm3Whk
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S7/SvEvBrd * C57BL/6 * CBA MGI:3620012
cn83
Trp53tm1Glo/Trp53tm4Glo
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S7/SvEvBrd * C57BL/6 * CBA MGI:5000506
cn84
Bmpr1atm2.1Bhr/Bmpr1atm2.1Bhr
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S7/SvEvBrd * C57BL/6 * CBA MGI:6404152
cn85
Lmx1btm1Rjo/Lmx1btm4.1Rjo
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S7/SvEvBrd * C57BL/6 * CBA MGI:4818573
cn86
Trp53tm3.1Glo/Trp53tm4Glo
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S7/SvEvBrd * C57BL/6 * CBA MGI:5000509
cn87
Dicer1tm1Snj/Dicer1tm1Snj
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S7/SvEvBrd * C57BL/6 * CBA MGI:3809305
cn88
Bmpr1atm1Bhr/Bmpr1atm2.1Bhr
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S7/SvEvBrd * C57BL/6 * CBA MGI:4941477
cn89
Tbx1tm1Bld/Tbx1tm3Bld
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S7/SvEvBrd * C57BL/6 * CBA MGI:4453459
cn90
Omgtm1.2Bzh/Omgtm1.2Bzh
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S7/SvEvBrd * C57BL/6 * CBA * SJL MGI:4399102
cn91
Mstntm1Swel/Mstntm1Swel
Tg(CAG-cre/Esr1*)5Amc/?
involves: 129S7/SvEvBrd-Hprt1 * C57BL/6 * CBA MGI:3711528
cn92
Rettm2(RET)Heno/Rettm1Cos
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S/Sv * C57BL/6 * CBA MGI:4820805
cn93
Rettm2(RET)Heno/Rettm2(RET)Jmi
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S/Sv * C57BL/6 * CBA MGI:4820814
cn94
Plxnd1tm1.1Tmj/Plxnd1tm1.1Tmj
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S/SvEv * 129S4/SvJaeSor * C57BL/6 * CBA MGI:3848824
cn95
Tbptm1Xjl/Tbp+
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S/SvEv * C57BL/6 * CBA MGI:5693885
cn96
Fktntm1Kcam/Fktntm1Kcam
Tg(CAG-cre/Esr1*)5Amc/?
involves: 129S/SvEv * C57BL/6 * CBA MGI:5435674
cn97
Pou4f2tm4Whk/Pou4f2+
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S/SvEv * C57BL/6 * CBA MGI:3838797
cn98
Tg(CAG-Bgeo/Lhx2,-GFP)#Lcar/0
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * CBA MGI:4453351
cn99
Rab35tm1.1Vha/Rab35tm1.1Vha
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129/Sv * 129S4/SvJaeSor * C57BL/6J * C57BL/6 * CBA MGI:6467551
cn100
Tg(CAG-cre/Esr1*)5Amc/?
Thratm1Ffla/Thra+
involves: 129/Sv * C57BL/6 * CBA MGI:3758925
cn101
Nlrp3tm1Hhf/Nlrp3+
Tg(CAG-cre/Esr1*)5Amc/?
involves: 129/Sv * C57BL/6 * CBA MGI:3850050
cn102
Nlrp3tm2Hhf/Nlrp3+
Tg(CAG-cre/Esr1*)5Amc/?
involves: 129/Sv * C57BL/6 * CBA MGI:3850052
cn103
Gfra1tm1Jmi/Gfra1tm2Jmi
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129/Sv * C57BL/6 * CBA * SJL MGI:3715267
cn104
Foxn1tm1.1Dmsu/Foxn1tm1.1Dmsu
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129/Sv * C57BL/6 * CBA * SJL MGI:4454657
cn105
Foxn1nu/Foxn1tm1.1Dmsu
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129/Sv * C57BL/6 * CBA * SJL MGI:4454658
cn106
Trip11tm1.1Psmi/Trip11tm1.2Psmi
Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo/?
Tg(CAG-cre/Esr1*)5Amc/?
involves: 129/Sv * C57BL/6 * SJL/J MGI:6154270
cn107
Tmem30atm1.1Xjz/Tmem30atm1.1Xjz
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129/SvEv * C57BL/6 * CBA MGI:6382630
cn108
Epas1tm1Mcs/Epas1tm1.1Mcs
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129X1/SvJ * C57BL/6 * CBA MGI:6724166
cn109
Rettm1Heno/Rettm2(RET)Heno
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129X1/SvJ * C57BL/6 * CBA MGI:4459060
cn110
Wnt9btm1.1Amc/Wnt9btm1.2Amc
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129X1/SvJ * C57BL/6 * CBA MGI:5428000
cn111
Baxtm1Sjk/Baxtm1Sjk
Rettm1Heno/Rettm3.1(Bcl2l1)Heno
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129X1/SvJ * C57BL/6 * CBA MGI:4459062
cn112
Gt(ROSA)26Sortm1(Smo/EYFP)Amc/?
Tg(CAG-cre/Esr1*)5Amc/?
involves: 129X1/SvJ * C57BL/6 * CBA MGI:3716204
cn113
Rettm1Heno/Rettm3.1(Bcl2l1)Heno
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129X1/SvJ * C57BL/6 * CBA MGI:4459061
cn114
Cxcl12tm1.1Ystz/Cxcl12tm1.2Ystz
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129X1/SvJ * C57BL/6 * CBA * FVB/N MGI:4888376
cn115
Nr1d1tm1.1Rev/Nr1d1tm1.1Rev
Nr1d2tm1.1Rev/Nr1d2tm1.1Rev
Tg(CAG-cre/Esr1*)5Amc/0
involves: BALB/cJ * C57BL/6 * C57BL/6J * CBA MGI:5426706
cn116
Pmltm1(PML/RARA)Ley/Pml+
Tg(CAG-cre/Esr1*)5Amc/0
involves: BALB/cJ * C57BL/6 * CBA MGI:5014087
cn117
Pou4f1tm1.1Gan/Pou4f1tm1.1Gan
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * C57BL/6J * CBA MGI:5607142
cn118
Pou4f2tm2.1Gan/Pou4f2tm2.1Gan
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * C57BL/6J * CBA MGI:5607145
cn119
Cop1tm1.1Vmd/Cop1tm2.1Vmd
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * C57BL/6N * CBA MGI:5013602
cn120
Sel1ltm1c(KOMP)Wtsi/Sel1ltm1c(KOMP)Wtsi
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * C57BL/6N * CBA * SJL MGI:5581523
cn121
Ccnd3tm2.1Pisc/Ccnd3tm2.1Pisc
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * CBA MGI:5468353
cn122
Aqp2tm1Bxy/Aqp2tm1Bxy
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * CBA MGI:3653933
cn123
Nr2e1tm1Rev/Nr2e1tm1Rev
Tg(CAG-cre/Esr1*)5Amc/?
involves: C57BL/6 * CBA MGI:3777343
cn124
Stk3tm1.1Yy/Stk3tm1Yy
Stk4tm1.1Yy/Stk4tm1.1Yy
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * CBA MGI:4422186
cn125
Kat7tm1.1Avo/Kat7tm1.1Avo
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * CBA MGI:4947714
cn126
Map2k7tm1Rjd/Map2k7tm1Rjd
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * CBA MGI:5297907
cn127
Map2k4tm1Ctr/Map2k4tm1Ctr
Map2k7tm1Rjd/Map2k7tm1Rjd
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * CBA MGI:5297908
cn128
Map2k4tm1Ctr/Map2k4tm1Ctr
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * CBA MGI:5297910
cn129
Lbx1tm1.1Khan/Lbx1tm1.1Khan
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * CBA MGI:5304417
cn130
Nrltm1Jcco/Nrltm1Jcco
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * CBA MGI:5490590
cn131
Map3k12tm1Lewc/Map3k12tm1Lewc
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * CBA MGI:5502227
cn132
Pdpntm2.1Mlkn/Pdpntm2.1Mlkn
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * CBA MGI:5552951
cn133
Ino80tm1Schg/Ino80tm1Schg
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * CBA MGI:5898009
cn134
Gt(ROSA)26Sortm1(CAG-MFN2*T105M)Dple/Gt(ROSA)26Sor+
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * CBA MGI:6198665
cn135
Nup85tm1.1Yter/Nup85tm1.1Yter
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * CBA MGI:6451097
cn136
Tcfl5tm1Frem/Tcfl5tm1Frem
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * CBA MGI:7316744
cn137
Tg(CAG-cre/Esr1*)5Amc/0
Tg(CAG-LacZ,-ACVR1*,-EGFP)35-1Mis/0
involves: C57BL/6 * CBA * DBA/2 MGI:3821885
cn138
Prom1tm1.1(DTA)Toko/Prom1tm1.1(DTA)Toko
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6 * CBA * SJL MGI:4360394
cn139
Abcg5tm1.1Hobb/Abcg5tm1.1Hobb
Abcg8tm1.1Hobb/Abcg8tm1.1Hobb
Tg(CAG-cre/Esr1*)5Amc/?
involves: C57BL/6 * CBA * SJL MGI:5607628
cn140
Nkx2-5tm1.1Gum/Nkx2-5tm1.1Gum
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6J MGI:5810739
cn141
Dhpstm2c(EUCOMM)Wtsi/Dhpstm2c(EUCOMM)Wtsi
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6J * C57BL/6N * CBA * SJL MGI:5903287
cn142
Atg7tm1Tchi/Atg7tm1Tchi
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6J * C57BL/6NCrlj * CBA/JNCrlj MGI:6870515
cn143
Kdm6atm1Cdcn/Kdm6atm1Cdcn
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6J * CBA MGI:6192376
cn144
Emc3em1Xjz/Emc3em1Xjz
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6J * CBA MGI:6376225
cn145
Kdm6atm1Cdcn/Y
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6J * CBA MGI:6192375
cn146
Fam210atm1c(EUCOMM)Wtsi/Fam210atm1c(EUCOMM)Wtsi
Tg(CAG-cre/Esr1*)5Amc/0
involves: C57BL/6N * CBA * SJL MGI:6159281
cn147
Pou4f1tm1.1Gan/Pou4f1tm1.1Gan
Pou4f2tm2.1Gan/Pou4f2tm2.1Gan
Tg(CAG-cre/Esr1*)5Amc/0
Not Specified MGI:5607147
cx148
Syngap1tm2Geno/Syngap1+
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S2/SvPas * C57BL/6 * CBA MGI:5469878
cx149
Nlrp3tm2Hhf/Nlrp3+
Tg(CAG-cre/Esr1*)5Amc/?
involves: 129/Sv * C57BL/6 * CBA MGI:3850051
cx150
Nlrp3tm1Hhf/Nlrp3+
Tg(CAG-cre/Esr1*)5Amc/?
involves: 129/Sv * C57BL/6 * CBA MGI:3850049
tg151
Tg(CAG-cre/Esr1*)5Amc/0 involves: C57BL/6 * CBA MGI:3845073
tg152
Tg(CAG-cre/Esr1*)5Amc/? involves: C57BL/6 * CBA MGI:3716206


Genotype
MGI:6114982
cn1
Allelic
Composition
Apptm1.1Tlyp/Apptm1.1Tlyp
Tg(CAG-cre/Esr1*)5Amc/?
Genetic
Background
B6.Cg-Apptm1.1Tlyp Tg(CAG-cre/Esr1*)5Amc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apptm1.1Tlyp mutation (0 available); any App mutation (68 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• in a subset of embryos, some TBR1+ cells (expressed in the lower cortical layer) are observed below the cortical plate after tamoxifen treatment
• following tamoxifen treatment, the majority of Reelin+ cells (expressed in the marginal zone) in some embryonic brains are displaced below the cortical plate, and, in other brains, Reelin+ cells are displaced to the intermediate zone
• number and morphology of astrocytes and microglia are similar to wild-type in the hippocampus and cerebral cortex following tamoxifen treatment at E12, 13, and 14 (harvested on E18)




Genotype
MGI:6197269
cn2
Allelic
Composition
Gt(ROSA)26Sortm7(Pik3ca*,EGFP)Rsky/Gt(ROSA)26Sor+
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
B6.Cg-Gt(ROSA)26Sortm7(Pik3ca*,EGFP)Rsky Tg(CAG-cre/Esr1*)5Amc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm7(Pik3ca*,EGFP)Rsky mutation (1 available); any Gt(ROSA)26Sor mutation (793 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice administered a single low dose (4 mg/kg) of tamoxifen to induce cre recombination survive 2 months and then die with multiple abnormalities
• tamoxifen-administered mice treated with rapamycin show improved survival but no improvement in organ abnormalities such as liver and spleen disorganization with aberrant vascularization
• mice start to rapidly die after 40 mg/kg tamoxifen administration, with 50% of mortality at day 9
• tamoxifen-administered mice treated with BYL719 are alive after 40 days, however interruption of BYL719 treatment 40 days after tamoxifen-administration leads to rapid death
• tamoxifen-administered mice treated with rapamycin show improved survival but no improvement in organ abnormalities such as liver and spleen disorganization with aberrant vascularization

growth/size/body
• kidney cysts in tamoxifen-administered mice
• organomegaly is seen in mice administered a single low dose of tamoxifen

cardiovascular system
• vessel abnormalities in tamoxifen-administered mice
• tamoxifen-administered mice treated with BYL719 show normal vessels
• ecstatic venous channels with a thin endothelial cell lining, surrounded by sparse, erratically distributed vascular smooth muscle cells and a disorganized extracellular matrix are seen in mice administered a low dose of tamoxifen
• severe vessel dilation in tamoxifen-administered mice
• intra-abdominal hemorrhages in tamoxifen-administered mice
• hepatic hemorrhages in tamoxifen-administered mice

cellular
• high number of proliferating cells in affected organs of tamoxifen-administered mice
• however, no changes in apoptosis are seen
• tamoxifen-administered mice treated with BYL719 show a reduction in proliferation

hematopoietic system
• loss of spleen microarchitecture integrity in tamoxifen-administered mice

immune system
• loss of spleen microarchitecture integrity in tamoxifen-administered mice
• expansion of lymphatic vessels in tamoxifen-administered mice

limbs/digits/tail
• mice administered a single low dose of tamoxifen progressively develop asymmetrical overgrowth of extremities, disseminated voluminous tumors and subcutaneous vascular abnormalities
• low-dose tamoxifen administered mice treated with BYL719 show improvement of the overgrowth of extremities, however, withdrawal of BYL719 leads to the development of asymmetric extremity hypertrophy within 4 weeks

liver/biliary system
• hepatic hemorrhages in tamoxifen-administered mice
• severe liver steatosis with vessel disorganization in tamoxifen-administered mice

muscle
• muscle hypertrophy in tamoxifen-administered mice
• mice treated with BYL719 7 days after cre induction show improved muscle hypertrophy

neoplasm
• low dose tamoxifen-administered mice develop tumors that are lipomatous tumors and severe vascular lesions mixing venous and arterial vessels
• low-dose tamoxifen administered mice treated with BYL719 show reduced and disappearance of visible tumors within 2 weeks
• withdrawal of BYL719 from the low-dose tamoxifen administered mice leads to recurrence of tumors
• low-dose tamoxifen-administered mice treated with rapamycin show no effect on tumor growth

renal/urinary system
• kidney cysts in tamoxifen-administered mice
• fibrosis of the kidney with aberrant vessels in tamoxifen-administered mice

skeleton
• scoliosis in tamoxifen-administered mice
• mice treated with BYL719 7 days after cre induction show improved scoliosis

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
CLOVES syndrome DOID:0080351 OMIM:612918
J:264410




Genotype
MGI:5510953
cn3
Allelic
Composition
Rtn4rtm2.1Stmr/Rtn4rtm2.2Stmr
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
B6.Cg-Rtn4rtm2.1Stmr/Rtn4rtm2.2Stmr Tg(CAG-cre/Esr1*)5Amc0
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rtn4rtm2.1Stmr mutation (0 available); any Rtn4r mutation (16 available)
Rtn4rtm2.2Stmr mutation (0 available); any Rtn4r mutation (16 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• after optic nerve crush, tamoxifen-treated mice exhibit stronger axonal regeneration compared with control mice though not as complete as in constitutive knock-out mice
• after spinal cord dorsal hemisection injury, tamoxifen-treated mice exhibit improvement of motor function and 5HT fiber density compared with control mice
• however, untreated mice exhibit normal regeneration




Genotype
MGI:5795687
cn4
Allelic
Composition
Camk2atm1.1Yelg/Camk2atm1.1Yelg
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
B6J.Cg-Camk2atm1.1Yelg Tg(CAG-cre/Esr1*)5Amc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Camk2atm1.1Yelg mutation (0 available); any Camk2a mutation (126 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• adult mice treated with tamoxifen show severe contextual fear learning deficits relative to control littermates, as revealed by a marked reduction in elicited freezing behavior
• in the hidden version of the Morris water maze, adult mice treated with tamoxifen search equally in all four quadrants with no clear preference for the target quadrant during the probe trial, unlike control littermates
• however, no significant differences in latency times to reach the hidden platform, thigmotaxis, swim speed, or path length are observed

nervous system
• adult mice treated with tamoxifen exhibit impaired synaptic plasticity
• adult mice treated with tamoxifen show impaired LTP induction at the CA3-CA1 synapse in the hippocampus in two independent stimulation protocols (100 Hz and theta-burst) relative to control littermates
• however, basal synaptic transmission and paired-pulse facilitation (PPF) are normal




Genotype
MGI:5925342
cn5
Allelic
Composition
Npc1m1N/Npc1tm1.1Apl
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
B6J.Cg-Npc1m1N/Npc1tm1.1Apl Tg(CAG-cre/Esr1*)5Amc
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Npc1m1N mutation (3 available); any Npc1 mutation (52 available)
Npc1tm1.1Apl mutation (0 available); any Npc1 mutation (52 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• average lifespan is 109 days post tamoxifen injection

nervous system
• widespread microgliosis in the cerebellum of tamoxifen-treated mice at 18 weeks of age
• accumulation of unesterified cholesterol in cerebellar lobule X in tamoxifen-treated mice at 18 weeks of age
• progressive anterior-to-posterior Purkinje cell loss in tamoxifen-treated mice
• cells in anterior lobules degenerate early and those in posterior lobules are more resistant to degeneration
• widespread astrocytosis in the cerebellum of tamoxifen-treated mice at 18 weeks of age
• tamoxifen-treated mice exhibit swollen axons in the cortex at 22 weeks of age
• widespread axonal spheroids in the cerebellum of tamoxifen-treated mice at 18 weeks of age
• tamoxifen-treated mice exhibit demyelination in the corpus callosum at 22 weeks of age
• widespread secondary demyelination in the cerebellum of tamoxifen-treated mice at 18 weeks of age

behavior/neurological
• mice injected with tamoxifen at 6 weeks of age exhibit impaired balance beam performance by 12 weeks which progresses with age

growth/size/body
• mice injected with tamoxifen at 6 weeks of age start to lose weight around 16 weeks of age

hematopoietic system
• widespread microgliosis in the cerebellum of tamoxifen-treated mice at 18 weeks of age

homeostasis/metabolism
• accumulation of unesterified cholesterol in cerebellar lobule X in tamoxifen-treated mice at 18 weeks of age

immune system
• widespread microgliosis in the cerebellum of tamoxifen-treated mice at 18 weeks of age

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Niemann-Pick disease DOID:14504 J:176888




Genotype
MGI:4839957
cn6
Allelic
Composition
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm7(SMO*/YFP)Amc
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
chimera involves: 129S4/SvJae * 129X1/SvJ * C57BL/6 * CBA * Swiss Webster
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sor mutation (8 available); any Gt(ROSA)26Sor mutation (793 available)
Gt(ROSA)26Sortm7(SMO*/YFP)Amc mutation (0 available); any Gt(ROSA)26Sor mutation (793 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• dorsal CNS hyperproliferation at E13.5 after being exposed at E8.5 to tamoxifen

limbs/digits/tail
• observed at E13.5 after being exposed at E8.5 to tamoxifen




Genotype
MGI:5523423
cn7
Allelic
Composition
Gnl3tm2.1Rylt/Gnl3tm2.1Rylt
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129 * 129S2/SvPas * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gnl3tm2.1Rylt mutation (0 available); any Gnl3 mutation (56 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• increase in the percentage of MEFs showing signs of replication-induced DNA damage after tamoxifen treatment
• tamoxifen treatment impairs the long-term proliferative potential of MEFs




Genotype
MGI:5523425
cn8
Allelic
Composition
Gnl3tm2.1Rylt/Gnl3tm2.1Rylt
Trp53tm1Tyj/Trp53tm1Tyj
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129 * 129S2/SvPas * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gnl3tm2.1Rylt mutation (0 available); any Gnl3 mutation (56 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (210 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• increase in the percentage of MEFs showing signs of replication-induced DNA damage after tamoxifen treatment
• tamoxifen treatment shortens the lifespan of MEFs
• tamoxifen treatment impairs the long-term proliferative potential of MEFs




Genotype
MGI:7282305
cn9
Allelic
Composition
Avpr2tm2.1Jwe/Y
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Avpr2tm2.1Jwe mutation (0 available); any Avpr2 mutation (1 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• 7- to 8-week-old males treated with tamoxifen for 6 days show an increase in water intake
• treatment with the selective EP4 receptor agonist ONO results in a 50% decrease in cumulative water consumption

renal/urinary system
• tamoxifen-treated males show a reduction in urine creatinine concentration
• tamoxifen-treated males show a reduction in urine potassium concentration
• tamoxifen-treated males show a reduction in urine sodium concentration
• however, serum sodium levels are normal
• urine produced by tamoxifen-treated males has very low osmolality
• urine osmolality is lower by about 25% even prior to tamoxifen treatment
• treatment with 1-desamino-8-D-AVP, a selective AVPR2 agonist, is unable to increase urine osmolality in tamoxifen-treated mice
• treatment with the selective EP4 receptor agonist ONO leads to dose-dependent increases in urine osmolality in tamoxifen-administered mice
• tamoxifen-treated males show a reduction in urine urea
• kidneys show distention of the renal pelvis after tamoxifen treatment
• ONO treatment completely prevents further expansion of renal pelvic space in tamoxifen-administered mice
• tamoxifen-treated males show an approximate 40% reduction of glomerular filtration rate
• ONO treatment restores normal glomerular filtration rate in tamoxifen-administered mice
• 7- to 8-week-old males treated with tamoxifen for 6 days show an increase in urine production
• treatment with the selective EP4 receptor agonist ONO leads to a reduction in urine output in tamoxifen-administered mice

homeostasis/metabolism
• tamoxifen-treated males show a reduction in urine creatinine concentration
• tamoxifen-treated males show a reduction in urine potassium concentration
• however, serum sodium levels are normal
• tamoxifen-treated males show a reduction in urine sodium concentration
• urine produced by tamoxifen-treated males has very low osmolality
• urine osmolality is lower by about 25% even prior to tamoxifen treatment
• treatment with 1-desamino-8-D-AVP, a selective AVPR2 agonist, is unable to increase urine osmolality in tamoxifen-treated mice
• treatment with the selective EP4 receptor agonist ONO leads to dose-dependent increases in urine osmolality in tamoxifen-administered mice
• tamoxifen-treated males show a reduction in urine urea

growth/size/body
• tamoxifen-treated males weigh approximately 25% less than controls

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
X-linked nephrogenic diabetes insipidus DOID:0081060 OMIM:304800
J:324922




Genotype
MGI:5824831
cn10
Allelic
Composition
Pdpntm2.1Mlkn/Pdpntm2.1Mlkn
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pdpntm2.1Mlkn mutation (0 available); any Pdpn mutation (27 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

VEGF-C-and galectin-8-induced lymphangiogenesis is diminished in Pdpntm2.1Mlkn/Pdpntm2.1Mlkn Tg(CAG-cre/Esr1*)5Amc/0 mice

immune system
• in corneal micropocket assays, corneas implanted with either VEGF-C or galectin-8 pellets in tamoxifen-treated mice exhibit significantly reduced lymphangiogenesis relative to similarly-implanted wild-type corneas, as quantified by the lymphatic vessel area on day 7 post-surgery




Genotype
MGI:5538607
cn11
Allelic
Composition
Tbx3tm3.1Moon/Tbx3tm3.1Moon
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tbx3tm3.1Moon mutation (0 available); any Tbx3 mutation (38 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Atrioventricular block in tamoxifen treated Tbx3tm3.1Moon/Tbx3tm3.1Moon Tg(CAG-cre/Esr1*)5Amc/0 mice

cardiovascular system
• in tamoxifen-treated mice
• second degree in tamoxifen-treated mice




Genotype
MGI:5691394
cn12
Allelic
Composition
Hap1tm2Xjl/Hap1tm2Xjl
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129 * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hap1tm2Xjl mutation (0 available); any Hap1 mutation (29 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• mice treated with tamoxifen at early postnatal times (P1), but not at late postnatal times or as adults, show increased immobility in the forced swim test and in the tail suspension test
• mice treated with tamoxifen at P21 do not exhibit impaired hippocampal neurogenesis under normal conditions, however after repeated restraint stress, these mice show an increase in immobility compared to non-stressed mutants and stressed controls
• mice treated with tamoxifen at an early age exhibit lower locomotor activity as adults

nervous system
• mice treated with tamoxifen at P1 show impaired neuronal differentiation in the hippocampus as indicated by a lower ratio of NeuN+/BrdU+ cells than in controls and a higher ratio of GFAP+/BrdU+ cells among BrdU+ cells
• a decrease in proliferating cells is seen in the hippocampal dentate gyrus when mice are treated with tamoxifen at P1, but not when mice are treated with tamoxifen at P21

cellular
• mice treated with tamoxifen at P1 show impaired neuronal differentiation in the hippocampus as indicated by a lower ratio of NeuN+/BrdU+ cells than in controls and a higher ratio of GFAP+/BrdU+ cells among BrdU+ cells
• a decrease in proliferating cells is seen in the hippocampal dentate gyrus when mice are treated with tamoxifen at P1, but not when mice are treated with tamoxifen at P21

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
endogenous depression DOID:1595 OMIM:608516
J:224698




Genotype
MGI:6712827
cn13
Allelic
Composition
Seh1ltm1Lzha/Seh1ltm1Lzha
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129 * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Seh1ltm1Lzha mutation (0 available); any Seh1l mutation (78 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• tamoxifen-treated mice show a translucent optic nerve indicating a severe deficiency of myelin formation




Genotype
MGI:6449234
cn14
Allelic
Composition
Dicer1tm1Bdh/Dicer1tm1Bdh
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129 * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dicer1tm1Bdh mutation (4 available); any Dicer1 mutation (71 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
muscle
• lower mean of regenerating myofiber cross-sectional area of tibialis anterior (TA) muscle 14 days after intramuscular injection of cardiotoxin (CTX), after induction of knockout with tamoxifen
• normal number of satellite cells and normal primary myoblast differentiation and viability after induction of knockout with tamoxifen




Genotype
MGI:4353177
cn15
Allelic
Composition
Pax3tm1.1Sjc/Pax3tm1.1Sjc
Pax7tm1.2Fan/Pax7tm1.2Fan
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pax3tm1.1Sjc mutation (0 available); any Pax3 mutation (41 available)
Pax7tm1.2Fan mutation (0 available); any Pax7 mutation (35 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
muscle
N
• following tamoxifen-treatment, muscle regeneration is normal as are the proliferative and myogenic properties of adult myoblasts




Genotype
MGI:4834592
cn16
Allelic
Composition
Tardbptm1.1Pcw/Tardbptm1.1Pcw
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tardbptm1.1Pcw mutation (1 available); any Tardbp mutation (55 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• after cre induction by tamoxifen, mice show decrease in body relative to controls

cellular
• increased fat oxidation after loss of Tardbp results in fat loss in adipocytes

adipose tissue
• inspection of animals dying after cre induction by tamoxifen shows loss of body fat in these mice
• analyses of carcasses show significant decreases in whole body fat mass, but not lean mass
• absence of fatty acid vacuoles in adipocytes in interscapular brown fat is detected
• adipocytes are present in brown fat, but lack of stored fat within adipocytes results in loss of fat content in animals after induction by tamoxifen
• dramatic fat loss is observed
• reduction of fatty acid vacuoles in adipocytes in subcutaneous fat is detected
• adipocytes are present in white fat, but lack of stored fat within adipocytes results in loss of fat content in animals after induction by tamoxifen

homeostasis/metabolism
• increased fat oxidation after loss of Tardbp results in fat loss in adipocytes




Genotype
MGI:3773016
cn17
Allelic
Composition
Sox4tm1Vlf/Sox4tm1Vlf
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sox4tm1Vlf mutation (0 available); any Sox4 mutation (14 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• when treated with tamoxifen, mice die between E13.5 and E14.5 likely due to regurgitation of blood into the heart

cardiovascular system
• when treated with tamoxifen
• at E13.5, mice exhibit incomplete septation of the ventricles when treated with tamoxifen
• endocardial cushions form at the level of the semilunar valve but functional flaps do not form when treated with tamoxifen

homeostasis/metabolism
• at E13.5 when treated with tamoxifen




Genotype
MGI:5318110
cn18
Allelic
Composition
Cdk1tm2.1Kald/Cdk1tm2.1Kald
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdk1tm2.1Kald mutation (0 available); any Cdk1 mutation (18 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• tamoxifen-treated mouse embryonic fibroblasts fail to exhibit DNA re-replication unlike control cells
• however, initial DNA replication is normal
• in mouse embryonic fibroblasts treated with tamoxifen
• in mouse embryonic fibroblasts treated with tamoxifen

neoplasm
• following tamoxifen treatment of tumor cells induced by activated Ras

homeostasis/metabolism
• tamoxifen-treated mouse embryonic fibroblasts fail to exhibit DNA re-replication unlike control cells
• however, initial DNA replication is normal




Genotype
MGI:4834589
cn19
Allelic
Composition
Tardbptm1.1Pcw/Tardbp+
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tardbptm1.1Pcw mutation (1 available); any Tardbp mutation (55 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• after cre induction by tamoxifen, mice show decrease in body weight relative to controls

adipose tissue
• absence of fatty acid vacuoles in adipocytes in interscapular brown fat is detected
• reduction of fatty acid vacuoles in adipocytes in subcutaneous fat is detected




Genotype
MGI:6194636
cn20
Allelic
Composition
Celf4tm1.1Frk/Celf4tm1.1Frk
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Celf4tm1.1Frk mutation (2 available); any Celf4 mutation (20 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• tamoxifen-induced deletion at 7 weeks of age is sufficient to cause a lowered threshold for handling-associated convulsive seizures
• tamoxifen-induced cre excision of Celf4 must occur by 1 day of age in order to develop a high incidence of spike wave discharge, and induced deletion at 5 to 7 days of age or later fails to result in increased absence seizures

nervous system
• tamoxifen-induced deletion at 7 weeks of age is sufficient to cause a lowered threshold for handling-associated convulsive seizures
• tamoxifen-induced cre excision of Celf4 must occur by 1 day of age in order to develop a high incidence of spike wave discharge, and induced deletion at 5 to 7 days of age or later fails to result in increased absence seizures




Genotype
MGI:5704117
cn21
Allelic
Composition
Tg(CAG-cre/Esr1*)5Amc/0
Ube3atm1Yelg/Ube3a+
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPasCrl * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
Ube3atm1Yelg mutation (0 available); any Ube3a mutation (48 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• mice with a maternally inherited allele treated with tamoxifen at 3, 6, or 14 weeks of age show alterations in marble burying, indicating no rescue of this phenotype when gene expression is re-established at those times
• tamoxifen treatment of mice with a maternally inherited allele immediately after birth via administration to lactating dams does not rescue the deficits in marble burying
• mice treated with tamoxifen at 3, 6, or 14 weeks of age show alterations in the forced swim test, indicating no rescue of this phenotype
• tamoxifen treatment of mice with a maternally inherited allele immediately after birth via administration to lactating dams does not rescue the deficits in the forced swim test
• mice with a maternally inherited allele treated with tamoxifen at 14 weeks (adults) do not show any rescue of motor coordination deficit at 28 weeks of age
• however, mice with a maternally inherited allele treated with tamoxifen at 6 weeks (adolescents) show partial rescue of motor coordination deficit at 22 weeks of age and mice treated with tamoxifen at 3 weeks (juveniles) show full rescue of motor coordination deficit at 16 weeks of age
• tamoxifen treatment of mice with a maternally inherited allele immediately after birth via administration to lactating dams rescues fully the motor coordination deficit
• mice with a maternally inherited allele treated with tamoxifen at 3, 6, or 14 weeks of age show alterations in the open field explorations, indicating no rescue of this phenotype
• however, tamoxifen treatment of mice with a maternally inherited allele immediately after birth via administration to lactating dams results in improved performance in the open field
• mice with a maternally inherited allele treated with tamoxifen at 3, 6, or 14 weeks of age show alterations in nest building, indicating no rescue of this phenotype
• tamoxifen treatment of mice with a maternally inherited allele immediately after birth via administration to lactating dams does not rescue the deficits in nest building
• mice with a maternally inherited allele treated with tamoxifen at 3 weeks of age show increased audiogenic seizure threshold, indicating no rescue of this phenotype

nervous system
• mice with a maternally inherited allele treated with tamoxifen at 3 weeks of age show increased audiogenic seizure threshold, indicating no rescue of this phenotype
• mice with a maternally inherited allele not treated with tamoxifen exhibit abnormal Schaffer collateral-CA1 long term potentiation indicating a hippocampal plasticity deficit
• mice with a maternally inherited allele show full recovery of hippocampal LTP when treated with tamoxifen at 3 and 14 weeks of age




Genotype
MGI:4453348
cn22
Allelic
Composition
Lhx2tm1Monu/Lhx2tm1Monu
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lhx2tm1Monu mutation (0 available); any Lhx2 mutation (10 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• most mice shaved and treated with Tamoxifen at 3 weeks of age do not regrow hair
• unable to develop beyond Sub-stage III and assemble a normal hair shaft




Genotype
MGI:4453346
cn23
Allelic
Composition
Lhx2tm1Monu/Lhx2tm1Dra
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lhx2tm1Dra mutation (0 available); any Lhx2 mutation (10 available)
Lhx2tm1Monu mutation (0 available); any Lhx2 mutation (10 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• most mice shaved and treated with Tamoxifen at 3 weeks of age do not regrow hair
• unable to develop beyond Sub-stage III and assemble a normal hair shaft




Genotype
MGI:3833891
cn24
Allelic
Composition
Supv3l1tm2.1Jkl/Supv3l1tm2.2Jkl
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Supv3l1tm2.1Jkl mutation (0 available); any Supv3l1 mutation (26 available)
Supv3l1tm2.2Jkl mutation (0 available); any Supv3l1 mutation (26 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Thymic atrophy in Supv3l1tm2.1Jkl/Supv3l1tm2.2Jkl Tg(CAG-cre/Esr1*)5Amc/0 mice

mortality/aging
• mice die by 15 weeks of age
• tamoxifen-treated mice die by 6 weeks of age

immune system
• in the lungs in tamoxifen-treated mice
• mice exhibit thymic atrophy that develops more rapidly in tamoxifen treated mice
• 6-fold in tamoxifen-treated mice compared to mice heterozygous for the floxed allele
• tamoxifen-treated mice exhibit decreased DN2, DN3, and DN4 cells compared to mice heterozygous for the floxed allele
• in tamoxifen-treated mice
• more than 10-fold in tamoxifen-treated mice
• chronic and acute in untreated and tamoxifen-treated mice

growth/size/body
• in tamoxifen-treated mice

adipose tissue
• mice exhibit adipose tissue loss that develops more rapidly in tamoxifen treated mice

respiratory system
• chronic and acute in untreated and tamoxifen-treated mice
• thickened in in tamoxifen-treated mice and untreated mice

muscle
• mice exhibit sarcopenia atrophy that develops more rapidly in tamoxifen treated mice

skeleton
• mice exhibit kyphosis that develops more rapidly in tamoxifen treated mice

endocrine/exocrine glands
• mice exhibit thymic atrophy that develops more rapidly in tamoxifen treated mice
• 6-fold in tamoxifen-treated mice compared to mice heterozygous for the floxed allele
• in tamoxifen-treated mice, the numbers of sebaceous glands is reduced compared to in untreated mice

cardiovascular system
• tamoxifen-treated mice exhibit focal vascular ectasia in the skin unlike in untreated mice
• mice treated topically with tamoxifen exhibit dilated vasculature at the site of application

behavior/neurological
• locomotor functions fail in moribund mice

digestive/alimentary system
• tamoxifen-treated mice exhibit an increase in apoptosis compared to untreated mice

hematopoietic system
• in the lungs in tamoxifen-treated mice
• mice exhibit thymic atrophy that develops more rapidly in tamoxifen treated mice
• 6-fold in tamoxifen-treated mice compared to mice heterozygous for the floxed allele
• tamoxifen-treated mice exhibit decreased DN2, DN3, and DN4 cells compared to mice heterozygous for the floxed allele
• in tamoxifen-treated mice
• more than 10-fold in tamoxifen-treated mice

cellular
• in the lungs in tamoxifen-treated mice

integument
N
• unlike in Supv3l1tm2Jkl/Supv3l1tm2Jkl floxed Tg(Mx1-cre)1Cgn mice, tamoxifen-treated mice exhibit normal hair growth
• mice exhibit adipose tissue loss that develops more rapidly in tamoxifen treated mice
• in tamoxifen-treated mice, the numbers of sebaceous glands is reduced compared to in untreated mice
• tamoxifen treated mice exhibit focal vascular ectasia, reduced adipose tissue, and atrophic muscle layer in the skin unlike in untreated mice
• apoptosis rates in the basal layer are increased in tamoxifen-treated mice compared to in untreated mice
• mild in tamoxifen-treated mice and at the site of application in mice treated topically with tamoxifen
• at the site of tamoxifen application when applied directly to the skin
• hypergranulosis develops in tamoxifen-treated mice and at the site of application in mice treated topically with tamoxifen
• in tamoxifen-treated mice
• in tamoxifen-treated mice and at the site of tamoxifen application when applied directly to the skin
• at the site of tamoxifen application when applied directly to the skin
• on the skin and tails of tamoxifen-treated mice and at the site of tamoxifen application when applied directly to the skin




Genotype
MGI:4361221
cn25
Allelic
Composition
St14tm2Bug/St14tm3Bug
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * Black Swiss * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
St14tm2Bug mutation (0 available); any St14 mutation (34 available)
St14tm3Bug mutation (0 available); any St14 mutation (34 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice are moribund within 9 to 10 days of tamoxifen treatment unlike similarly treated control mice

digestive/alimentary system
• tamoxifen-treated mice exhibit disruption of tight junctions unlike similarly treated wild-type mice
• tamoxifen-treated mice exhibit dissolution of tissue architecture and pronounced edema of crypts and submucosa in the large intestine unlike in similarly treated control mice
• tamoxifen-treated mice exhibit edema of the large intestine crypts unlike in similarly treated control mice
• tamoxifen-treated mice exhibit edema of the large intestine crypts and submucosa unlike in similarly treated control mice
• in tamoxifen-treated mice
• tamoxifen-treated mice exhibit a loss of intestinal barrier and increased intestinal permeability unlike similarly treated control mice
• tamoxifen-treated mice exhibit a 1.5-fold increase in epithelial cell transit through colonic crypts compared with similarly treated control mice
• tamoxifen-treated mice exhibit an increase in intestinal cell turnover compared with similarly treated control mice

craniofacial
• tamoxifen-treated mice exhibit scaling and inflammation of the orofacial surfaces unlike similarly treated control mice

endocrine/exocrine glands
• tamoxifen-treated mice exhibit edema of the large intestine crypts unlike in similarly treated control mice

growth/size/body
• tamoxifen-treated mice exhibit scaling and inflammation of the orofacial surfaces unlike similarly treated control mice
• in tamoxifen-treated mice despite normal food ingestion
• in tamoxifen-treated mice

homeostasis/metabolism
• tamoxifen-treated mice exhibit edema of the large intestine crypts and submucosa unlike in similarly treated control mice

integument
• in tamoxifen-treated mice
• tamoxifen-treated mice exhibit follicular hyperplasia compared with similarly treated control mice
• in tamoxifen-treated mice
• tamoxifen-treated mice exhibit retention and hyperproliferative ichthyosis unlike similarly treated control mice
• tamoxifen-treated mice exhibit dermal fibrosis unlike similarly treated control mice




Genotype
MGI:3833890
cn26
Allelic
Composition
Supv3l1tm2Jkl/Supv3l1tm2Jkl
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Supv3l1tm2Jkl mutation (0 available); any Supv3l1 mutation (26 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Kyphosis and scaling on feet develop in Supv3l1tm2Jkl/Supv3l1tm2Jkl Tg(CAG-cre/Esr1*)5Amc/0 mice following tamoxifen treatment

mortality/aging
• mice die by 15 weeks of age
• tamoxifen-treated mice die by 6 weeks of age

immune system
• in the lungs in tamoxifen-treated mice
• mice exhibit thymic atrophy that develops more rapidly in tamoxifen treated mice
• 6-fold in tamoxifen-treated mice compared to mice heterozygous for the floxed allele
• tamoxifen-treated mice exhibit decreased DN2, DN3, and DN4 cells compared to mice heterozygous for the floxed allele
• in tamoxifen-treated mice
• more than 10-fold in tamoxifen-treated mice
• chronic and acute in untreated and tamoxifen-treated mice

growth/size/body
• in tamoxifen-treated mice

adipose tissue
• mice exhibit adipose tissue loss that develops more rapidly in tamoxifen treated mice

respiratory system
• chronic and acute in untreated and tamoxifen-treated mice
• thickened in in tamoxifen-treated mice and untreated mice

muscle
• mice exhibit sarcopenia atrophy that develops more rapidly in tamoxifen treated mice

skeleton
• mice exhibit kyphosis that develops more rapidly in tamoxifen treated mice

endocrine/exocrine glands
• mice exhibit thymic atrophy that develops more rapidly in tamoxifen treated mice
• 6-fold in tamoxifen-treated mice compared to mice heterozygous for the floxed allele
• in tamoxifen-treated mice, the numbers of sebaceous glands is reduced compared to in untreated mice

cardiovascular system
• tamoxifen-treated mice exhibit focal vascular ectasia in the skin unlike in untreated mice
• mice treated topically with tamoxifen exhibit dilated vasculature at the site of application

behavior/neurological
• locomotor functions fail in moribund mice

digestive/alimentary system
• tamoxifen-treated mice exhibit an increase in apoptosis compared to untreated mice

hematopoietic system
• in the lungs in tamoxifen-treated mice
• mice exhibit thymic atrophy that develops more rapidly in tamoxifen treated mice
• 6-fold in tamoxifen-treated mice compared to mice heterozygous for the floxed allele
• tamoxifen-treated mice exhibit decreased DN2, DN3, and DN4 cells compared to mice heterozygous for the floxed allele
• in tamoxifen-treated mice
• more than 10-fold in tamoxifen-treated mice

cellular
• in the lungs in tamoxifen-treated mice

integument
N
• unlike in Supv3l1tm2Jkl/Supv3l1tm2Jkl floxed Tg(Mx1-cre)1Cgn mice, tamoxifen-treated mice exhibit normal hair growth
• mice exhibit adipose tissue loss that develops more rapidly in tamoxifen treated mice
• in tamoxifen-treated mice, the numbers of sebaceous glands is reduced compared to in untreated mice
• tamoxifen treated mice exhibit focal vascular ectasia, reduced adipose tissue, and atrophic muscle layer in the skin unlike in untreated mice
• apoptosis rates in the basal layer are increased in tamoxifen-treated mice compared to in untreated mice
• mild in tamoxifen-treated mice and at the site of application in mice treated topically with tamoxifen
• at the site of tamoxifen application when applied directly to the skin
• hypergranulosis develops in tamoxifen-treated mice and at the site of application in mice treated topically with tamoxifen
• in tamoxifen-treated mice
• in tamoxifen-treated mice and at the site of tamoxifen application when applied directly to the skin
• at the site of tamoxifen application when applied directly to the skin
• on the skin and tails of tamoxifen-treated mice and at the site of tamoxifen application when applied directly to the skin




Genotype
MGI:5466536
cn27
Allelic
Composition
Mcattm1.1Ssmi/Mcattm1.1Ssmi
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mcattm1.1Ssmi mutation (0 available); any Mcat mutation (5 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Hair loss and dry skin in tamoxifen treated Mcattm1.1Ssmi/Mcattm1.1Ssmi Tg(CAG-cre/Esr1*)5Amc/0 mice

mortality/aging
• severely affected tamoxifen-treated mice develop pruritus that leads to self-inflicted scratch wounds and necessitates euthanasia
• tamoxifen-treated mice that do not require euthanasia exhibit mean survival time of 293 days post-induction

hematopoietic system
• in tamoxifen-treated mice
• myeloid hematopoiesis in the bone marrow of some tamoxifen-treated mice
• in some tamoxifen-treated mice
• in some tamoxifen-treated mice
• in some tamoxifen-treated mice
• in some tamoxifen-treated mice
• in some tamoxifen-treated mice
• in some tamoxifen-treated mice
• in some tamoxifen-treated mice
• minor in some female tamoxifen-treated mice
• minor in some female tamoxifen-treated mice
• tamoxifen-treated mice that develop anemia exhibit increased number and size of reticulocyte compared with control mice
• in some tamoxifen-treated mice
• anemic tamoxifen-treated mice exhibit reduced red blood cell lifespan compared with control mice

behavior/neurological
N
• tamoxifen-treated mice exhibit normal balance and motor coordination
• in tamoxifen-treated mice
• in tamoxifen-treated mice
• severely affected tamoxifen-treated mice develop pruritus that leads to self-inflicted scratch wounds and necessitates euthanasia
• shivering in tamoxifen-treated mice
• in tamoxifen-treated mice
• tamoxifen-treated mice walk with splayed hind limbs and drag their posterior unlike control mice
• in tamoxifen-treated mice
• reduced exploration and overall activity in an open field test in tamoxifen-treated mice
• tamoxifen-treated mice on a constantly spinning rotarod exhibit reduced endurance compared with control mice

homeostasis/metabolism
• tamoxifen-treated mice on a constantly spinning rotarod exhibit reduced endurance compared with control mice
• in tamoxifen-treated mice
• tamoxifen-treated mice exhibit elevated plasma lactate compared with control mice
• decreased in tamoxifen-treated mice
• in tamoxifen-treated mice
• in tamoxifen-treated mice
• in tamoxifen-treated mice
• tamoxifen-treated mice exhibit compromised fatty acid synthesis due to reduced availability of precursors for lipoylation of key mitochondrial enzymes compared with control mice
• tamoxifen-treated mice exhibit elevated plasma ketone bodies compared with control mice

integument
• in tamoxifen-treated mice
• beginning 3 to 4 months after tamoxifen-treatment, coats have lost their normal luster compared with controls
• beginning 3 to 4 months after tamoxifen-treatment eventually resulting in severe baldness
• in tamoxifen-treated mice
• in tamoxifen-treated mice
• in severely affected tamoxifen-treated mice that leads to self-inflicted scratch wounds, necessitating euthanasia

digestive/alimentary system
N
• tamoxifen-treated mice exhibit normal digestion
• from prolapsed rectum in anemic tamoxifen-treated mice
• however, no blood is observed in the feces
• in 9 of 10 anemic tamoxifen-treated mice

cardiovascular system
• from prolapsed rectum in anemic tamoxifen-treated mice
• however, no blood is observed in the feces

growth/size/body
• tamoxifen-treated mice fail to gain weight
• after 6 months in tamoxifen-treated mice
• in tamoxifen-treated mice

immune system
• myeloid hematopoiesis in the bone marrow of some tamoxifen-treated mice
• minor in some female tamoxifen-treated mice
• minor in some female tamoxifen-treated mice
• lymphoid atrophy in some tamoxifen-treated mice
• in tamoxifen-treated mice

adipose tissue
• in tamoxifen-treated mice
• in tamoxifen-treated mice

cellular
• tamoxifen-treated mice exhibit compromised mitochondrial respiration due to defects in protein lipoylation and respiratory complexes compared with wild-type mice
• tamoxifen-treated mice exhibit compromised mitochondrial respiration due to defects in protein lipoylation and respiratory complexes compared with wild-type mice

muscle
• in tamoxifen-treated mice
• increased glycogen and lactate levels in skeletal muscle of tamoxifen-treated mice

skeleton
• in tamoxifen-treated mice




Genotype
MGI:3712287
cn28
Allelic
Composition
Mecp2tm2Bird/Mecp2+
Tg(CAG-cre/Esr1*)5Amc/?
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mecp2tm2Bird mutation (1 available); any Mecp2 mutation (37 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• at 4 to 12 months of age, mice exhibit a progressive development of RTT-like symptoms (inertia, gait, hindlimb clasping, tremor, irregular breathing and poor general condition)
• however, tamoxifen treatment after the onset of symptoms reverses symptom progression
• at 4 to 12 months of age
• however, tamoxifen treatment after the onset of symptoms reverses symptom progression
• at 4 to 12 months of age
• however, tamoxifen treatment after the onset of symptoms reverses symptom progression

nervous system
• mice develop a reduction in long term potentiation
• however, treatment with tamoxifen returns long term potentiation to normal levels

respiratory system
• at 4 to 12 months of age
• however, tamoxifen treatment after the onset of symptoms reverses symptom progression

growth/size/body
• mice exhibit excess weight gain
• however, tamoxifen treatment after the onset of symptoms reverses weight gain




Genotype
MGI:3832684
cn29
Allelic
Composition
Mecp2tm2Bird/Y
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mecp2tm2Bird mutation (1 available); any Mecp2 mutation (37 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 9 of 17 mice treated with tamoxifen at 3 to 4 weeks of age die soon after treatment
• however, tamoxifen-tocixity is not responsible for observed deaths, 8 of 17 mice treated with tamoxifen at 3 to 4 weeks of age have a normal life span, and mice treated with tamoxifen from week 12 to 17 exhibit normal lethality

behavior/neurological
N
• the surviving 8 of 17 mice treated with tamoxifen at 3 to 4 weeks of age exhibit normal behavior/neurological phenotypes
• at 12 weeks mice display low stance, inertia, tremor, arrhythmic breathing, splayed himdlimb and moderate hindlimb clasping
• during the last 4 weeks of life, mice exhibit a progressive development of RTT-like symptoms (inertia, gait, hindlimb clasping, tremor, irregular breathing and poor general condition)
• mice treated with tamoxifen at 12 to 17 weeks of age exhibit only mild RTT-like symptoms
• at 12 weeks, mice display moderate hindlimb clasping
• mice treated with tamoxifen at 12 to 17 weeks of age exhibit only mild RTT-like symptoms
• at 12 weeks
• mice treated with tamoxifen at 12 to 17 weeks of age exhibit only mild RTT-like symptoms

respiratory system
• at 12 weeks
• mice treated with tamoxifen at 12 to 17 weeks of age exhibit only mild RTT-like symptoms




Genotype
MGI:5524264
cn30
Allelic
Composition
Nrg1tm3Cbm/Nrg1tm3Cbm
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nrg1tm3Cbm mutation (0 available); any Nrg1 mutation (27 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
muscle
• small diameter with degeneration of the outer capsule in tamoxifen-treated mice
• however, innervation is normal
• in tamoxifen-treated mice

behavior/neurological
• tamoxifen-treated mice hang on to an inverted grid 3 to 4 times less than controls mice
• strongly impaired in a beam-walking test

nervous system
• however, innervation is normal
• small diameter with degeneration of the outer capsule in tamoxifen-treated mice
• in tamoxifen-treated mice




Genotype
MGI:4830343
cn31
Allelic
Composition
Recktm1Ito/Recktm1.1Noda
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Recktm1.1Noda mutation (0 available); any Reck mutation (36 available)
Recktm1Ito mutation (1 available); any Reck mutation (36 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice treated with tamoxifen at E11 die after E15.5

cardiovascular system
• at E15.5, blood vessels in tamoxifen-treated mice are large and irregularly shaped compared to in wild-type mice
• brain vasculature in tamoxifen-treated mice is disorganized and interrupted by large spaces and cavities unlike in wild-type mice
• the blood vessels in the livers of tamoxifen-treated mice exhibit larger luminal spaces than in wild-type mice
• at E15.5, blood vessels in tamoxifen-treated mice are large and irregularly shaped compared to in wild-type mice
• brain vasculature in tamoxifen-treated mice is disorganized and interrupted by large spaces and cavities unlike in wild-type mice
• the blood vessels in the livers of tamoxifen-treated mice exhibit larger luminal spaces than in wild-type mice
• in tamoxifen-treated mice
• at E15.5 in tamoxifen-treated mice

growth/size/body
• at E15.5 in tamoxifen-treated mice

liver/biliary system
• the blood vessels in the livers of tamoxifen-treated mice exhibit larger luminal spaces than in wild-type mice

nervous system
• brain vasculature in tamoxifen-treated mice is disorganized and interrupted by large spaces and cavities unlike in wild-type mice

integument
• at E15.5 in tamoxifen-treated mice




Genotype
MGI:5287435
cn32
Allelic
Composition
Ppp2r1atm1.1Wltr/Ppp2r1atm1.2Wltr
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/Sv * 129S4/SvJaeSor * C57BL/6 * CBA * FVB/NCrl
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppp2r1atm1.1Wltr mutation (1 available); any Ppp2r1a mutation (25 available)
Ppp2r1atm1.2Wltr mutation (0 available); any Ppp2r1a mutation (25 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die 6 days after tamoxifen treatment

behavior/neurological
• tamoxifen-treated mice exhibit difficulty walking compared with control mice
• in tamoxifen-treated mice

growth/size/body
• in tamoxifen-treated mice beyond the initial drop associated with tamoxifen treatment alone




Genotype
MGI:5903288
cn33
Allelic
Composition
Dohhtm1.1Sbal/Dohhtm1.1Sbal
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * BALB/cJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dohhtm1.1Sbal mutation (0 available); any Dohh mutation (12 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• in two tamoxifen-treated mice
• diffuse in one tamoxifen-treated mouse
• in one tamoxifen-treated mouse

mortality/aging
• 1 to 5 weeks after tamoxifen treatment

growth/size/body
• in tamoxifen-treated mice
• in tamoxifen-treated mice due to wasting syndrome

renal/urinary system
• in one tamoxifen-treated mouse
• enhanced ferrous iron incorporation in the kidney of 2 of 4 tamoxifen-treated mice

liver/biliary system
• in two tamoxifen-treated mice
• diffuse in one tamoxifen-treated mouse

homeostasis/metabolism
• enhanced ferrous iron incorporation in the kidney of 2 of 4 tamoxifen-treated mice

hematopoietic system
N
• tamoxifen-treated mice exhibit normal bone marrow cellularity




Genotype
MGI:4360189
cn34
Allelic
Composition
Inpp5etm1.1Ssch/Inpp5etm1.2Ssch
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Inpp5etm1.1Ssch mutation (0 available); any Inpp5e mutation (16 available)
Inpp5etm1.2Ssch mutation (0 available); any Inpp5e mutation (16 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• mice display increased body weight after tamoxifen treatment
• glomerular cysts are seen in 6 month old tamoxifen treated mice

renal/urinary system
• glomerular cysts are seen in 6 month old tamoxifen treated mice

vision/eye
• after tamoxifen treatment the retinal photoreceptor layer is completely absent




Genotype
MGI:3767641
cn35
Allelic
Composition
Bub1tm1Ssta/Bub1tm1Ssta
Tg(CAG-cre/Esr1*)5Amc/?
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bub1tm1Ssta mutation (0 available); any Bub1 mutation (37 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• after mice are treated with tamoxifen for 8 weeks, tubules exhibit decreased celullarity and diameter
• tubules containing only Sertoli cells are often observed
• after mice are treated with tamoxifen for 8 weeks, testis weight is decreased by 50% of wild-type
• after mice are treated with tamoxifen for 8 weeks, mitotic clusters of cells observed are often stuck in anaphase and abnormal chromosome content is observed
• after mice are treated with tamoxifen for 8 weeks, no male germ cells are observed
• after mice are treated with tamoxifen for 8 weeks, sperm production is reduced by 80% of wild-type
• after treated with tamoxifen for 4 weeks, adult males become infertile

cellular
• after mice are treated with tamoxifen for 8 weeks, no male germ cells are observed
• after mice are treated with tamoxifen for 8 weeks, sperm production is reduced by 80% of wild-type
• after mice are treated with tamoxifen for 8 weeks, male testes have reduced mitotic index

growth/size/body
• when mice are treated with tamoxifen beginning at E10.5, by E18.5 mice resemble E10.5 to E11.5 mice
• when mice are treated with tamoxifen beginning at E10.5, by E18.5 mice resemble E10.5 to E11.5 mice

endocrine/exocrine glands
• after mice are treated with tamoxifen for 8 weeks, tubules exhibit decreased celullarity and diameter
• tubules containing only Sertoli cells are often observed
• after mice are treated with tamoxifen for 8 weeks, testis weight is decreased by 50% of wild-type




Genotype
MGI:4438398
cn36
Allelic
Composition
Edn2tm1.1Nat/Edn2tm1.1Nat
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Edn2tm1.1Nat mutation (1 available); any Edn2 mutation (14 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Impaired lung morphology in Edn2tm1Ywa/Edn2tm1Ywa mice and tamoxifen-treated Edn2tm1.1Nat/Edn2tm1.1Nat Tg(CAG-cre/Esr1*)5Amc/0 mice

mortality/aging
• in mice treated with tamoxifen at P0
• however, adult mice treated with tamoxifen exhibit normal survival
• in mice treated with tamoxifen at P0

homeostasis/metabolism
• decreased body temperature in response to cold exposure in mice treated with tamoxifen
• blood pH is more acidic in tamoxifen-treated mice
• in tamoxifen-treated mice
• in mice treated with tamoxifen at P0 or 6 weeks of age
• in mice treated with tamoxifen at P0 or 6 weeks of age
• in tamoxifen-treated mice
• blood pH is more acidic in tamoxifen-treated mice

growth/size/body
• in mice treated with tamoxifen at P0 or 6 weeks of age
• in mice treated with tamoxifen at P0 or 6 weeks of age

respiratory system
• tamoxifen-treated mice exhibit enlarged air spaces with simplification of the alveolar structure
• simplified structure in tamoxifen-treated mice

adipose tissue
• after 10 weeks of tamoxifen-induced activation




Genotype
MGI:5438129
cn37
Allelic
Composition
Sdhdtm1Jlob/Sdhdtm2Jlob
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sdhdtm1Jlob mutation (1 available); any Sdhd mutation (13 available)
Sdhdtm2Jlob mutation (1 available); any Sdhd mutation (13 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• in tamoxifen-treated mice

nervous system
N
• tamoxifen-treatment does not affect brain catecholaminergic neurons matured at birth

cardiovascular system
• tamoxifen-treated mice exhibit a trend towards degeneration of the carotid body

neoplasm
N
• tamoxifen-treated mice do not develop tumors




Genotype
MGI:5305034
cn38
Allelic
Composition
Dscamtm1Pfu/Dscamtm1Pfu
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dscamtm1Pfu mutation (0 available); any Dscam mutation (65 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
• following tamoxifen treatment at E13 or E16 dopaminergic amacrine cells and neurites are clumped
• following tamoxifen treatment at P0
• following tamoxifen treatment at P0 2?3 fasciculated groups of melanopsin positive retinal ganglion cells are seen in each retina

nervous system
• following tamoxifen treatment at E13 or E16 dopaminergic amacrine cells and neurites are clumped
• following tamoxifen treatment at P0, 2?3 fasciculated groups of retinal ganglion cells are seen in each retina
• however with tamoxifen treatment at P0 or in adults no fasiculation of amacrine cell neurites is seen
• following tamoxifen treatment at E13 or E16 dopaminergic amacrine cells and neurites are clumped
• following tamoxifen treatment at P0
• following tamoxifen treatment at P0 2?3 fasciculated groups of melanopsin positive retinal ganglion cells are seen in each retina

cellular
• following tamoxifen treatment at E13 or E16 dopaminergic amacrine cells and neurites are clumped
• following tamoxifen treatment at P0, 2?3 fasciculated groups of retinal ganglion cells are seen in each retina
• however with tamoxifen treatment at P0 or in adults no fasiculation of amacrine cell neurites is seen




Genotype
MGI:3767640
cn39
Allelic
Composition
Bub1tm1Ssta/Bub1tm1.1Ssta
Tg(CAG-cre/Esr1*)5Amc/?
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bub1tm1.1Ssta mutation (0 available); any Bub1 mutation (37 available)
Bub1tm1Ssta mutation (0 available); any Bub1 mutation (37 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• sister chromatid cohesion is defective in tamoxifen-treated mouse embryonic fibroblasts
• the spindle assembly checkpoint is defective in tamoxifen-treated mouse embryonic fibroblasts
• unlike untreated cells, tamoxifen-treated mouse embryonic fibroblasts stop proliferating in culture




Genotype
MGI:5431829
cn40
Allelic
Composition
Kcnq1ot1tm2.1Ckan/Kcnq1ot1+
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA * SD7
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kcnq1ot1tm2.1Ckan mutation (0 available); any Kcnq1ot1 mutation (0 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• loss of methylation in the somatic differentially methylated regions following tamoxifen treatment at E8.5 when the Kcnq1ot1 allele is inherited paternally
• loss of imprinting of ubiquitously imprinted genes following tamoxifen treatment at E8.5 when the Kcnq1ot1 allele is inherited paternally
• however, silencing of placental-specific imprinted genes is variably maintained
• no alteration of imprinting status when the Kcnq1ot1 allele is inherited maternally




Genotype
MGI:3838126
cn41
Allelic
Composition
Numa1tm1.1Dwc/Numa1tm1.1Dwc
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Numa1tm1.1Dwc mutation (0 available); any Numa1 mutation (51 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Spindle defects in primay Numa1tm1.1Dwc/Numa1tm1.1Dwc Tg(CAG-cre/Esr1*)5Amc/0 fibroblasts

cellular
N
• despite spindle defects, bulk chromosome segregation is largely normal
• tamoxifen-treated mouse embryonic fibroblasts (MEFs) exhibit detachment of microtubule-nucleating structures from the ends of the mitotic spindles unlike wild-type cells
• 50% of metaphase-like tamoxifen-treated MEFs have at least one centrosome that is not clearly associated with a spindle pole unlike in wild-type cells
• tension between sister kinetochores in pole-focused spindles in tamoxifen-treated MEFs exposed to MG132 is 33% less than in wild-type cells
• more like tamoxifen-treated MEFs exhibit pole defocusing and centrosome detachment than in wild-type cells
• tamoxifen-treated mouse embryonic fibroblasts (MEFs) fail to increase in number after release from growth arrest unlike wild-type cells




Genotype
MGI:7266814
cn42
Allelic
Composition
Htttm1Mem/Htttm6Mem
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA * Swiss Webster
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Htttm1Mem mutation (1 available); any Htt mutation (121 available)
Htttm6Mem mutation (0 available); any Htt mutation (121 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• mice administered tamoxifen after P21 exhibit progressive neurological abnormalities; all abnormalities reported below are in mice treated with tamoxifen from P21-P26
• tamoxifen-treated mice exhibit clasping
• mice administered tamoxifen from P21 to P26 exhibit abnormalities of motor coordination at 6 months of age
• mice administered tamoxifen after P21 show Straub tail at one year of age
• tamoxifen-treated mice exhibit gait disturbances at one year of age, including flattened pelvic elevation, abnormally wide hindlimb stance, and occasional hopping and stiffness
• gait abnormalities worsen over time such that 1-year-old mice lack the typical uniformity of step alternation and exhibit smaller gait strides
• 1-year-old tamoxifen-treated mice exhibit smaller gait strides
• mice administered tamoxifen from P21 to P26 exhibit a hyperkinetic phenotype at 6 months of age
• tamoxifen-treated mice exhibit handling induced seizures, characterized by alternating clonic movement of forelimbs, clonic and versive movements of the head, chewing movement and facial myoclonus, flagpole tail dodrsiflexion, followed by intermittent eye blinking, immobility, head nodding and clonic mouth jerks

growth/size/body
• mice administered tamoxifen from P21 to P26 consistently show lower weight during adult life

muscle
• 16-month-old mice exhibit atrophy of hindlimb muscles when tamoxifen is administered after P21

nervous system
• tamoxifen-treated mice exhibit handling induced seizures, characterized by alternating clonic movement of forelimbs, clonic and versive movements of the head, chewing movement and facial myoclonus, flagpole tail dodrsiflexion, followed by intermittent eye blinking, immobility, head nodding and clonic mouth jerks
• the number of degenerating neurons in the outer cortical layers of tamoxifen-treated mice, especially in layer III/IV is increased
• layer VI thickness and numbers of neurons are reduced in the motor cortex of 12-month-old tamoxifen-treated mice
• the number of degenerating neurons in the deep layer motor cortex are increased in 12-month-old tamoxifen-treated mice
• the reduction in motor cortex layer VI is seen as early as 3 months of age, however the number of neurons in layer VI is comparable to wild-type at this age
• majority of tamoxifen-treated mice exhibit smaller cerebellar lobules
• P21 mice show fewer APC+ smooth- and ramified-type oligodendrocytes
• 3-month-old mice show a reduction of smooth- and ramified-type oligodendrocytes in layer VI of the motor cortex, with an increase of stellar-type oligodendrocytes
• however, overall number of APC+ oligodendrocytes is normal in 3-month-old tamoxifen-treated mice
• oligodendrocyte progenitors derived from primary embryonic neuronal stem cells display progressive maturation abnormalities, with impairments in the transition from proliferating progenitors to post-mitotic precursors and subsequent maturation and myelination
• 83.3% of 12-month-old tamoxifen-treated mice exhibit striatal reactive gliosis, with exceedingly severe gliosis in the globus pallidum
• reactive astrogliosis in superficial and cortical layers already at 3 months of age
• marker analysis indicates the presence of deficits in early neural lineage specification, migration, and regional organization, with impairments in the maturation of striatal compartmentalization
• loss of the typical palisade appearance of pseudostratified neuroepithelium encompassing Mash1+ neuronal progenitors within the E15.5 lateral ganglionic eminence
• all fetuses (E14.5, E15.5, and E17.5) and early postnatal mice (P2, P10, and P21) exhibit analogous masses consisting of heterotopic evaginations of germinative zone-derived cells from the posterior ventromedial aspect of the lateral ganglionic eminence indicating subpallial ventricular heterotopias
• a number of non-degenerative cortical neurons of tamoxifen-treated mice, particularly those in layer III/IV, exhibit intracytoplasmic inclusions corresponding to concentric membrane-bound laminated inclusions of zebra bodies
• tamoxifen-treated mice develop progressive striatal neurodegenerative pathology and cortical deep layer degeneration
• 27.3% of 12-month-old tamoxifen-treated mice show degenerative changes in the posterior ventrolateral striatum and the endopiriform claustrum
• motor cortex of tamoxifen-treated mice shows axons of larger caliber displaying Wallerian-like degenerative morphology
• 12-month-old tamoxifen-treated mice exhibit hypomyelinated axons in cortical deep layers, as well as axons with myelin balloons and tuberovesicular structures
• myelination defects preferentially affect axons of larger caliber, with reduced periodicity of myelin lamellae in large axons
• similar myelin defects are seen on white matter tracts containing axonal bundles traveling across the striatum

skeleton
• 16-month-old mice exhibit lordokyphosis when tamoxifen is administered after P21

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Huntington's disease DOID:12858 OMIM:143100
J:260244




Genotype
MGI:3693848
cn43
Allelic
Composition
Six3tm2Gco/Six3tm2.1Gco
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Six3tm2.1Gco mutation (0 available); any Six3 mutation (11 available)
Six3tm2Gco mutation (0 available); any Six3 mutation (11 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
• defects are observed starting at E10.5
• reduction in size of invaginating lens pit is observed in mildly and moderately affected embryos
• at E14.5, some embryos have an abnormally persistent lens stalk
• differentiation of lens is not affected in mildly or moderately affected mutant lenses
• in severely affected lenses at E10.5, no lens-like structures are present
• at E12.5, in mild cases, lens vesicle is small but relatively normal, small and abnormal in moderated cases and completely absent in severely affected embryos and neuroretinal is malformed also
• at E14.5 some embryos show disorganized lens fibers
• lens is absent in some mutants
• cataracts are present in some mice
• some mice show drastically reduced lens size
• shape of vesicle is defective




Genotype
MGI:3809283
cn44
Allelic
Composition
Gdnftm1Bbd/Gdnftm1Jlob
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gdnftm1Bbd mutation (0 available); any Gdnf mutation (12 available)
Gdnftm1Jlob mutation (0 available); any Gdnf mutation (12 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• tamoxifen treatment leads to the death of catecholaminergic neurons in the brain
• 210 days after tamoxifen treatment, there is a substantial lose (about 50%) of tyrosine hydroxylase positive neurons in the substantia nigra adult mice
• there is also a drop in the total number of neurons in the substantia nigra after tamoxifen treatment
• 210 days after tamoxifen treatment, there is a substantial lose (about 2.5-fold) of tyrosine hydroxylase positive neurons in the ventral tegmentum of adult mice
• there is also a drop in the total number of neurons in the ventral tegmentum after tamoxifen treatment
• neurons are diminished in the locus ceruleus 210 days after tamoxifen treatment
• fiber density of tyrosine hydroxylase positive neurons are diminished 210 days after tamoxifen treatment
• fiber density of tyrosine hydroxylase positive neurons are diminished 210 days after tamoxifen treatment

behavior/neurological
• 100 days after tamoxifen injection, mice have reduced activity in open field tests with about 25% less activity
• resting time of mice in open field tests increases significantly 100 days after tamoxifen treatment
• this hypoactivity worsens with the passage of time

cardiovascular system
• tyrosine hydroxylase positive neurons are diminished by more than half 210 days after tamoxifen-treatment




Genotype
MGI:5784520
cn45
Allelic
Composition
Glstm2.1Sray/Gls+
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Glstm2.1Sray mutation (1 available); any Gls mutation (31 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• attenuated locomotor response to amphetamine in tamoxifen-treated mice as compared to controls
• amphetamine-induced hyperlocomotion is blocked in open field test
• decrease in fine movements, but not rearing, following administration of amphetamine in tamoxifen-treated mice as compared to controls




Genotype
MGI:5440734
cn46
Allelic
Composition
Wnt5atm1.1Tpy/Wnt5atm1.1Tpy
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
Wnt5atm1.1Tpy mutation (0 available); any Wnt5a mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• abnormal wound channels containing fewer invaginations at day 6 and lacking crypt like structures at day 8 are seen after colonic mucosal injury in tamoxifen treated mice

homeostasis/metabolism
• abnormal wound channels containing fewer invaginations at day 6 and lacking crypt like structures at day 8 are seen after colonic mucosal injury in tamoxifen treated mice




Genotype
MGI:5795834
cn47
Allelic
Composition
Pnkptm1.1Pmc/Pnkptm1.1Pmc
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pnkptm1.1Pmc mutation (0 available); any Pnkp mutation (31 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• mice treated with tamoxifen at P10 (3 doses every 2 days) exhibit apoptosis in the dentate gyrus at P20

growth/size/body
• mice treated with tamoxifen at P7 exhibit a decreased body size at P13
• mice treated with tamoxifen at P10 (3 doses every 2 days) exhibit a modest effect on brain size at P20

nervous system
• mice treated with tamoxifen at P10 (3 doses every 2 days) exhibit apoptosis in the dentate gyrus at P20
• mice treated with tamoxifen at P7 exhibit decreased brain size
• however, mice treated with tamoxifen at P21 (3 doses every 2 days) exhibit little overall effect on brain size or structure
• mice treated with tamoxifen at P7 exhibit a reduction in cortical size
• mice treated with tamoxifen at P21 (3 doses every 2 days) exhibit a decrease in oligodendrocyte numbers in the dentate gyrus but not in the cortex at P33
• mice treated with tamoxifen at P21 show a reduction of mature neurons in the dentate gyrus, the hippocampal CA3 region and the cerebellum
• myelin-producing oligodendrocytes from mice treated with tamoxifen at P21 show a reduction in myelination
• mice treated with tamoxifen at P10 (3 doses every 2 days) exhibit a loss of myelination in the dentate gyrus at P20
• mice treated with tamoxifen at P14 (3 doses every 2 days) exhibit a loss of myelination of oligodendrocytes at P30




Genotype
MGI:4839181
cn48
Allelic
Composition
Rapgef2tm1.1Hous/Rapgef2tm1.1Hous
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rapgef2tm1.1Hous mutation (1 available); any Rapgef2 mutation (50 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most mice treated with tamoxifen at E11.5 and E13.5 die E17.5 and E18.5 with remaining mice dying at E19.5 to E10.5
• however, mice treated with tamoxifen at E17.5 and E19.5 exhibit the same lethality as in similarly treated Rapgef2tm1.1Hous homozygotes

hematopoietic system
• mice treated with tamoxifen at E11.5 and E13.5 exhibit impaired fetal liver hematopoiesis with reduced differentiation of erythroid progenitor cells compared with similarly treated Rapgef2tm1.1Hous homozygotes
• at E16.5 in the livers of mice treated with tamoxifen at E11.5 and E13.5

cardiovascular system
• at E17.5, mice treated with tamoxifen at E11.5 and E13.5 lack major embryonic blood vessels unlike wild-type mice

growth/size/body
• in mice treated with tamoxifen at E17.5 and E19.5

liver/biliary system
• at E16.5 in mice treated with tamoxifen at E11.5 and E13.5

integument
• at E17.5 in mice treated with tamoxifen at E11.5 and E13.5




Genotype
MGI:4415303
cn49
Allelic
Composition
Ate1tm1Avar/Ate1tm2.1Avar
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ate1tm1Avar mutation (0 available); any Ate1 mutation (30 available)
Ate1tm2.1Avar mutation (0 available); any Ate1 mutation (30 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Small and lean phenotype of Ate1tm1Avar/Ate1tm2.1Avar Tg(CAG-cre/Esr1*)5Amc/0 mice

mortality/aging
• 15% (18 of 119 mice) die over 42 days after TM treatment
• 46% of mice younger than 30 days at the beginning of TM treatment die within 42 days after TM treatment
• 12% of mice die if they are older than 30 days (up to 56 days) at the beginning of TM treatment

growth/size/body
• hearts are disproportionately large
• decreased growth
• attaining only 70% of normal weight
• no decrease in their consumption of food
• during the first 3 weeks after TM treatment, rapid loss of weight
• all the phenotypes below are induced by tamoxifen (TM) treatment
• 5% smaller average body length (p<0.08)
• resistant to high-fat diet induced obesity
• kidneys are disproportionately large

behavior/neurological
• higher than normal food intake
• within a week after TM treatment increased food consumption (125%) which continues up to 8 months
• 53% (95 of 180) of surviving mice appear ''scruffy'', versus 3% (8 of 244) of wild type
• enhanced startle response
• most mice (96 of 180) are strikingly hyperkinetic in the open field test
• travel 3-fold greater distance in an open field
• 10-fold higher propensity for seizures
• 3.1% mice (38 of 1,232) have tonic-clonic seizures during routine cage changes and handling of mice, versus 0.3% of wild type mice

adipose tissue
• strikingly lower content of the peritoneal white adipose tissue (WAT), on average only 16% of WAT in wild type mice
• contain little or no visceral fat
• decrease average diameter of intrascapular brown adipocytes
• the average diameter of WAT adipocytes is 30% of that of the wild type mice
• exhibit ectopic induction of the uncoupling protein 1 (Ucp1) in white adipose tissue

homeostasis/metabolism
• resistant to high-fat diet induced obesity
• strongly hypersensitive to cold
• decreased fasting blood glucose level (88.6 mg/dl versus 125.3 mg/dl)
• lower glucose levels 6 hr after administration of glucose (80.9 mg/dl versus 109.7 mg/dl)
• no other significant differences in blood composition
• lower core body temperature on average 35.1C (36.7C in wild type)
• the average water content and dry weight was 80.5% and 19.5%, respectively, versus 79.9% and 20.1% of wild type brains
• increased metabolic rate (resting metabolic rate, RMR)
• consume on average 46.12 ml of oxygen per kg per min, versus 29.3 ml of oxygen per kg per min
• decreased expression of mRNA encoding proopiomelanocortin (POMC) in hypothalami
• normal respiratory exchange ratio (RER)

nervous system
• 10-fold higher propensity for seizures
• 3.1% mice (38 of 1,232) have tonic-clonic seizures during routine cage changes and handling of mice, versus 0.3% of wild type mice
• the average water content and dry weight was 80.5% and 19.5%, respectively, versus 79.9% and 20.1% of wild type brains
• brains appear swollen and bigger
• the average brain weight, as a percentage of total body weight (TBW) are 3.09%, versus 1.96% of wild type mice
• no differences in cell proliferation (5-ethynyl-29-deoxyuridine (EdU) incorporation)

skeleton
• the skulls appear to be thinner and softer
• 66% (109 of 180) of surviving mice have a kyphotic posture, versus 2% (5 of 244) of wild type

reproductive system
• lumens of seminiferous tubules contain few sperm cells, in a disorganized arrangement
• lumens of seminiferous tubules contain few sperm cells
• testis extracts contain the 85-kDa fragment of poly(ADP-ribose)-polymerase (PARP) but no full-length PARP, indicating extensive apoptosis
• males are infertile

cardiovascular system
• hearts are disproportionately large

renal/urinary system
• kidneys are disproportionately large

cellular
• lumens of seminiferous tubules contain few sperm cells, in a disorganized arrangement
• lumens of seminiferous tubules contain few sperm cells
• increased retention of 14C in their brains, livers, spleens, kidneys and hearts

digestive/alimentary system
• increased intestinal import of 14C-protein

pigmentation
• 10% (8 of 80) of surviving mice develop patches of red hair among their normally black hair

endocrine/exocrine glands
• testis extracts contain the 85-kDa fragment of poly(ADP-ribose)-polymerase (PARP) but no full-length PARP, indicating extensive apoptosis

craniofacial
• the skulls appear to be thinner and softer

integument
• 10% (8 of 80) of surviving mice develop patches of red hair among their normally black hair




Genotype
MGI:3842509
cn50
Allelic
Composition
Kmt5atm1.1Dare/Kmt5atm1.2Dare
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kmt5atm1.1Dare mutation (0 available); any Kmt5a mutation (50 available)
Kmt5atm1.2Dare mutation (0 available); any Kmt5a mutation (50 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• tamoxifen-treated embryonic stem cells exhibit global chromosomal decondensation at interphase compared to in wild-type cells
• tamoxifen-treated embryonic stem cells exhibit increased DNA damage compared to wild-type cells
• tamoxifen-treated embryonic stem cells exhibit decreased DNA synthesis compared to in wild-type cells
• tamoxifen-treated embryonic stem cells exhibit a defect in cell growth at G2/M phase unlike wild-type cells
• 24 hours after tamoxifen treatment, embryonic stem cells undergo apoptosis unlike wild-type cells

homeostasis/metabolism
• tamoxifen-treated embryonic stem cells exhibit increased DNA damage compared to wild-type cells
• tamoxifen-treated embryonic stem cells exhibit decreased DNA synthesis compared to in wild-type cells




Genotype
MGI:5301413
cn51
Allelic
Composition
Mecomtm1Aspe/Mecomtm2.1Aspe
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/SvImJ * C57BL/6 * C57BL/6J * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mecomtm1Aspe mutation (1 available); any Mecom mutation (52 available)
Mecomtm2.1Aspe mutation (1 available); any Mecom mutation (52 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• tamoxifen-treated mice lack long-term repopulating cells (or high proliferative potential colony-forming cells; HPP-CFC) unlike wild-type mice
• granulocyte and macrophage progenitors (CFU-G and CFU-M, respectively) are increase compared with wild-type mice
• tamoxifen-treated mice exhibit fewer multipotent progenitors (CFU-GEMM) and granulocyte-macrophage progenitor (CFU-GM) compared with wild-type mice




Genotype
MGI:5301414
cn52
Allelic
Composition
Mecomtm2.1Aspe/Mecomtm2.1Aspe
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/SvImJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mecomtm2.1Aspe mutation (1 available); any Mecom mutation (52 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• tamoxifen-treated mice lack long-term repopulating cells (or high proliferative potential colony-forming cells; HPP-CFC) unlike wild-type mice
• granulocyte and macrophage progenitors (CFU-G and CFU-M, respectively) are increase 3- to 4-fold compared with wild-type mice
• tamoxifen-treated mice exhibit fewer multipotent progenitors (CFU-GEMM) and granulocyte-macrophage progenitor (CFU-GM) compared with wild-type mice




Genotype
MGI:5086257
cn53
Allelic
Composition
Cxadrtm1.1Ics/Cxadrtm1.1Ics
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * C57BL/6J * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cxadrtm1.1Ics mutation (1 available); any Cxadr mutation (9 available)
Tg(CAG-cre/Esr1*)5Amc mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• mice treated with tamoxifen at 4 weeks of age show a reduced tendency to freeze when transferred to a novel environment

cardiovascular system
• most discs are severely changed with disconnection between myofilaments and the presence of big vacuoles-containing parts of membranes in tamoxifen treated mice
• the outline of the junction is also changed with the distance between zonula adherens being wider and containing clot like contents in some areas
• complete atrioventricular block with temporal dissociation between atrial depolarization and ventricular depolarization in mice treated with tamoxifen at 4 weeks of age at 24 weeks after the last tamoxifen treatment

digestive/alimentary system
• atrophy and metaplastic phenotype are present as early as 3 weeks after tamoxifen treatment and is maintained up to 18 months after tamoxifen treatment
• almost a complete lack of acinar cells in mice treated with tamoxifen at 4 weeks of age
• in mice treated with tamoxifen at 4 weeks of age
• dilated intestine in mice treated with tamoxifen at 4 weeks of age at up to 18 months after the last tamoxifen treatment

endocrine/exocrine glands
• in tamoxifen treated mice 2 -3 days after the last treatment
• in tamoxifen treated mice 2 -3 days after the last treatment
• in mice treated with tamoxifen at 4 weeks of age the pancreas consists of mainly adipose tissue in which apparently normal islets of Langerhans are interspersed