About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Tek-cre)1Ywa
transgene insertion 1, Masashi Yanagisawa
MGI:2450311
Summary 158 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Nrastm1Tyj/Nras+
Tg(Tek-cre)1Ywa/0
B6.Cg-Nrastm1Tyj Tg(Tek-cre)1Ywa MGI:7544842
cn2
Snai1tm1.1Stjw/Snai1tm1.1Stjw
Tg(Tek-cre)1Ywa/0
B6.Cg-Snai1tm1.1Stjw Tg(Tek-cre)1Ywa MGI:5659607
cn3
Arg1tm1Pmu/Arg1tm1Pmu
Tg(Tek-cre)1Ywa/?
B6.Cg-Tg(Tek-cre)1Ywa Arg1tm1Pmu MGI:3826863
cn4
Ccm2tm1Etl/Ccm2tm1Etl
Tg(Tek-cre)1Ywa/0
B6.Cg-Tg(Tek-cre)1Ywa Ccm2tm1Etl MGI:3837692
cn5
Fcgrttm1Esw/Fcgrttm1Esw
Tg(Tek-cre)1Ywa/0
B6.Cg-Tg(Tek-cre)1Ywa Fcgrttm1Esw MGI:3838507
cn6
Igf1rtm2Arge/Igf1r+
Tg(Tek-cre)1Ywa/0
B6.Cg-Tg(Tek-cre)1Ywa Igf1rtm2Arge MGI:5568546
cn7
Itga5tm2Hyn/Itga5tm2Hyn
Tg(Tek-cre)1Ywa/0
B6.Cg-Tg(Tek-cre)1Ywa Itga5tm2Hyn MGI:4818938
cn8
Nrp1tm2Ddg/Nrp1tm2Ddg
Tg(Tek-cre)1Ywa/0
involves: 129 * C57BL/6 MGI:3512126
cn9
Nrp1tm2Ddg/Nrp1tm2.1Ddg
Tg(Tek-cre)1Ywa/0
involves: 129 * C57BL/6 MGI:3512130
cn10
Itga5tm1Hyn/Itga5tm2Hyn
Tg(H2-K1-tsA58)6Kio/0
Tg(Tek-cre)1Ywa/0
involves: 129 * C57BL/6 * C57BL/10 * CBA/Ca * SJL MGI:4818936
cn11
Cd40lgtm1Parl/Y
Tg(Tek-cre)1Ywa/0
involves: 129 * C57BL/6 * CD-1 * SJL MGI:5585444
cn12
Cd40lgtm1Parl/Cd40lgtm1Parl
Tg(Tek-cre)1Ywa/0
involves: 129 * C57BL/6 * CD-1 * SJL MGI:5585446
cn13
Acvr1tm1Glh/Acvr1tm1Vk
Gt(ROSA)26Sortm1.2(CAG-EGFP)Glh/Gt(ROSA)26Sor+
Tg(Tek-cre)1Ywa/0
involves: 129 * C57BL/6 * FVB/N * SJL MGI:7278774
cn14
Sox7tm1.1Nat/Sox7tm1.1Nat
Tg(Tek-cre)1Ywa/0
involves: 129 * C57BL/6 * SJL MGI:7550407
cn15
F8tm1.1Rmnt/F8tm1.1Rmnt
Tg(Tek-cre)1Ywa/0
involves: 129 * C57BL/6 * SJL MGI:5582835
cn16
Ccm2ltm1Mlkn/Ccm2ltm1Mlkn
Ccm2tm1Mlkn/Ccm2+
Heg1tm1Mlkn/Heg1tm2.1Mlkn
Tg(Tek-cre)1Ywa/0
involves: 129 * C57BL/6 * SJL MGI:5439515
cn17
Ccm2ltm1Mlkn/Ccm2ltm1Mlkn
Heg1tm1Mlkn/Heg1tm2.1Mlkn
Tg(Tek-cre)1Ywa/0
involves: 129 * C57BL/6 * SJL MGI:5439509
cn18
Gata4tm1Grg/Gata4tm1.1Wtp
Tg(Tek-cre)1Ywa/0
involves: 129 * C57BL/6 * SJL MGI:5427937
cn19
Gata5tm1.1Nemr/Gata5tm1.1Nemr
Tg(Tek-cre)1Ywa/0
involves: 129 * C57BL/6 * SJL MGI:5296321
cn20
Notch1tm1Agt/Notch1tm1Agt
Tg(Tek-cre)1Ywa/0
involves: 129 * C57BL/6 * SJL MGI:3710249
cn21
Gt(ROSA)26Sortm1Sho/0
Itga5tm2Hyn/Itga5tm1Hyn
Itgavtm1Hyn/Itgavtm2Hyn
Tg(Tek-cre)1Ywa/0
involves: 129 * C57BL/6 * SJL MGI:4818940
cn22
Gt(ROSA)26Sortm1Sho/0
Itga5tm2Hyn/Itga5tm1Hyn
Itgavtm2Hyn/Itgav+
Tg(Tek-cre)1Ywa/0
involves: 129 * C57BL/6 * SJL MGI:4818939
cn23
Itga5tm1Hyn/Itga5tm2Hyn
Tg(Tek-cre)1Ywa/0
involves: 129 * C57BL/6 * SJL MGI:4818935
cn24
Juntm1Pa/Juntm4Wag
Tg(Tek-cre)1Ywa/0
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * C57BL/6J * SJL MGI:7562249
cn25
Gt(ROSA)26Sortm1(PDGFB)Cbet/Gt(ROSA)26Sortm1(PDGFB)Cbet
Pdgfbtm1Cbet/Pdgfbtm1Cbet
Tg(Fabp4-lacZ)4Mosh/0
Tg(Tek-cre)1Ywa/0
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * FVB/N * SJL MGI:4849467
cn26
Gt(ROSA)26Sortm1(PDGFB)Cbet/Gt(ROSA)26Sor+
Pdgfbtm1Cbet/Pdgfbtm1Cbet
Tg(Fabp4-lacZ)4Mosh/0
Tg(Tek-cre)1Ywa/0
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * FVB/N * SJL MGI:4849465
cn27
Gt(ROSA)26Sortm1(PDGFB)Cbet/Gt(ROSA)26Sor+
Pdgfbtm1Cbet/Pdgfbtm1Cbet
Tg(Tek-cre)1Ywa/0
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * SJL MGI:4849464
cn28
Gt(ROSA)26Sortm1(PDGFB)Cbet/Gt(ROSA)26Sortm1(PDGFB)Cbet
Pdgfbtm1Cbet/Pdgfbtm1Cbet
Tg(Tek-cre)1Ywa/0
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * SJL MGI:4849466
cn29
Arap3tm1.1Sve/Arap3tm1.2Sve
Tg(Tek-cre)1Ywa/0
involves: 129P2/OlaHsd * BALB/cJ * C57BL/6 * SJL MGI:5428758
cn30
Ednrbtm1Yko/Ednrbtm1Yko
Tg(Tek-cre)1Ywa/0
involves: 129P2/OlaHsd * Bkl:BKW * C57BL/6 * SJL MGI:3804904
cn31
Nrp1tm1Hfu/Nrp1tm2Ddg
Tg(Tek-cre)1Ywa/0
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * SJL MGI:5432163
cn32
Gt(ROSA)26Sortm18(Zeb2)Jhai/Gt(ROSA)26Sor+
Tg(Tek-cre)1Ywa/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * C57BL/6 * CD-1 * SJL MGI:6195748
cn33
Gt(ROSA)26Sortm18(Zeb2)Jhai/Gt(ROSA)26Sortm18(Zeb2)Jhai
Tg(Tek-cre)1Ywa/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * C57BL/6 * CD-1 * SJL MGI:6195747
cn34
Smad5tm1Huy/Smad5tm1.1Huy
Tg(Tek-cre)1Ywa/0
involves: 129P2/OlaHsd * C57BL/6 * CD-1 * SJL MGI:3710362
cn35
Tg(Tek-cre)1Ywa/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * C57BL/6 * CD-1 * SJL MGI:6195749
cn36
Cxcl12tm1Tng/Cxcl12tm1.1Link
Tg(Tek-cre)1Ywa/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N * SJL MGI:5468943
cn37
Adam10tm2Psa/Adam10tm2Psa
Tg(Tek-cre)1Ywa/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:6852794
cn38
Juntm4Wag/Juntm4Wag
Tg(Tek-cre)1Ywa/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:7562246
cn39
Nus1tm1.1Qrm/Nus1tm1.1Qrm
Tg(Tek-cre)1Ywa/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:6361029
cn40
Sox9tm1Gsr/Sox9tm1Gsr
Tg(Tek-cre)1Ywa/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3710208
cn41
Pik3cbtm1Bvan/Pik3cbtm1Bvan
Tg(Tek-cre)1Ywa/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3796333
cn42
Pik3catm3Bvan/Pik3catm3Bvan
Tg(Tek-cre)1Ywa/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3796332
cn43
Itgavtm2Hyn/Itgavtm2.1Hyn
Tg(Tek-cre)1Ywa/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:5306154
cn44
Gna13tm1Soff/Gna13tm2Cgh
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129S4/SvJae * C57BL/6 * SJL MGI:3590664
cn45
Nr2f2tm2.1Tsa/Nr2f2tm2.1Tsa
Rbpjtm1Hon/Rbpjtm1Hon
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6 * SJL MGI:4441397
cn46
Nr2f2tm2.1Tsa/Nr2f2tm2.1Tsa
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6 * SJL MGI:4441398
cn47
Fzd4tm1Nat/Fzd4tm2.1Nat
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ MGI:4948329
cn48
Agrntm1Rwb/Agrntm1Rwb
Tg(APPswe,PSEN1dE9)85Dbo/?
Tg(Tek-cre)1Ywa/?
involves: 129S1/Sv * 129X1/SvJ * C3H * C57BL/6 * SJL MGI:5692156
cn49
Gata4tm1.1Sad/Gata4+
Glyr1em1Dsr/Glyr1+
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * C57BL/6J * SJL MGI:7279301
cn50
Cd2bp2tm1.1Tbh/Cd2bp2tm1.1Tbh
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6N * SJL MGI:6392049
cn51
Ndst1tm1Je/Ndst1tm1Je
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3589869
cn52
Ndst1tm1Je/Ndst1tm1Je
Robo4tm1Kzh/Robo4+
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5562651
cn53
Ndst1tm1Je/Ndst1tm1Je
Robo4tm1Kzh/Robo4tm1Kzh
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5562654
cn54
Fzd4tm1Nat/Fzd4tm2.1Nat
Tg(Tek-cre)1Ywa/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:4412188
cn55
Hif1atm3Rsjo/Hif1atm3Rsjo
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:4418479
cn56
Foxp1tm2.1Eem/Foxp1tm2.1Eem
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:4829789
cn57
Prox1tm1Gco/Prox1tm2Gco
Tg(Tek-cre)1Ywa/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3759503
cn58
Agrntm1Rwb/Agrntm1Rwb
Tg(Tek-cre)1Ywa/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5692155
cn59
Nf1tm1Par/Nf1tm1Par
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3710234
cn60
Ctnnb1tm2Kem/Ctnnb1tm2.1Kem
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3710231
cn61
Ndst1tm1Je/Ndst1tm1Je
Ndst2tm1Lkj/Ndst2tm1Lkj
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3589870
cn62
Ndst1tm1Je/Ndst1tm1Je
Slit3tm1.1Dor/Slit3tm1.1Dor
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5562649
cn63
Ctnnb1tm2Kem/Ctnnb1tm2Kem
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5581949
cn64
Ctnnb1tm2Kem/Ctnnb1+
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5581948
cn65
Ptgestm1.1Gaf/Ptgestm1.1Gaf
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5570546
cn66
Gt(ROSA)26Sortm1(Bmi1)Aiwa/Gt(ROSA)26Sor+
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5496651
cn67
Ndst1tm1Je/Ndst1tm1Je
Slit3tm1.1Dor/Slit3+
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5562648
cn68
Gata4tm1.1Sad/Gata4tm1.1Sad
Tg(Tek-cre)1Ywa/?
involves: 129S1/Sv * 129X1/SvJ * CD-1 MGI:3053001
cn69
Prox1tm2Gco/Prox1+
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * C57BL/6 * NMRI * SJL MGI:3611343
cn70
Zfpm2tm1Sho/Zfpm2tm2Sho
Tg(Tek-cre)1Ywa/0
involves: 129S1/Sv * C57BL/6 * SJL MGI:3851403
cn71
Rasa3tm1.1Llp/Rasa3tm1.1Llp
Tg(Tek-cre)1Ywa/?
involves: 129S1/SvImJ * C57BL/6J * SJL/J MGI:6510800
cn72
Pros1tm1Grl/Pros1tm1Grl
Tg(Tek-cre)1Ywa/0
involves: 129S1/SvImJ * C57BL/6 * SJL MGI:5499117
cn73
Nfatc1tm1Glm/Nfatc1tm1Glm
Tg(Tek-cre)1Ywa/0
Gt(ROSA)26Sortm1Sho/Gt(ROSA)26Sor+
involves: 129S2/SvPas * 129S4/SvJaeSor * C57BL/6 * SJL MGI:5432552
cn74
Msx1tm1Rem/Msx1tm1Rem
Msx2tm1Yvla/Msx2tm1Yvla
Tg(Tek-cre)1Ywa/0
involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 * NMRI * SJL MGI:5297712
cn75
Itgavtm2Hyn/Itgavtm2.1Hyn
Tg(Tek-cre)1Ywa/?
involves: 129S2/SvPas * C57BL/6 * FVB * SJL MGI:3759849
cn76
Smarca4tm1.2Pcn/Smarca4tm1.2Pcn
Tg(Tek-cre)1Ywa/0
involves: 129S2/SvPas * C57BL/6 * SJL MGI:5699726
cn77
Egr2tm3Pch/Egr2tm3Pch
Tg(Tek-cre)1Ywa/0
involves: 129S2/SvPas * C57BL/6 * SJL MGI:5762545
cn78
Tg(Tek-cre)1Ywa/0
Thbdtm2Rdr/Thbdtm2Wlr
involves: 129S2/SvPas * C57BL/6 * SJL MGI:3844980
cn79
Xbp1tm1.1Geno/Xbp1tm1.1Geno
Tg(Tek-cre)1Ywa/0
involves: 129S2/SvPas * C57BL/6 * SJL MGI:5576524
cn80
Vgll4tm1b(EUCOMM)Hmgu/Vgll4tm1c(EUCOMM)Hmgu
Yap1tm1.1Fcam/Yap1+
Tg(Tek-cre)1Ywa/0
involves: 129S4/SvJae * C57BL/6N * CBA * SJL MGI:6360911
cn81
Pkd1tm1Ggg/Pkd1tm2Ggg
Tg(Tek-cre)1Ywa/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:4843167
cn82
Socs1tm1Ayos/Socs1tm1Ayos
Tg(Tek-cre)1Ywa/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:3783710
cn83
Ppargtm2Rev/Ppargtm2Rev
Tg(Tek-cre)1Ywa/?
involves: 129S4/SvJae * C57BL/6 * SJL MGI:5444193
cn84
Slc25a37tm1.1Kapl/Slc25a37tm1.2Kapl
Tg(Tek-cre)1Ywa/?
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6J * C57BL/6NCr * SJL MGI:5014818
cn85
Pgptm1.1Ango/Pgptm1.1Ango
Tg(Tek-cre)1Ywa/0
involves: 129S4/SvJaeSor * C57BL/6 * C57BL/6J * SJL MGI:6150907
cn86
Pdgfrbtm14(Pdgfrb)Sor/Pdgfrb+
Tg(Tek-cre)1Ywa/0
involves: 129S4/SvJaeSor * C57BL/6 * SJL MGI:5140931
cn87
Cd99l2tm1.1Dvst/Cd99l2tm1.1Dvst
Tg(Tek-cre)1Ywa/0
involves: 129S6/SvEvTac * BALB/c * C57BL/6 MGI:6147345
cn88
Krit1tm1Kwhi/Krit1tm1.1Kwhi
Tg(Tek-cre)1Ywa/0
involves: 129S6/SvEvTac * C57BL/6 * C57BL/6NCrl * SJL MGI:5661914
cn89
Adgrg6em2Jlp/Adgrg6em2Jlp
Gt(ROSA)26Sortm1(ADGRG6)Jlp/Gt(ROSA)26Sor+
Tg(Tek-cre)1Ywa/0
involves: 129S6/SvEvTac * C57BL/6 * C57BL/6NCrl * SJL MGI:7442273
cn90
Gt(ROSA)26Sortm1(ADGRG6)Jlp/Gt(ROSA)26Sor+
Tg(Tek-cre)1Ywa/0
involves: 129S6/SvEvTac * C57BL/6 * C57BL/6NCrl * SJL MGI:7442271
cn91
Zfpm1tm4Sho/Zfpm1tm4Sho
Tg(Gata1-Zfpm1)1Sho/0
Tg(Tek-cre)1Ywa/0
involves: 129S6/SvEvTac * C57BL/6 * CD-1 * SJL MGI:3586390
cn92
Acvr1tm1Glh/Acvr1+
Gt(ROSA)26Sortm1.2(CAG-EGFP)Glh/Gt(ROSA)26Sor+
Tg(Tek-cre)1Ywa/0
involves: 129S6/SvEvTac * C57BL/6J * FVB/N * SJL MGI:7278772
cn93
Vgll4tm1b(EUCOMM)Hmgu/Vgll4tm1c(EUCOMM)Hmgu
Gt(ROSA)26Sortm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Tg(Tek-cre)1Ywa/0
involves: 129S6/SvEvTac * C57BL/6NCrl * CBA * SJL MGI:6360909
cn94
S1pr1tm1Rlp/S1pr1tm2Rlp
Tg(Tek-cre)1Ywa/?
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:2681954
cn95
Hdac7tm1Eno/Hdac7tm2Eno
Tg(Tek-cre)1Ywa/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:3695494
cn96
Efemp2tm1.1Hiya/Efemp2tm1.2Hiya
Tg(Tek-cre)1Ywa/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:4947946
cn97
Hey2tm1Eno/Hey2tm2Eno
Tg(Tek-cre)1Ywa/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:3711336
cn98
Stat5btm1Mam/Stat5btm1Mam
Tg(Tek-cre)1Ywa/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:4844106
cn99
Stat5atm2Mam/Stat5atm2Mam
Stat5btm1Mam/Stat5btm1Mam
Tg(Tek-cre)1Ywa/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:4844105
cn100
Pbx1tm1Mlc/Pbx1tm3.1Mlc
Tg(Tek-cre)1Ywa/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:4352855
cn101
Edn1tm1Ywa/Edn1tm1Ywa
Tg(Tek-cre)1Ywa/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:5490276
cn102
Ppp3r1tm2Grc/Ppp3r1tm2Grc
Tg(Tek-cre)1Ywa/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:4366032
cn103
Gja1tm1Dlg/Gja1tm1Dlg
Tg(Tek-cre)1Ywa/0
involves: 129S7/SvEvBrd * C57BL/6 MGI:2176965
cn104
Tbx1tm1Bld/Tbx1tm3Bld
Tg(Tek-cre)1Ywa/0
involves: 129S7/SvEvBrd * C57BL/6 MGI:3046801
cn105
Rbpjtm1Hon/Rbpjtm1Hon
Tg(Tek-cre)1Ywa/0
involves: 129S7/SvEvBrd * C57BL/6 * SJL MGI:4441396
cn106
Tbx1tm1Bld/Tbx1tm3Bld
Tg(Tek-cre)1Ywa/0
involves: 129S7/SvEvBrd * C57BL/6 * SJL MGI:4453460
cn107
Tg(CAG-lacZ,-BMPR1A*,-EGFP)1Mis/0
Tg(Tek-cre)1Ywa/0
involves: 129S7/SvEvBrd * C57BL/6 * SJL MGI:5444494
cn108
Fkbp1atm1.1Shou/Fkbp1atm1Zuk
Tg(Tek-cre)1Ywa/0
involves: 129S7/SvEvBrd * C57BL/6 * SJL MGI:5490245
cn109
Gt(ROSA)26Sortm1Fia/Gt(ROSA)26Sor+
Nf1tm1Fcr/Nf1tm1Par
Tg(Tek-cre)1Ywa/0
involves: 129S/SvEv * 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3689708
cn110
Nf1tm1Fcr/Nf1tm1Par
Tg(Tek-cre)1Ywa/0
involves: 129S/SvEv * 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3689709
cn111
Plxnd1tm1.1Tmj/Plxnd1tm1.1Tmj
Tg(Tek-cre)1Ywa/0
involves: 129S/SvEv * 129S4/SvJaeSor * C57BL/6 * SJL MGI:3848821
cn112
Pkd2tm1.1Tjwt/Pkd2tm1.1Tjwt
Tg(Tek-cre)1Ywa/0
involves: 129S/SvEv * 129X1/SvJ * C57BL/6 * SJL MGI:4843169
cn113
Ets1tm1Jml/Ets1tm1Jml
Ets2tm5.1Rgo/Ets2tm5.1Rgo
Tg(Tek-cre)1Ywa/0
involves: 129S/SvEv * C57BL/6 * FVB/N MGI:4353416
cn114
Sox7tm1Dsco/Sox7tm1Dsco
Tg(Tek-cre)1Ywa/0
involves: 129S/SvEv * C57BL/6 * SJL MGI:7543477
cn115
Sox7tm1Dsco/Sox7tm1.1Dsco
Tg(Tek-cre)1Ywa/0
involves: 129S/SvEv * C57BL/6 * SJL MGI:7543476
cn116
Ppargc1btm1.2Rev/Ppargc1btm1.2Rev
Tg(Tek-cre)1Ywa/0
involves: 129/Sv * C57BL/6 * C57BL/6J * SJL MGI:4461914
cn117
Foxm1tm1Rhc/Foxm1tm1Rhc
Tg(Tek-cre)1Ywa/0
involves: 129X1/SvJ * C57BL/6 * SJL MGI:3710341
cn118
Ctnnb1tm1Mmt/Ctnnb1+
Tg(Tek-cre)1Ywa/0
involves: 129X1/SvJ * C57BL/6 * SJL MGI:5581955
cn119
Chd7tm2a(EUCOMM)Wtsi/Chd7tm2a(EUCOMM)Wtsi
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * C57BL/6J * C57BL/6N * SJL MGI:7493911
cn120
Foxc2tm1.1Miu/Foxc2tm1.1Miu
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * C57BL/6J * SJL MGI:6879489
cn121
Eogttm1.1Okaj/Eogttm1.1Okaj
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * C57BL/6J * SJL MGI:7640065
cn122
Chd3tm1.1Cya/Chd3tm1.1Cya
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * C57BL/6J * SJL MGI:6456932
cn123
Chd3tm1.1Cya/Chd3tm1.1Cya
Chd4tm1.1Kge/Chd4tm1.1Kge
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * C57BL/6J * SJL MGI:6456933
cn124
Snrktm2Rra/Snrktm2Rra
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * C57BL/6J * SJL MGI:5792712
cn125
Gt(ROSA)26Sortm1(CAG-Etv2,-GFP)Hkata/Gt(ROSA)26Sor+
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * SJL MGI:5527434
cn126
Bcas3tm1Msin/Bcas3tm1Msin
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * SJL MGI:6195768
cn127
Npr1tm1.1Kkan/Npr1tm1.1Kkan
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * SJL MGI:5792676
cn128
Spns2tm1.1Nmoc/Spns2tm1.1Nmoc
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * SJL MGI:5426398
cn129
Hacd2tm1b(EUCOMM)Hmgu/Hacd2tm1c(EUCOMM)Hmgu
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * C57BL/6N * SJL MGI:7447126
cn130
Commd9tm1c(KOMP)Wtsi/Commd9tm1c(KOMP)Wtsi
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * C57BL/6N * SJL MGI:5796350
cn131
Eps15tm1c(KOMP)Wtsi/Eps15tm1c(KOMP)Wtsi
Eps15l1tm1.1Noff/Eps15l1tm1.1Noff
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * C57BL/6N * SJL MGI:6509036
cn132
Eps15tm1c(KOMP)Wtsi/Eps15tm1c(KOMP)Wtsi
Eps15l1tm2.1Noff/Eps15l1tm2.1Noff
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * C57BL/6N * SJL MGI:6509037
cn133
Pfn1tm1Foxp/Pfn1tm1Foxp
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * C57BL/6NTac * SJL MGI:5470091
cn134
Gt(ROSA)26Sortm18(Zeb2)Jhai/Gt(ROSA)26Sortm18(Zeb2)Jhai
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * CD-1 * SJL MGI:6195746
cn135
Tg(CAG-cat,-Ptpn11*Q510E)#Krnz/0
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * FVB/N * SJL MGI:5828598
cn136
Mfsd2atm1c(KOMP)Wtsi/Mfsd2atm1c(KOMP)Wtsi
Tg(Tek-cre)1Ywa/0
involves: C57BL/6J * C57BL/6N MGI:5806300
cn137
Vgll4tm1b(EUCOMM)Hmgu/Vgll4tm1c(EUCOMM)Hmgu
Tg(Tek-cre)1Ywa/0
involves: C57BL/6N * CBA * SJL MGI:6360907
cn138
Anxa3tm1c(EUCOMM)Hmgu/Anxa3tm1c(EUCOMM)Hmgu
Tg(Tek-cre)1Ywa/0
involves: C57BL/6N * SJL MGI:6416300
cn139
Ccm2tm2.1Sbn/Ccm2tm2.1Sbn
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * SJL MGI:5085318
cn140
Tmem100tm1.1Ysai/Tmem100tm2.1Ysai
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * SJL MGI:5432907
cn141
Pdcd10tm1Kwhi/Pdcd10tm1Kwhi
Tg(Tek-cre)1Ywa/?
involves: C57BL/6 * SJL MGI:5052326
cn142
Sart3tm1.1Hbro/Sart3+
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * SJL MGI:5052129
cn143
Irx3tm3Hui/Irx3tm3Hui
Irx5tm3Hui/Irx5tm3Hui
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * SJL MGI:5444490
cn144
Etv2tm1Vkou/Etv2tm1Vkou
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * SJL MGI:5474868
cn145
Plekhg5tm1Jbar/Plekhg5tm1Jbar
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * SJL MGI:5484864
cn146
Hprt1tm1(H1-RNAi:Tmsb4x)Prri/Hprt1+
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * SJL MGI:5487451
cn147
Gt(ROSA)26Sortm4(EWSR1/ATF1)Mrc/Gt(ROSA)26Sor+
Tg(Tek-cre)1Ywa/?
involves: C57BL/6 * SJL MGI:5495315
cn148
Adgrg6em3Jlp/Adgrg6em3Jlp
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * SJL MGI:7442264
cn149
Phf6tm1.1Avo/Y
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * SJL MGI:6507173
cn150
Prkaa2tm1.1Sjm/Prkaa2tm1.1Sjm
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * SJL MGI:6449118
cn151
Ccm2tm1Kwhi/Ccm2tm1.1Kwhi
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * SJL MGI:3838812
cn152
Lama5tm1Lsor/Lama5tm1Lsor
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * SJL MGI:5555041
cn153
Lmnatm1Bliu/Lmna+
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * SJL MGI:6423604
cn154
Ddah1tm1Geno/Ddah1tm1Geno
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * SJL MGI:5897606
cn155
Adgrg6em2Jlp/Adgrg6em3Jlp
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * SJL MGI:7442268
cn156
Tnfrsf21tm2Gne/Tnfrsf21tm2Gne
Tg(Tek-cre)1Ywa/0
involves: C57BL/6 * SJL MGI:5312098
cn157
F11rtm1Dej/F11rtm1.1Dej
Tg(Tek-cre)1Ywa/0
Not Specified MGI:3054867
tg158
Tg(Tek-cre)1Ywa/Tg(Tek-cre)1Ywa involves: C57BL/6 * SJL MGI:6415042


Genotype
MGI:7544842
cn1
Allelic
Composition
Nrastm1Tyj/Nras+
Tg(Tek-cre)1Ywa/0
Genetic
Background
B6.Cg-Nrastm1Tyj Tg(Tek-cre)1Ywa
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nrastm1Tyj mutation (1 available); any Nras mutation (43 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• live embryos are recovered at normal numbers at E14.5; however, all embryos die by E17.5

cardiovascular system
• at E13.5, three of 5 hearts exhibit myocardial hypertrabeculation
• at E13.5, three of 5 hearts exhibit a thin compact layer with a deeply invaginated trabecular layer
• at E13.5, two of 5 hearts exhibit DORV
• at E13.5, two of 5 hearts show ventricular septal defects (VSDs)
• at E13.5, two of 5 hearts exhibit pulmonary valve stenosis

muscle
• at E13.5, three of 5 hearts exhibit myocardial hypertrabeculation
• at E13.5, three of 5 hearts exhibit a thin compact layer with a deeply invaginated trabecular layer




Genotype
MGI:5659607
cn2
Allelic
Composition
Snai1tm1.1Stjw/Snai1tm1.1Stjw
Tg(Tek-cre)1Ywa/0
Genetic
Background
B6.Cg-Snai1tm1.1Stjw Tg(Tek-cre)1Ywa
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Snai1tm1.1Stjw mutation (0 available); any Snai1 mutation (9 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• by E11.5 and E12.5, approximately 50 and 100% of mice die, respectively

cardiovascular system
• cranial blood vessels fail to undergo remodeling events
• decreased vascularization with fewer fetal blood vessels invading
• cranial blood vessels fail to undergo remodeling events
• at E11.5 about 50% of embryos are necrotic with no intact vascular structures
• intersomitic vessels form but are unable to organize or full infiltrate the somites, displaying significant decreases in vessel length and branch points
• impaired vascularization of the tail with the formation of truncated and disorganized networks
• decrease in the number of mesenchymal cells in the atrioventricular canal

embryo
• decreased vascularization with fewer fetal blood vessels invading
• at E10.5 and E11.5 crown to rump length is decreased by 32 and 47%, respectively, compared to control littermates
• severely defective remodeling of the primary vascular plexus at E10.5

growth/size/body
• at E10.5 and E11.5 crown to rump length is decreased by 32 and 47%, respectively, compared to control littermates

nervous system
• cranial blood vessels fail to undergo remodeling events




Genotype
MGI:3826863
cn3
Allelic
Composition
Arg1tm1Pmu/Arg1tm1Pmu
Tg(Tek-cre)1Ywa/?
Genetic
Background
B6.Cg-Tg(Tek-cre)1Ywa Arg1tm1Pmu
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Arg1tm1Pmu mutation (2 available); any Arg1 mutation (25 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• very little urea is produced by peritoneal macrophages in response to IL-4 and IL-10 incubation due to a lack of arginase activity
• macrophages produce more nitrous oxide in response to LPS stimulation or Mycobacterium bovis infection
• mice infected with M. tuberculosis have lower bacterial counts than wild-type littermates in the lungs after the initial bacterial growth period
• there is also lower bacterial load in the spleens of the mice 70 days after infection with M. tuberculosis
• lung granulomas in these infected mice occupy a smaller fraction of the total lung area and have a more pronounced lymphocytic infiltrate

homeostasis/metabolism
• there is more NO activity in liver granulomas of mice infected with M. tuberculosis
• macrophages produce more nitrous oxide in response to LPS stimulation or Mycobacterium bovis infection

hematopoietic system
• very little urea is produced by peritoneal macrophages in response to IL-4 and IL-10 incubation due to a lack of arginase activity
• macrophages produce more nitrous oxide in response to LPS stimulation or Mycobacterium bovis infection




Genotype
MGI:3837692
cn4
Allelic
Composition
Ccm2tm1Etl/Ccm2tm1Etl
Tg(Tek-cre)1Ywa/0
Genetic
Background
B6.Cg-Tg(Tek-cre)1Ywa Ccm2tm1Etl
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ccm2tm1Etl mutation (0 available); any Ccm2 mutation (47 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• embryonic lethality occurs between E10.5 and E11.5

embryo
• E10.5 embryonic blood vessels do not invade the labyrinthine layer to the same extent as seen in control placentas
• yolk sac vessels of E10.5 embryos remain in a honeycomb pattern instead of developing into the large vitelline vessels
• 58% of E10.5 embryos have marked general delay of development
• 19% of E10.5 embryos have little to no signs of developmental delays
• 23% of E10.5 embryos have general growth arrest, a failure to complete turning and/or signs of resorption
• somite vasculature is poorly defined in E10.5 embyros
• E10.5 placenta has few nucleated red blood cells
• E9.5 homozygous embryos can be distinguished from other genotypes by their pale, wrinkled yolk sacs
• at E10.5, the different layers of the placenta are difficult to define and appear poorly organized

cardiovascular system
• at E9.5, the dorsal aorta is irregular in appearance and thinner than controls
• at E10.5, the dorsal aorta is highly irregular in appearance and has narrow lumens
• in most embryos the dorsal aorta fails to fuse and instead remain present as two stenotic DA
• mural cells are hardly detectable in the dorsal aorta of E10.5 embryos
• in the head of E10.5 embryos, the cephalic plexus vasculature fails to remodel into a hierarchical branched network
• a coarse vascular network with poorly organized vessels makes it difficult to distinguish the internal carotid artery or primary head veins
• E10.5 embryonic blood vessels do not invade the labyrinthine layer to the same extent as seen in control placentas
• cardinal veins of E10.5 embryos are dilated
• yolk sac vessels of E10.5 embryos remain in a honeycomb pattern instead of developing into the large vitelline vessels
• there is a paucity of cells in the cushions in the atrioventricular canal of E10.5 embryos
• sinus venosus of E10.5 embryos are dilated
• E10.5 embryos have enlarged atria to the degree that the more severe cases have distortion of the embryo
• in E10.5 embryos that do not have severe growth arrest, the heart is 17% bigger than controls
• ventricular trabeculations are strongly reduced in E10.5 embryos with, in some extreme cases, detachment of the endocardial cells from the myocardium
• most E10.5 embryos suffer from pericardial edema to varying degrees
• half of E10.5 embryos have hemorrhaging in the pericardial cavity and in the trunk

homeostasis/metabolism
• most E10.5 embryos suffer from pericardial edema to varying degrees
• half of E10.5 embryos have hemorrhaging in the pericardial cavity and in the trunk

nervous system
• in the head of E10.5 embryos, the cephalic plexus vasculature fails to remodel into a hierarchical branched network
• a coarse vascular network with poorly organized vessels makes it difficult to distinguish the internal carotid artery or primary head veins
• in the head of E10.5 embryos, the cephalic plexus vasculature fails to remodel into a hierarchical branched network

growth/size/body
• in E10.5 embryos that do not have severe growth arrest, the heart is 17% bigger than controls




Genotype
MGI:3838507
cn5
Allelic
Composition
Fcgrttm1Esw/Fcgrttm1Esw
Tg(Tek-cre)1Ywa/0
Genetic
Background
B6.Cg-Tg(Tek-cre)1Ywa Fcgrttm1Esw
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fcgrttm1Esw mutation (1 available); any Fcgrt mutation (60 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• half-life of IgG1 antibodies (measured by clearance of injected human IgG1) is much shorter than controls with a mean half-life of 8.2 hours compared to 169.8 hours for controls
• serum levels of IgG1 are 4-fold less than controls

homeostasis/metabolism
• albumin levels are about half that of controls

hematopoietic system
• serum levels of IgG1 are 4-fold less than controls




Genotype
MGI:5568546
cn6
Allelic
Composition
Igf1rtm2Arge/Igf1r+
Tg(Tek-cre)1Ywa/0
Genetic
Background
B6.Cg-Tg(Tek-cre)1Ywa Igf1rtm2Arge
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Igf1rtm2Arge mutation (1 available); any Igf1r mutation (85 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• blunted endothelial regeneration after arterial injury compared with wild-type cells
• blunted endothelial regeneration after arterial injury compared with wild-type cells

homeostasis/metabolism
• blunted endothelial regeneration after arterial injury compared with wild-type cells




Genotype
MGI:4818938
cn7
Allelic
Composition
Itga5tm2Hyn/Itga5tm2Hyn
Tg(Tek-cre)1Ywa/0
Genetic
Background
B6.Cg-Tg(Tek-cre)1Ywa Itga5tm2Hyn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Itga5tm2Hyn mutation (2 available); any Itga5 mutation (45 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

cardiovascular system
• in 90% of 10- to 20-week-old mice

cellular
• in 90% of 10- to 20-week-old mice




Genotype
MGI:3512126
cn8
Allelic
Composition
Nrp1tm2Ddg/Nrp1tm2Ddg
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nrp1tm2Ddg mutation (1 available); any Nrp1 mutation (82 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 25/25 mutant mice died perinatally

cardiovascular system
• exhibit multiple cardiac defects
• misplacement of coronary arteries




Genotype
MGI:3512130
cn9
Allelic
Composition
Nrp1tm2Ddg/Nrp1tm2.1Ddg
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nrp1tm2.1Ddg mutation (0 available); any Nrp1 mutation (82 available)
Nrp1tm2Ddg mutation (1 available); any Nrp1 mutation (82 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mid-to-late embryonic lethality

cardiovascular system
• systemic vascular deficiencies at E12.5 such as distended vessels in the abdominal wall
• brain vessels were large and underdeveloped
• lack of medium and small-diameter branched vessels in the abdominal wall and brain vessels were not branched
• exhibited bilateral atrial enlargement




Genotype
MGI:4818936
cn10
Allelic
Composition
Itga5tm1Hyn/Itga5tm2Hyn
Tg(H2-K1-tsA58)6Kio/0
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129 * C57BL/6 * C57BL/10 * CBA/Ca * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Itga5tm1Hyn mutation (1 available); any Itga5 mutation (45 available)
Itga5tm2Hyn mutation (2 available); any Itga5 mutation (45 available)
Tg(H2-K1-tsA58)6Kio mutation (2 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• endothelial cells showed reduced adhesion to fibronectin




Genotype
MGI:5585444
cn11
Allelic
Composition
Cd40lgtm1Parl/Y
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129 * C57BL/6 * CD-1 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd40lgtm1Parl mutation (0 available); any Cd40lg mutation (15 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• mice exhibit normal hemograms and response to thromogenesis

homeostasis/metabolism
N
• mice exhibit normal prothrombin tine and activated partial thromboplastin time

immune system




Genotype
MGI:5585446
cn12
Allelic
Composition
Cd40lgtm1Parl/Cd40lgtm1Parl
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129 * C57BL/6 * CD-1 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd40lgtm1Parl mutation (0 available); any Cd40lg mutation (15 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• mice exhibit normal hemograms and response to thromogenesis

homeostasis/metabolism
N
• mice exhibit normal prothrombin tine and activated partial thromboplastin time

immune system




Genotype
MGI:7278774
cn13
Allelic
Composition
Acvr1tm1Glh/Acvr1tm1Vk
Gt(ROSA)26Sortm1.2(CAG-EGFP)Glh/Gt(ROSA)26Sor+
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129 * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Acvr1tm1Glh mutation (0 available); any Acvr1 mutation (44 available)
Acvr1tm1Vk mutation (0 available); any Acvr1 mutation (44 available)
Gt(ROSA)26Sortm1.2(CAG-EGFP)Glh mutation (0 available); any Gt(ROSA)26Sor mutation (968 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• pinch injury of adult gastrocnemius muscle results in a 50-fold increase in heterotopic ossification volume compared to mice that have one wild-type allele of Acvr1

skeleton
• pinch injury of adult gastrocnemius muscle results in a 50-fold increase in heterotopic ossification volume compared to mice that have one wild-type allele of Acvr1




Genotype
MGI:7550407
cn14
Allelic
Composition
Sox7tm1.1Nat/Sox7tm1.1Nat
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sox7tm1.1Nat mutation (1 available); any Sox7 mutation (21 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryo
• at E10.5, embryos show evidence of delayed development
• at E10.5, embryos show failure of yolk sac vascular remodeling

growth/size/body
• at E10.5, embryos show evidence of delayed development




Genotype
MGI:5582835
cn15
Allelic
Composition
F8tm1.1Rmnt/F8tm1.1Rmnt
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
F8tm1.1Rmnt mutation (1 available); any F8 mutation (24 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism




Genotype
MGI:5439515
cn16
Allelic
Composition
Ccm2ltm1Mlkn/Ccm2ltm1Mlkn
Ccm2tm1Mlkn/Ccm2+
Heg1tm1Mlkn/Heg1tm2.1Mlkn
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ccm2ltm1Mlkn mutation (0 available); any Ccm2l mutation (14 available)
Ccm2tm1Mlkn mutation (0 available); any Ccm2 mutation (47 available)
Heg1tm1Mlkn mutation (0 available); any Heg1 mutation (56 available)
Heg1tm2.1Mlkn mutation (0 available); any Heg1 mutation (56 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• some survivors are detected




Genotype
MGI:5439509
cn17
Allelic
Composition
Ccm2ltm1Mlkn/Ccm2ltm1Mlkn
Heg1tm1Mlkn/Heg1tm2.1Mlkn
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ccm2ltm1Mlkn mutation (0 available); any Ccm2l mutation (14 available)
Heg1tm1Mlkn mutation (0 available); any Heg1 mutation (56 available)
Heg1tm2.1Mlkn mutation (0 available); any Heg1 mutation (56 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

cardiovascular system

muscle




Genotype
MGI:5427937
cn18
Allelic
Composition
Gata4tm1Grg/Gata4tm1.1Wtp
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gata4tm1.1Wtp mutation (0 available); any Gata4 mutation (36 available)
Gata4tm1Grg mutation (1 available); any Gata4 mutation (36 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Hypocellular endocardial cushions in Gata4tm1.1Wtp/Gata4tm1Grg Tg(Tek-cre)1Ywa/0 mice

cardiovascular system
• hypocellular endocardial cushions are noted at E10.5
• however, no myocardial thinning is seen

growth/size/body
N
• viable with no signs of embryonic growth retardation




Genotype
MGI:5296321
cn19
Allelic
Composition
Gata5tm1.1Nemr/Gata5tm1.1Nemr
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gata5tm1.1Nemr mutation (0 available); any Gata5 mutation (17 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Bicuspid aortic valve in Gata5tm1.2Nemr/Gata5tm1.2Nemr Tg(Tek-cre)1Ywa/0 mice

cardiovascular system
• mice exhibit the fusion of the right-coronary and noncoronary valve leaflets unlike in control mice
• in 3 of 14 mice compared with 1 of 31 control mice




Genotype
MGI:3710249
cn20
Allelic
Composition
Notch1tm1Agt/Notch1tm1Agt
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Notch1tm1Agt mutation (0 available); any Notch1 mutation (115 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

growth/size/body
• embryos show a pronounced delay in posterior development, with some showing incomplete embryonic turning

embryo
• blood vessels fail to invade the placental labyrinth
• seen in some embryos
• at E9.5, embryos display growth arrest at the 16-to 20-somite stage
• embryos show a pronounced delay in posterior development, with some showing incomplete embryonic turning
• the forebrain neural tube is degenerated, with abundant pyknotic and fragmented nuclei
• somites are poorly defined, with signs of apoptosis
• embryos fail to remodel the primary vascular plexus to form large and small blood vessels of the mature yolk sac

cardiovascular system
• intersomitic blood vessels are poorly defined, with signs of apoptosis
• blood vessels fail to invade the placental labyrinth
• exhibit a marked reduction in vessel organization and a persistent, immature vascular plexus, suggesting a block in vascular maturation and angiogenic remodeling
• intact vasculogenesis but impaired secondary angiogenic sprouting and remodeling
• embryos show a decreased number of branching blood vessels throughout the embryo
• the anterior cardinal vein appears hypoplastic
• the heart displays delayed looping beginning at E9.5
• pericardial effusion is seen at E9.5 but not earlier
• starting at E9.5, there is intraembryonic hemorrhage into the pericardium and tails
• starting at E9.5, there is intraembryonic hemorrhage into the pericardium

cellular
• widespread apoptosis in neural cells and the inner endothelial lining of the aorta

nervous system
• the forebrain neural tube is degenerated, with abundant pyknotic and fragmented nuclei

homeostasis/metabolism
• pericardial effusion is seen at E9.5 but not earlier
• starting at E9.5, there is intraembryonic hemorrhage into the pericardium

muscle




Genotype
MGI:4818940
cn21
Allelic
Composition
Gt(ROSA)26Sortm1Sho/0
Itga5tm2Hyn/Itga5tm1Hyn
Itgavtm1Hyn/Itgavtm2Hyn
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sho mutation (4 available); any Gt(ROSA)26Sor mutation (968 available)
Itga5tm1Hyn mutation (1 available); any Itga5 mutation (45 available)
Itga5tm2Hyn mutation (2 available); any Itga5 mutation (45 available)
Itgavtm1Hyn mutation (1 available); any Itgav mutation (53 available)
Itgavtm2Hyn mutation (2 available); any Itgav mutation (53 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• die at E14.5 of severe dorsal edema and sometimes hemorrhage

cardiovascular system
• aorta vascular ring
• absent ascending aorta
• in one of two surviving mice
• ventricular septation defects

cellular
• in one of two surviving mice




Genotype
MGI:4818939
cn22
Allelic
Composition
Gt(ROSA)26Sortm1Sho/0
Itga5tm2Hyn/Itga5tm1Hyn
Itgavtm2Hyn/Itgav+
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sho mutation (4 available); any Gt(ROSA)26Sor mutation (968 available)
Itga5tm1Hyn mutation (1 available); any Itga5 mutation (45 available)
Itga5tm2Hyn mutation (2 available); any Itga5 mutation (45 available)
Itgavtm2Hyn mutation (2 available); any Itgav mutation (53 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• at P21 fewer mice are alive than wild type

cardiovascular system
• in several of the mice
• ventricular septation defects

cellular
• in several of the mice




Genotype
MGI:4818935
cn23
Allelic
Composition
Itga5tm1Hyn/Itga5tm2Hyn
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Itga5tm1Hyn mutation (1 available); any Itga5 mutation (45 available)
Itga5tm2Hyn mutation (2 available); any Itga5 mutation (45 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype




Genotype
MGI:7562249
cn24
Allelic
Composition
Juntm1Pa/Juntm4Wag
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Juntm1Pa mutation (1 available); any Jun mutation (12 available)
Juntm4Wag mutation (0 available); any Jun mutation (12 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryo
N
• at E10.5, embryos show a similar pattern of Tfap2a expression in the developing cardiac outflow tract (OFT) and pharyngeal arches relative to controls, suggesting normal cardiac neural crest cell migration




Genotype
MGI:4849467
cn25
Allelic
Composition
Gt(ROSA)26Sortm1(PDGFB)Cbet/Gt(ROSA)26Sortm1(PDGFB)Cbet
Pdgfbtm1Cbet/Pdgfbtm1Cbet
Tg(Fabp4-lacZ)4Mosh/0
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(PDGFB)Cbet mutation (0 available); any Gt(ROSA)26Sor mutation (968 available)
Pdgfbtm1Cbet mutation (0 available); any Pdgfb mutation (15 available)
Tg(Fabp4-lacZ)4Mosh mutation (1 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• mural cell (pericytes and vascular smooth muscle cells) densities are close to normal




Genotype
MGI:4849465
cn26
Allelic
Composition
Gt(ROSA)26Sortm1(PDGFB)Cbet/Gt(ROSA)26Sor+
Pdgfbtm1Cbet/Pdgfbtm1Cbet
Tg(Fabp4-lacZ)4Mosh/0
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(PDGFB)Cbet mutation (0 available); any Gt(ROSA)26Sor mutation (968 available)
Pdgfbtm1Cbet mutation (0 available); any Pdgfb mutation (15 available)
Tg(Fabp4-lacZ)4Mosh mutation (1 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mural cell (pericytes and vascular smooth muscle cells) densities are lower than in wild-type mice




Genotype
MGI:4849464
cn27
Allelic
Composition
Gt(ROSA)26Sortm1(PDGFB)Cbet/Gt(ROSA)26Sor+
Pdgfbtm1Cbet/Pdgfbtm1Cbet
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(PDGFB)Cbet mutation (0 available); any Gt(ROSA)26Sor mutation (968 available)
Pdgfbtm1Cbet mutation (0 available); any Pdgfb mutation (15 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• mice exhibit increased blood-brain barrier (BBB) permeability compared with wild-type mice
• however, imatinib-treatment reverses increased BBB permeability without improving blood vessel morphology
• astrocyte end-feet are mis-localized compared to in wild-type mice

cardiovascular system
• capillary diameter is increased compared to in wild-type mice
• capillary density is reduced compared to in wild-type mice
• pericyte coverage is less than in wild-type mice but not as severely as in Pdgfbtm3.1Cbet homozygotes
• mice exhibit increased blood-brain barrier (BBB) permeability compared with wild-type mice
• however, imatinib-treatment reverses increased BBB permeability without improving blood vessel morphology




Genotype
MGI:4849466
cn28
Allelic
Composition
Gt(ROSA)26Sortm1(PDGFB)Cbet/Gt(ROSA)26Sortm1(PDGFB)Cbet
Pdgfbtm1Cbet/Pdgfbtm1Cbet
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(PDGFB)Cbet mutation (0 available); any Gt(ROSA)26Sor mutation (968 available)
Pdgfbtm1Cbet mutation (0 available); any Pdgfb mutation (15 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• mice exhibit increased blood-brain barrier (BBB) permeability compared with wild-type mice
• however, imatinib-treatment reverses increased BBB permeability
• astrocyte end-feet are mis-localized compared to in wild-type mice

cardiovascular system
• capillary diameter is increased compared to in wild-type mice
• capillary density is reduced compared to in wild-type mice
• pericyte coverage is less than in wild-type mice but not as severely as in Pdgfbtm3.1Cbet homozygotes
• mice exhibit increased blood-brain barrier (BBB) permeability compared with wild-type mice
• however, imatinib-treatment reverses increased BBB permeability




Genotype
MGI:5428758
cn29
Allelic
Composition
Arap3tm1.1Sve/Arap3tm1.2Sve
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129P2/OlaHsd * BALB/cJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Arap3tm1.1Sve mutation (0 available); any Arap3 mutation (61 available)
Arap3tm1.2Sve mutation (0 available); any Arap3 mutation (61 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• die around E11
• identical to mice homozygous for Arap3tm1.2Sve

cardiovascular system
• the capillary network is replaced with a large accumulation of endothelial cells
• identical to mice homozygous for Arap3tm1.2Sve
• defect in vascular maturation and remodeling, especially apparent in the midbrain
• unevenly sized vessel lumens, some of which are large, giving an impression of accumulations of endothelial cells

embryo
• identical to mice homozygous for Arap3tm1.2Sve
• unevenly sized vessel lumens, some of which are large, giving an impression of accumulations of endothelial cells
• defect in labyrinth formation
• identical to mice homozygous for Arap3tm1.2Sve
• wrinkled yolk sac at E10.5
• the primary vascular plexus fails to remodel

growth/size/body

integument
• at E10.5

nervous system
• the capillary network is replaced with a large accumulation of endothelial cells




Genotype
MGI:3804904
cn30
Allelic
Composition
Ednrbtm1Yko/Ednrbtm1Yko
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129P2/OlaHsd * Bkl:BKW * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ednrbtm1Yko mutation (0 available); any Ednrb mutation (103 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• mutants do not develop cardiac hypertrophy on a regular diet or salt-sensitive hypertension
• vasodilator response to S6c, a selective Ednrb agonist, is attenuated in mutant aortic rings compared to controls
• acetylcholine-induced vasodilation is impaired
• however, S6c-induced tracheal smooth muscle cell contraction is unaltered

homeostasis/metabolism
• plasma endothelin-1 concentration is increased
• decrease in endogenous release of NO

muscle
• vasodilator response to S6c, a selective Ednrb agonist, is attenuated in mutant aortic rings compared to controls
• acetylcholine-induced vasodilation is impaired
• however, S6c-induced tracheal smooth muscle cell contraction is unaltered




Genotype
MGI:5432163
cn31
Allelic
Composition
Nrp1tm1Hfu/Nrp1tm2Ddg
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nrp1tm1Hfu mutation (2 available); any Nrp1 mutation (82 available)
Nrp1tm2Ddg mutation (1 available); any Nrp1 mutation (82 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• reduced gonadotropin-releasing hormone neurons

cardiovascular system




Genotype
MGI:6195748
cn32
Allelic
Composition
Gt(ROSA)26Sortm18(Zeb2)Jhai/Gt(ROSA)26Sor+
Tg(Tek-cre)1Ywa/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CD-1 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm18(Zeb2)Jhai mutation (0 available); any Gt(ROSA)26Sor mutation (968 available)
Tg(Tek-cre)1Ywa mutation (6 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice develop tumors after 15.5 weeks of age, with a complete shift towards hematopoietic neoplastic lesions (100%), mainly precursor T-cell lymphoma (85.7%)
• T-cell antigen receptor rearrangement analysis suggests either mono- or oligoclonal origin for all the thymic tumors

endocrine/exocrine glands
• mice develop tumors after 15.5 weeks of age, with a complete shift towards hematopoietic neoplastic lesions (100%), mainly precursor T-cell lymphoma (85.7%)
• T-cell antigen receptor rearrangement analysis suggests either mono- or oligoclonal origin for all the thymic tumors




Genotype
MGI:6195747
cn33
Allelic
Composition
Gt(ROSA)26Sortm18(Zeb2)Jhai/Gt(ROSA)26Sortm18(Zeb2)Jhai
Tg(Tek-cre)1Ywa/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CD-1 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm18(Zeb2)Jhai mutation (0 available); any Gt(ROSA)26Sor mutation (968 available)
Tg(Tek-cre)1Ywa mutation (6 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice develop tumors after 12.7 weeks of age, with a complete shift towards hematopoietic neoplastic lesions (100%), mainly precursor T-cell lymphoma (87.5%)
• cell antigen receptor rearrangement analysis suggests either mono- or oligoclonal origin for all the thymic tumors
• thymomas have an immature/early T-cell precursor leukemia signature
• 12.5% of tumors are myeloid leukemia
• thymomas have an immature/early T-cell precursor leukemia signature
• thymic tumors lack mature T-cell markers such as surface CD3 and CD8 and exhibit a higher percentage of cells that express the stem/progenitor marker cKit or CD44

endocrine/exocrine glands
• mice develop tumors after 12.7 weeks of age, with a complete shift towards hematopoietic neoplastic lesions (100%), mainly precursor T-cell lymphoma (87.5%)
• cell antigen receptor rearrangement analysis suggests either mono- or oligoclonal origin for all the thymic tumors




Genotype
MGI:3710362
cn34
Allelic
Composition
Smad5tm1Huy/Smad5tm1.1Huy
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CD-1 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Smad5tm1.1Huy mutation (0 available); any Smad5 mutation (23 available)
Smad5tm1Huy mutation (0 available); any Smad5 mutation (23 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• mutants exhibit normal blood vessel development and blood vessel morphology in adults




Genotype
MGI:6195749
cn35
Allelic
Composition
Tg(Tek-cre)1Ywa/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CD-1 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Tek-cre)1Ywa mutation (6 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mice develop neoplastic lesions from both vascular (40.5%) and hematopoietic origins (54.8%), mainly T-cell lymphomas, at an average age of 25.5 weeks

neoplasm
• mice develop neoplastic lesions from both vascular (40.5%) and hematopoietic origins (54.8%), mainly T-cell lymphomas, at an average age of 25.5 weeks




Genotype
MGI:5468943
cn36
Allelic
Composition
Cxcl12tm1Tng/Cxcl12tm1.1Link
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cxcl12tm1.1Link mutation (1 available); any Cxcl12 mutation (24 available)
Cxcl12tm1Tng mutation (1 available); any Cxcl12 mutation (24 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• hematopoietic stem cell numbers and cycling are normal
• bone marrow cells exhibit multilineage long-term repopulating defects
• however, self-renewal capacity is restored by transplantation into a wild-type environment




Genotype
MGI:6852794
cn37
Allelic
Composition
Adam10tm2Psa/Adam10tm2Psa
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adam10tm2Psa mutation (1 available); any Adam10 mutation (37 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• endometrial endothelial cells are unable to support a normal decidualization reaction resulting in pregnancy loss between 5.5 days post conception (dpc) and 6.5 dpc
• genes associated with embryonic and trophoblast lineage development and decidualization are downregulated, consistent with the observed pregnancy loss
• however, corpora lutea (CL) histology and the distribution pattern of endothelial cells in the CL are normal at 5.5 dpc
• at 5.5 dpc, the decidualization reaction is less widely distributed throughout the stroma and less organized than in controls; however, the ability of endometrial stromal cells to differentiate into decidual cells is normal
• after induction of artificial decidualization, the weights of scratched uterine horns are significantly lower than those of controls, indicating that decidualization is impaired independently of embryonic signals
• at 5.5 dpc, implantation sites are round instead of oval and have a smaller diameter than control sites; the area of the proximal decidual zone is significantly reduced and a less developed embryonic body is observed
• at 5.5 dpc, embryonic crypt formation is abnormal and large red blood cell-filled spaces are frequently seen close to the implantation sites, indicating aberrant blood vessel formation
• at 5.5 dpc, the area of the endometrial fraction is significantly reduced, and implantation sites show a disorganized vasculature with an increase in endothelial cell coverage
• however, no significant changes in tissue perfusion, hypoxia levels, cell proliferation in the endometrium, or distribution of immune cells are observed in the implantation site
• at 5.5 dpc, the implanting embryo remains localized in the anti-mesometrial side of the lumen rather than having invaded the maternal decidua as in controls
• at 5.5 dpc, luminal closure is incomplete
• at 5.5 dpc, all analyzed females are pregnant but show a ~20% reduction in the number of implantation sites relative to control females
• most or all implantation sites are completely resorbed by 6.5 dpc
• when mated with control Adam10tm2Psa homozygous males for a total of 4 months, 6 of 8 females fail to give birth
• when mated with control males for a 4 month-period, 2 of 8 females produce a relatively small number of offspring (9 pups or 10 pups each, over the course of 3 litters); on average, females give birth to a total of 2.3 +/- 4.4 pups per mouse over 4 months versus 22.88 +/- 3.1 pups per control female
• when mated with wild-type males (129S1/SvImj), 2 of 5 females produce a total of 8 pups in 2 litters, with an average of 1.6 +/- 2.6 pups per female over 4 months
• when females are mated with control males for a 4 month-period, average litter size 3.18 +/- 0.8 versus 9.96 +/- 2.2 in control x control matings
• when females are mated with wild-type males (129S1/SvImj), average litter size is only 2.7 +/- 2.1

embryo
• at 5.5 dpc, the decidualization reaction is less widely distributed throughout the stroma and less organized than in controls; however, the ability of endometrial stromal cells to differentiate into decidual cells is normal
• after induction of artificial decidualization, the weights of scratched uterine horns are significantly lower than those of controls, indicating that decidualization is impaired independently of embryonic signals

cardiovascular system
• females show a disorganized vasculature during the initiation of decidualization: at 5.5 dpc, vessels closer to the implantation sites are abnormally large, vein-like, and organized in honeycomb-like structures, unlike in controls
• an accumulation of CD31 + cells surrounding the luminal epithelium and increased vascularization of the area proximal to the implantation site are observed, unlike in the control area where vascular density is reduced
• increased endomucin (Emcn) and VEGFR2 staining of the enlarged abnormal vasculature surrounding the embryo in implantation sites is suggestive of a defect in endothelial ADAM10/Notch signaling
• females show a significant increase in the area covered by CD31 + endothelial cells in the endometrium at 5.5 dpc, but not at earlier time points (3.5 or 4.5 dpc) during pregnancy




Genotype
MGI:7562246
cn38
Allelic
Composition
Juntm4Wag/Juntm4Wag
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Juntm4Wag mutation (0 available); any Jun mutation (12 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• mice are present at the expected Mendelian ratios at E15.5-P0, indicating normal embryonic survival until late gestation or even until birth

cardiovascular system
N
• at E15.5-P0, none of 10 mice examined exhibit any aortic arch artery remodeling defects
• at E15.5, three of 7 (43%) embryos show thinning of the compact myocardium of the right ventricle
• however, no compact zone thinning is noted in the left ventricle
• at E15.5-P0, one of 7 (14%) embryos exhibits a double outlet right ventricle (DORV)
• at E15.5, mitral valve leaflets are thickened and hyperplastic in one embryo
• at E15.5-P0, one of 7 (14%) embryos shows mitral valve hyperplasia
• at E15.5-P0, three of 7 (43%) embryos show a perimembranous VSD
• at P0, pulmonary valve leaflets are thickened and hyperplastic in one embryo
• at E15.5-P0, one of 7 (14%) embryos shows pulmonary valve hyperplasia

muscle
• at E15.5, three of 7 (43%) embryos show thinning of the compact myocardium of the right ventricle
• however, no compact zone thinning is noted in the left ventricle




Genotype
MGI:6361029
cn39
Allelic
Composition
Nus1tm1.1Qrm/Nus1tm1.1Qrm
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nus1tm1.1Qrm mutation (0 available); any Nus1 mutation (19 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

growth/size/body

embryo
• E10, but not E9, yolk sac shows aberrant blood vessel development

cardiovascular system
• cerebral blood vessels are truncated and exhibit disrupted organization instead of having a well-organized tree-like pattern
• cerebral blood vessels are highly dilated, being normal at E8.5 but becoming dilated by E9.5
• cerebral blood vessels are truncated and exhibit disrupted organization instead of having a well-organized tree-like pattern
• the communicating artery is lost and disruption of major artery patterning is seen
• E10, but not E9, yolk sac shows aberrant blood vessel development
• however, no defect in cardiac development is seen and no obvious bronchial arch artery defects are seen
• E10, but not E9, yolk sac shows aberrant blood vessel development

nervous system
• cerebral blood vessels are truncated and exhibit disrupted organization instead of having a well-organized tree-like pattern
• cerebral blood vessels are highly dilated, being normal at E8.5 but becoming dilated by E9.5




Genotype
MGI:3710208
cn40
Allelic
Composition
Sox9tm1Gsr/Sox9tm1Gsr
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sox9tm1Gsr mutation (2 available); any Sox9 mutation (32 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

cardiovascular system
• endocardial cushions within the outflow tract appear grossly reduced in size
• in the atrioventricular canal, there is malalignment of the atrial septum, although the septum does meet the endocardial cushions in more distal areas
• endocardial cushions are hypoplastic and fail to elongate and form atrioventricular valve primordia at E13.5
• at E12.5, cell proliferation within the endocardial cushion is reduced by 75%
• defects in valve maturation
• atrioventricular valve primordia do not form at E13.5
• incomplete formation of the atrial septum
• mutants exhibit increased blood pooling

homeostasis/metabolism




Genotype
MGI:3796333
cn41
Allelic
Composition
Pik3cbtm1Bvan/Pik3cbtm1Bvan
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pik3cbtm1Bvan mutation (1 available); any Pik3cb mutation (152 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• vascular development is normal




Genotype
MGI:3796332
cn42
Allelic
Composition
Pik3catm3Bvan/Pik3catm3Bvan
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pik3catm3Bvan mutation (1 available); any Pik3ca mutation (64 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

embryo
• by E10.5, mice exhibit a defective remodeling of the primary yolk sac plexus

cardiovascular system
• at E10.5, mice develop vascular abnormalities similar to those observed in Pik3catm1Bvan homozygotes




Genotype
MGI:5306154
cn43
Allelic
Composition
Itgavtm2Hyn/Itgavtm2.1Hyn
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Itgavtm2.1Hyn mutation (0 available); any Itgav mutation (53 available)
Itgavtm2Hyn mutation (2 available); any Itgav mutation (53 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• mice exhibit normal cerebral vasculature




Genotype
MGI:3590664
cn44
Allelic
Composition
Gna13tm1Soff/Gna13tm2Cgh
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gna13tm1Soff mutation (0 available); any Gna13 mutation (12 available)
Gna13tm2Cgh mutation (0 available); any Gna13 mutation (12 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• at E9.5 36% of mutants are dead and by E11.5 88% are dead

cardiovascular system
• large vessels are missing and unusually large vascular spaces are present; however this phenotype is more obvious in Gna13tm1Soff homozygous mice
• pericardial swelling
• variable bleeding into cavities and tissues is seen; however this phenotype is more obvious in Gna13tm1Soff homozygous mice

embryo
• large vessels are missing and unusually large vascular spaces are present; however this phenotype is more obvious in Gna13tm1Soff homozygous mice
• the yolk sac is wrinkled

growth/size/body

integument




Genotype
MGI:4441397
cn45
Allelic
Composition
Nr2f2tm2.1Tsa/Nr2f2tm2.1Tsa
Rbpjtm1Hon/Rbpjtm1Hon
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nr2f2tm2.1Tsa mutation (0 available); any Nr2f2 mutation (27 available)
Rbpjtm1Hon mutation (2 available); any Rbpj mutation (193 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• fewer embryos than expected are found at E10.0

immune system
• at E10.0, number of Prox1+ve lymphatic endothelial cells is dramatically reduced




Genotype
MGI:4441398
cn46
Allelic
Composition
Nr2f2tm2.1Tsa/Nr2f2tm2.1Tsa
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129S7/SvEvBrd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nr2f2tm2.1Tsa mutation (0 available); any Nr2f2 mutation (27 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• at E10.0, number of Prox1+ve lymphatic endothelial cells is dramatically reduced




Genotype
MGI:4948329
cn47
Allelic
Composition
Fzd4tm1Nat/Fzd4tm2.1Nat
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fzd4tm1Nat mutation (1 available); any Fzd4 mutation (29 available)
Fzd4tm2.1Nat mutation (1 available); any Fzd4 mutation (29 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
N
• kidney size is normal




Genotype
MGI:5692156
cn48
Allelic
Composition
Agrntm1Rwb/Agrntm1Rwb
Tg(APPswe,PSEN1dE9)85Dbo/?
Tg(Tek-cre)1Ywa/?
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C3H * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Agrntm1Rwb mutation (1 available); any Agrn mutation (101 available)
Tg(APPswe,PSEN1dE9)85Dbo mutation (6 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• elevated Amyloid beta in females mice

homeostasis/metabolism
• elevated Amyloid beta in females mice




Genotype
MGI:7279301
cn49
Allelic
Composition
Gata4tm1.1Sad/Gata4+
Glyr1em1Dsr/Glyr1+
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gata4tm1.1Sad mutation (1 available); any Gata4 mutation (36 available)
Glyr1em1Dsr mutation (0 available); any Glyr1 mutation (30 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• VSD in all newborns, majority with atrio-ventricular septal defects (AVSDs)

mortality/aging
• 63% newborns die by age P1

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
atrioventricular septal defect DOID:0050651 OMIM:606215
OMIM:614430
OMIM:614474
J:322763




Genotype
MGI:6392049
cn50
Allelic
Composition
Cd2bp2tm1.1Tbh/Cd2bp2tm1.1Tbh
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd2bp2tm1.1Tbh mutation (0 available); any Cd2bp2 mutation (26 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging




Genotype
MGI:3589869
cn51
Allelic
Composition
Ndst1tm1Je/Ndst1tm1Je
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ndst1tm1Je mutation (4 available); any Ndst1 mutation (46 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• in an air-pouch model leukocyte infiltration is reduced to about half that of wild-type
• chemokine induced-immigration of neutrophils is reduced by about 50%
• a reduction of about 40% in firm adhesion of neutrophils to mutant endothelial cells is seen
• rolling velocity is about 40% greater on mutant endothelial cells at 1 dyne/cm2 of shear force
• about 40% fewer neutrophils infiltrate the peritoneal cavity in response to intraperitoneal thioglycollate injection
• about 32% less ear thickening is seen in a model of contact dermatitis induced by oxazolone

cellular
• in an air-pouch model leukocyte infiltration is reduced to about half that of wild-type
• chemokine induced-immigration of neutrophils is reduced by about 50%
• a reduction of about 40% in firm adhesion of neutrophils to mutant endothelial cells is seen
• rolling velocity is about 40% greater on mutant endothelial cells at 1 dyne/cm2 of shear force
• endothelial cell proliferation is reduced in central tendon
• however, mural cell recruitment is normal

hematopoietic system
• in an air-pouch model leukocyte infiltration is reduced to about half that of wild-type
• chemokine induced-immigration of neutrophils is reduced by about 50%
• a reduction of about 40% in firm adhesion of neutrophils to mutant endothelial cells is seen
• rolling velocity is about 40% greater on mutant endothelial cells at 1 dyne/cm2 of shear force

cardiovascular system
• vascularization defects in the developing diaphragm
• central tendon of the diaphragm at E15.5 contains a larger avascular region than in controls and at E16.6, formation of the capillary bed in this region remains incomplete
• the central tendon shows reduced vessel density and many missing connections at E15.5 and E16.5
• the primary plexus of blood vessels in diaphragmatic muscle shows fewer vascular floors, reduced vascular density, some slender and cord-like capillaries, and capillary density remains reduced at E18.5
• however capillary density appears normal in the brain, liver, kidney, heart, lung, spleen and thymus
• SLIT3-induced angiogenesis is greatly diminished in cornea micropocket experiments

embryo
• adults show reduced branches of large vessels in the anterior muscular region of septum transversum

homeostasis/metabolism
• increase in hypoxia in diaphragm

liver/biliary system
• in most mice, liver is the only herniated organ although in a few cases, the small intestine is involved

muscle
• diaphragm covering the liver is thinner at P1
• vascularization defects in the developing diaphragm
• the primary plexus of blood vessels in diaphragmatic muscle shows fewer vascular floors, reduced vascular density, some slender and cord-like capillaries, and capillary density remains reduced at E18.5
• increase in apoptosis in the diaphragm tendon
• cell proliferation of tenocytes in the diaphragm is reduced
• the central tendon and liver remain fused at P1 unlike in wild-type where they are completely separated
• decrease in thickness and disorganized fibrils are seen in the primordial tendon at E15.5, indicating that genesis of the central tendon in the diaphragm is disrupted
• central tendon at E15.5 contains a larger avascular region than in controls and at E16.6, formation of the capillary bed in this region remains incomplete
• the central tendon shows reduced vessel density and many missing connections at E15.5 and E16.5
• mice show fewer tip endothelial cells (which guide angiogenic sprouting) in central tendon than in controls
• filopodia of tip cells are fewer in number and much shorter
• 40% of mice develop congenital diaphragmatic hernia at P2, with penetrance increasing to 60% in adults
• hernia occurs at the anterior midline of the septum transversum in the diaphragm
• hernia size does not progress with age
• muscular region of the diaphragm is thinner at E15.5
• however, fasciculi in the muscle are organized and sarcomeres appear normal
• cell proliferation of tenocytes in the diaphragm is reduced
• collagen bundle in the diaphragm is poorly expressed and disorganized, with fewer tenocytes

skeleton
• the central tendon and liver remain fused at P1 unlike in wild-type where they are completely separated
• decrease in thickness and disorganized fibrils are seen in the primordial tendon at E15.5, indicating that genesis of the central tendon in the diaphragm is disrupted
• central tendon at E15.5 contains a larger avascular region than in controls and at E16.6, formation of the capillary bed in this region remains incomplete
• the central tendon shows reduced vessel density and many missing connections at E15.5 and E16.5
• mice show fewer tip endothelial cells (which guide angiogenic sprouting) in central tendon than in controls
• filopodia of tip cells are fewer in number and much shorter
• cell proliferation of tenocytes in the diaphragm is reduced
• collagen bundle in the diaphragm is poorly expressed and disorganized, with fewer tenocytes

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
congenital diaphragmatic hernia DOID:3827 OMIM:142340
OMIM:222400
OMIM:610187
J:208012




Genotype
MGI:5562651
cn52
Allelic
Composition
Ndst1tm1Je/Ndst1tm1Je
Robo4tm1Kzh/Robo4+
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ndst1tm1Je mutation (4 available); any Ndst1 mutation (46 available)
Robo4tm1Kzh mutation (0 available); any Robo4 mutation (87 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mice show delayed diaphragm vascularization and have more severe branching defects, including missing connections, lack of sprouting, and formation of coiled ends compared to single conditional Ndst1 homozygotes

muscle
• mice show delayed diaphragm vascularization and have more severe branching defects, including missing connections, lack of sprouting, and formation of coiled ends compared to single conditional Ndst1 homozygotes
• 88% of mice develop congenital diaphragmatic hernia




Genotype
MGI:5562654
cn53
Allelic
Composition
Ndst1tm1Je/Ndst1tm1Je
Robo4tm1Kzh/Robo4tm1Kzh
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ndst1tm1Je mutation (4 available); any Ndst1 mutation (46 available)
Robo4tm1Kzh mutation (0 available); any Robo4 mutation (87 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• diaphragm shows a large avascular region in the anterior tendon and reduced total vessel length and branch point numbers

muscle
• diaphragm shows a large avascular region in the anterior tendon and reduced total vessel length and branch point numbers
• 92% of mice develop congenital diaphragmatic hernia




Genotype
MGI:4412188
cn54
Allelic
Composition
Fzd4tm1Nat/Fzd4tm2.1Nat
Tg(Tek-cre)1Ywa/?
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fzd4tm1Nat mutation (1 available); any Fzd4 mutation (29 available)
Fzd4tm2.1Nat mutation (1 available); any Fzd4 mutation (29 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
• rod and cone signals are not transmitted effectively
• vascular development on the vitreal face of the retina is retarded
• intra retinal capillaries are completely absent
• vessels from the vitreal surface penetrate the retina and end in ball-like structures
• large vessels are dilated and artery to vein anastomoses develop
• incomplete recombination in retinas creates mosaics in which capillaries form in some region
• vessels from conditionally knocked out regions can integrate into wild type capillary beds
• electroretinogram a wave is relatively normal
• electroretinogram b wave is markedly reduced

behavior/neurological
• rod and cone signals are not transmitted effectively
• rod and cone signals are not transmitted effectively

nervous system
• leakage of IgG into the cerebellum

cardiovascular system
• leakage of IgG into the cerebellum
• vascular development on the vitreal face of the retina is retarded
• intra retinal capillaries are completely absent
• vessels from the vitreal surface penetrate the retina and end in ball-like structures
• large vessels are dilated and artery to vein anastomoses develop
• incomplete recombination in retinas creates mosaics in which capillaries form in some region
• vessels from conditionally knocked out regions can integrate into wild type capillary beds




Genotype
MGI:4418479
cn55
Allelic
Composition
Hif1atm3Rsjo/Hif1atm3Rsjo
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hif1atm3Rsjo mutation (3 available); any Hif1a mutation (48 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• endothelial cells exhibit reduced VEGF-induced angiogenesis compared with similarly treated wild-type mice
• transplanted tumors exhibit a 50% in tumor vessel density compared with tumors transplanted into wild-type mice
• under hypoxic culture conditions, endothelial cells exhibit reduced VEGF-induced capillary structure formation compared with similarly treated wild-type cells
• endothelial cells exhibit reduced VEGF-induced migration in matrigel compared with similarly treated wild-type mice
• endothelial cells exhibit reduced VEGF-directed migration in hypoxic culture conditions compared with similarly treated wild-type cells
• however, random migration is normal
• VEGF-induced endothelial cell proliferation in matrigel is reduced compared with wild-type mice

neoplasm
• transplanted tumors are 60% lighter than those transplanted into wild-type mice with severe central necrosis due to decreased tumor angiogenesis

homeostasis/metabolism
• with reduced capillary sprouting

cellular
• endothelial cells exhibit reduced VEGF-induced migration in matrigel compared with similarly treated wild-type mice
• endothelial cells exhibit reduced VEGF-directed migration in hypoxic culture conditions compared with similarly treated wild-type cells
• however, random migration is normal
• VEGF-induced endothelial cell proliferation in matrigel is reduced compared with wild-type mice




Genotype
MGI:4829789
cn56
Allelic
Composition
Foxp1tm2.1Eem/Foxp1tm2.1Eem
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxp1tm2.1Eem mutation (0 available); any Foxp1 mutation (75 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

cardiovascular system
N
• despite cre expression patterns, coronary vessel development is relatively unperturbed
• thickened outflow tract at E14.5
• however, outflow tract septation is normal
• ventricular septal defect at E14.5
• display minor ventricular thinning at E12.4
• by E14.5 most mice show extensive ventricular thinning
• significant reduction in proliferation in the compact zone myocardium and the trabecular myocardium at E12.5

muscle
• significant reduction in proliferation in the compact zone myocardium and the trabecular myocardium at E12.5

cellular
• significant reduction in proliferation in the compact zone myocardium and the trabecular myocardium at E12.5




Genotype
MGI:3759503
cn57
Allelic
Composition
Prox1tm1Gco/Prox1tm2Gco
Tg(Tek-cre)1Ywa/?
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Prox1tm1Gco mutation (0 available); any Prox1 mutation (43 available)
Prox1tm2Gco mutation (0 available); any Prox1 mutation (43 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• no deep lymphatic vessels are observed




Genotype
MGI:5692155
cn58
Allelic
Composition
Agrntm1Rwb/Agrntm1Rwb
Tg(Tek-cre)1Ywa/?
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Agrntm1Rwb mutation (1 available); any Agrn mutation (101 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• expression of the Agrn gene is restricted to endothelial cells
• no obvious failure of integrity in the blood-brain barrier

cardiovascular system
• decreased diameter of microvessels




Genotype
MGI:3710234
cn59
Allelic
Composition
Nf1tm1Par/Nf1tm1Par
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf1tm1Par mutation (4 available); any Nf1 mutation (158 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• 8 of 11 embryos exhibit a thinned myocardium
• 8 of 11 embryos show an enlarged atrioventricular cushion
• seen in 8 of 11 embryos
• 10 of 11 embryos exhibit ventricular septal defects

homeostasis/metabolism

muscle
• 8 of 11 embryos exhibit a thinned myocardium




Genotype
MGI:3710231
cn60
Allelic
Composition
Ctnnb1tm2Kem/Ctnnb1tm2.1Kem
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm2.1Kem mutation (0 available); any Ctnnb1 mutation (48 available)
Ctnnb1tm2Kem mutation (1 available); any Ctnnb1 mutation (48 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 50% die by E11.5 and 100% die by E13.5

cardiovascular system
• in the head, the vascular network is less organized, with vessels of irregular diameter and shape and often blind ending vessels and lacunae-like bifurcations are observed
• cephalic vessels show an inconstant diameter and often form acute turns and branching
• endocardial and vascular endothelial cells are more elongated, resulting in a continuously thinner endothelial layer
• endothelial cells present a higher degree of fenestration; these structures are discontinuities in the cell membranes
• endothelial cells have altered intercellular junctional organization, with thinner and longer bundles of actin filaments
• the labyrinthine layer is less vascularized, there is a reduction in the number of fetal blood vessels that penetrate into the labyrinthine area and they remain concentrated in the chorionic plate
• vitelline vessels have a smaller diameter
• however, the primary vascular plexus is present and correctly organized
• thin endocardium
• frequently have extensive liquid accumulation in the pericardial cavity
• about 50% of embryos have hemorrhages in different vascular areas such as the head and the dorsal vessels

embryo
• vitelline vessels have a smaller diameter
• however, the primary vascular plexus is present and correctly organized
• the labyrinthine layer is less vascularized, there is a reduction in the number of fetal blood vessels that penetrate into the labyrinthine area and they remain concentrated in the chorionic plate
• reduced in thickness
• umbilical vessels are often increased in number, have a smaller diameter and are abnormally branched or anastomosed
• seen at E10.5 but not E8.5

homeostasis/metabolism
• frequently have extensive liquid accumulation in the pericardial cavity




Genotype
MGI:3589870
cn61
Allelic
Composition
Ndst1tm1Je/Ndst1tm1Je
Ndst2tm1Lkj/Ndst2tm1Lkj
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ndst1tm1Je mutation (4 available); any Ndst1 mutation (46 available)
Ndst2tm1Lkj mutation (0 available); any Ndst2 mutation (27 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• no pups carrying the cre transgene are born




Genotype
MGI:5562649
cn62
Allelic
Composition
Ndst1tm1Je/Ndst1tm1Je
Slit3tm1.1Dor/Slit3tm1.1Dor
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ndst1tm1Je mutation (4 available); any Ndst1 mutation (46 available)
Slit3tm1.1Dor mutation (1 available); any Slit3 mutation (78 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
muscle
• 100% of mice develop central tendon congenital diaphragmatic hernia compared to 57% of conditional Ndst1 homozygotes and 86% of Slit3 homozygotes




Genotype
MGI:5581949
cn63
Allelic
Composition
Ctnnb1tm2Kem/Ctnnb1tm2Kem
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm2Kem mutation (1 available); any Ctnnb1 mutation (48 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• fewer than expected mice are born

skeleton

hematopoietic system

immune system




Genotype
MGI:5581948
cn64
Allelic
Composition
Ctnnb1tm2Kem/Ctnnb1+
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm2Kem mutation (1 available); any Ctnnb1 mutation (48 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype



Genotype
MGI:5570546
cn65
Allelic
Composition
Ptgestm1.1Gaf/Ptgestm1.1Gaf
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgestm1.1Gaf mutation (0 available); any Ptges mutation (47 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• following wire injury, mice exhibit accelerated intimal hyperplasia with increased intima to media ratio and stenosis percent compared with control mice
• decreased IL1beta-stimulated prostaglandin E2
• increased IL1beta-stimulated prostaglandin D2 and I2 levels

cardiovascular system
N
• whether fed standard chow or a high salt diet, mice exhibit normal modulation of blood pressure and thrombogenesis
• following wire injury, mice exhibit accelerated intimal hyperplasia with increased intima to media ratio and stenosis percent compared with control mice




Genotype
MGI:5496651
cn66
Allelic
Composition
Gt(ROSA)26Sortm1(Bmi1)Aiwa/Gt(ROSA)26Sor+
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(Bmi1)Aiwa mutation (0 available); any Gt(ROSA)26Sor mutation (968 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• mice exhibit normal steady state hematopoiesis and colony-forming capacity of hematopoietic stem and progenitor cells
• during serial transplantation
• hematopoietic stem cells exhibit enhanced expansion ex vivo and protection against loss of self-renewal capacity during serial transplantation compared with wild-type cells
• hematopoietic stem cells exhibit resistance to oxidative stress compared with wild-type cells
• however, no radioprotection is observed
• during serial transplantation

cellular
• during serial transplantation




Genotype
MGI:5562648
cn67
Allelic
Composition
Ndst1tm1Je/Ndst1tm1Je
Slit3tm1.1Dor/Slit3+
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ndst1tm1Je mutation (4 available); any Ndst1 mutation (46 available)
Slit3tm1.1Dor mutation (1 available); any Slit3 mutation (78 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
muscle
• mice develop central tendon congenital diaphragmatic hernia with the same penetrance as seen in single Ndst1 conditional homozygotes




Genotype
MGI:3053001
cn68
Allelic
Composition
Gata4tm1.1Sad/Gata4tm1.1Sad
Tg(Tek-cre)1Ywa/?
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gata4tm1.1Sad mutation (1 available); any Gata4 mutation (36 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• despite the absence of Gata4 in the endocardium, trabeculae were found in E10.5 embryos




Genotype
MGI:3611343
cn69
Allelic
Composition
Prox1tm2Gco/Prox1+
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * NMRI * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Prox1tm2Gco mutation (0 available); any Prox1 mutation (43 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most mutants die within a few days of birth but some survive to adulthood

immune system
• leakage of chyle from the mesenteric vessels is seen in neonates that die postnatally, but not in surviving adults
• lymph vessels are mispatterned and dilated similar to Prox1tm1Gco heterozygotes

digestive/alimentary system
• accumulation of lipid is seen in the intestine walls

growth/size/body
• some mutants display weight gain similar to Prox1tm1Gco heterozygotes, but the occurrence is decreased

homeostasis/metabolism
• at E14.5 edema is seen identical to that in Prox1tm1Gco heterozygotes
• mutants that die within a few days of birth have milky chylous ascites in the peritoneal cavity and thoracic cavity; however, leakage is not seen in surviving adults

cardiovascular system
• leakage of chyle from the mesenteric vessels is seen in neonates that die postnatally, but not in surviving adults

respiratory system
• mutants that die within a few days of birth have milky chylous ascites in the peritoneal cavity and thoracic cavity; however, leakage is not seen in surviving adults




Genotype
MGI:3851403
cn70
Allelic
Composition
Zfpm2tm1Sho/Zfpm2tm2Sho
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Tek-cre)1Ywa mutation (6 available)
Zfpm2tm1Sho mutation (2 available); any Zfpm2 mutation (47 available)
Zfpm2tm2Sho mutation (1 available); any Zfpm2 mutation (47 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• survival rate to weaning is normal

cardiovascular system
N
• coronary plexus, endocardial cushions and compact myocardial layer develop normally
• adults have normal tricuspid and mitral valves




Genotype
MGI:6510800
cn71
Allelic
Composition
Rasa3tm1.1Llp/Rasa3tm1.1Llp
Tg(Tek-cre)1Ywa/?
Genetic
Background
involves: 129S1/SvImJ * C57BL/6J * SJL/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rasa3tm1.1Llp mutation (0 available); any Rasa3 mutation (62 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system

mortality/aging
• all die in utero at E12.5 and E13.5 with severe hemorrhage and diminished fetal liver erythropoiesis

embryo

hematopoietic system




Genotype
MGI:5499117
cn72
Allelic
Composition
Pros1tm1Grl/Pros1tm1Grl
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S1/SvImJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pros1tm1Grl mutation (1 available); any Pros1 mutation (44 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• embryos and adults are viable

cardiovascular system
N
• mice exhibit normal vascular permeability in the liver

homeostasis/metabolism
• focal fibrin deposits are not associated with vascular occlusion or hemorrhage




Genotype
MGI:5432552
cn73
Allelic
Composition
Nfatc1tm1Glm/Nfatc1tm1Glm
Tg(Tek-cre)1Ywa/0
Gt(ROSA)26Sortm1Sho/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S2/SvPas * 129S4/SvJaeSor * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sho mutation (4 available); any Gt(ROSA)26Sor mutation (968 available)
Nfatc1tm1Glm mutation (0 available); any Nfatc1 mutation (47 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• boundary of the proximal outflow tract (pOFT) and distal outflow tract (dOFT) at the outflow tract bend is distrupted, with an extension of endocardium-derived mesenchyme into the dOFT cushion in mutants




Genotype
MGI:5297712
cn74
Allelic
Composition
Msx1tm1Rem/Msx1tm1Rem
Msx2tm1Yvla/Msx2tm1Yvla
Tg(Tek-cre)1Ywa/0
Genetic
Background
involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 * NMRI * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Msx1tm1Rem mutation (1 available); any Msx1 mutation (18 available)
Msx2tm1Yvla mutation (0 available); any Msx2 mutation (23 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• carotid artery diamter and vascular smooth muscle cell (VSMC) are observed




Genotype
MGI:3759849
cn75
Allelic
Composition
Itgavtm2Hyn/Itgavtm2.1Hyn
Tg(Tek-cre)1Ywa/?
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * FVB * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Itgavtm2.1Hyn mutation (0 available); any Itgav mutation (53 available)
Itgavtm2Hyn mutation (2 available); any Itgav mutation (53 available)
Tg(Tek-cre)1Ywa mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median lifespan is reduced to 44 weeks compared to wild-type mice that live past 80 weeks
• mice die of intestinal constriction

immune system
• mesenteric lymph node dendritic cells cultured with CD4+CD25- T cells produce only 1% regulatory T cells compared to 4% to 5% by control dendritic cells
• CD11chighCD103+ dendritic cells implicated in gut-homing are reduced in the mesenteric lymph nodes compared to in Itgavtm2Hyn heterozygote controls
• however, bone marrow dendritic cells produce normal amount of regulatory T cells when cultured with CD4+CD25- T cells
• the number of regulatory T cells in the colon is decreased by 50% compared to in Itgavtm2Hyn heterozygote controls and are predominantly adaptive regulatory T cells
• the number of regulatory T cells in the spleen and mesenteric lymph nodes is increased compared to in Itgavtm2Hyn heterozygote controls and are predominantly natural regulatory T cells
• Peyer's patches are enlarged and contain an increased proportion of activated CD4+ cells compared to control mice
• mesenteric lymph nodes are enlarged (15+/-1.1x106 cells compared to 7.1+/-0.23 x106 cells in Itgavtm2Hyn heterozygote controls at 3 weeks ,and 34.2+/-6.7 x106 cells compared to 8.6+/-1.6 x106 cells in Itgavtm2Hyn heterozygote controls at 12 weeks) and contain an increased proportion of activated CD4+ cells (20+/-0.81 x106 cells compared to 11+/-1.3 x106 cells in Itgavtm2Hyn heterozygote controls at week 3, and 31.7+/-0.40 x106 cells compared to 15+/-0.81 x106 cells in Itgavtm2Hyn heterozygote controls at week 12)
• macrophages exhibit impaired ability to phagocytose and remove apoptotic cells with twice as many uncleared apoptotic cells present in the intestine
• macrophages are no longer sensitive to the inhibitory effects of RGD peptide
• levels of interferon-gamma in serum and the intestine are elevated compared to in Itgavtm2Hyn heterozygote controls
• IL-4 levels in serum and the intestine and IL-5 and IL-6 levels in the intestine are elevated compared to in Itgavtm2Hyn heterozygote controls
• however, IL-12 and IL-23 levels in the intestine are normal
• TNF-alpha levels in the intestine are elevated compared to in Itgavtm2Hyn heterozygote controls
• mice contain higher levels of autoantibodies including ones against tropomyosin, phosphotidylserine, double-stranded DNA and anti-nuclear antibodies compared to in Itgavtm2Hyn heterozygote controls
• mice develop inflammation in the peritoneum, in the liver, and 40% of mice nasal cavity and respiratory tract
• after 14 weeks of age, mice exhibit inflammation in the colon and cecum with infiltration of lymphocytes, monocytes and plasma cells
• inflammation is chronic and progressive leading to ulcers, acute inflammatory infiltrate and crypt abscesses by week 20 with extensive epithelial proliferation, regeneration and adenocarcinoma from 40 weeks

digestive/alimentary system
• by 20 weeks of age, mice exhibit extensive epithelial proliferation and regeneration
• by 20 weeks of age
• by 20 weeks of age