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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Trp53tm1Tyj
targeted mutation 1, Tyler Jacks
MGI:1857263
Summary 259 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Trp53tm1Tyj/Trp53tm1Tyj 129S6.129-Trp53tm1Tyj Rb1tm1.1Jyjw MGI:3769499
hm2
Trp53tm1Tyj/Trp53tm1Tyj 129-Trp53tm1Tyj/J MGI:3849871
hm3
Trp53tm1Tyj/Trp53tm1Tyj B6.129S2-Trp53tm1Tyj/J MGI:3849876
hm4
Trp53tm1Tyj/Trp53tm1Tyj involves: 129S2/SvPas MGI:3584474
hm5
Trp53tm1Tyj/Trp53tm1Tyj involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J MGI:3616345
hm6
Trp53tm1Tyj/Trp53tm1Tyj involves: 129S2/SvPas * BALB/c MGI:3695127
hm7
Trp53tm1Tyj/Trp53tm1Tyj involves: 129S2/SvPas * C57BL/6 MGI:2174782
hm8
Trp53tm1Tyj/Trp53tm1Tyj involves: 129S2/SvPas * C57BL/6 * CBA MGI:5751693
hm9
Trp53tm1Tyj/Trp53tm1Tyj involves: 129S2/SvPas * C57BL/6 * FVB/N MGI:5688516
hm10
Trp53tm1Tyj/Trp53tm1Tyj involves: 129S2/SvPas * FVB/N MGI:4420446
ht11
Trp53tm1Tyj/Trp53+ involves: 129P2/OlaHsd * 129S2/SvPas * BALB/c * C57BL/6 MGI:3818474
ht12
Trp53tm1Tyj/Trp53+ involves: 129S2/SvPas MGI:3584473
ht13
Trp53tm1Tyj/Trp53+ involves: 129S2/SvPas * BALB/cJ * C57BL/6 MGI:5463925
ht14
Trp53tm1Tyj/Trp53+ involves: 129S2/SvPas * C57BL/6 MGI:2174783
ht15
Trp53tm1Tyj/Trp53+ involves: 129S2/SvPas * C57BL/6 * CBA MGI:5751694
ht16
Trp53tm1Tyj/Trp53+ involves: 129S2/SvPas * C57BL/6 * FVB/N MGI:5688517
ht17
Trp53tm1Tyj/Trp53+ involves: 129S2/SvPas * C57BL/6J MGI:3629208
ht18
Trp53tm1Tyj/Trp53tm3.1Tyj involves: 129S2/SvPas * 129S4/SvJae MGI:3584471
ht19
Trp53tm1Tyj/Trp53tm2.1Tyj involves: 129S2/SvPas * 129S4/SvJae MGI:3584464
ht20
Trp53tm1Tyj/Trp53tm1.1Umol involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 * C57BL/6NTac MGI:5790354
ht21
Trp53tm1Tyj/Trp53tm2.1Umol involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 * C57BL/6NTac MGI:5790358
ht22
Trp53tm1Tyj/Trp53tm3.1Glo involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6 MGI:3722619
cn23
Trp53tm1Tyj/Trp53tm1.1Dgk involves: 129S * 129X1/SvJ * C57BL/6 MGI:5306614
cn24
Telo2tm1Tdl/Telo2tm1.1Tdl
Trp53tm1Tyj/Trp53tm1Tyj
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
involves: 129 * 129P2/OlaHsd * 129S2/SvPas * C57BL/6J MGI:3819400
cn25
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz/Gt(ROSA)26Sortm1(cre/ERT)Nat
Trp53tm1Tyj/Trp53+
involves: 129 * 129S2/SvPas * C57BL/6 MGI:4443108
cn26
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz/Gt(ROSA)26Sortm1(cre/ERT)Nat
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129 * 129S2/SvPas * C57BL/6 MGI:4443109
cn27
Gnl3tm2.1Rylt/Gnl3tm2.1Rylt
Trp53tm1Tyj/Trp53tm1Tyj
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129 * 129S2/SvPas * C57BL/6 * CBA MGI:5523425
cn28
Terf1tm1.1Blas/Terf1tm1.1Blas
Tg(KRT5-cre)1Tak/0
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129 * C3H * C57BL/6 * SJL MGI:4357787
cn29
Cops5tm1Rpar/Cops5tm1Rpar
Tg(Lck-cre)548Jxm/0
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129 * C57BL/6 * CBA * SJL MGI:3783542
cn30
Rps6tm1Gtho/Rps6+
Trp53tm1Tyj/Trp53tm1Tyj
Tg(KRT5-cre)5132Jlj/0
involves: 129 * C57BL/6J * DBA/2J MGI:6260011
cn31
Rps6tm1Gtho/Rps6+
Trp53tm1Tyj/Trp53+
Tg(KRT5-cre)5132Jlj/0
involves: 129 * C57BL/6J * DBA/2J MGI:6260013
cn32
Brca2tm1Brn/Brca2tm1Brn
Ptch1tm1Mps/Ptch1+
Trp53tm1Tyj/Trp53+
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:3831342
cn33
Brca2tm1Brn/Brca2tm1Brn
Ptch1tm1Mps/Ptch1+
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:3831343
cn34
Cdkn2ctm1Bbd/Cdkn2ctm1Bbd
Trp53tm1Brn/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL MGI:3710322
cn35
Nle1tm1Cba/Nle1tm1.1Cota
Gt(ROSA)26Sortm2(cre/ERT2)Brn/Gt(ROSA)26Sor+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * 129S2/SvPas MGI:5553372
cn36
Krastm4Tyj/Kras+
Map2k7tm1.1Twad/Map2k7tm1.2Twad
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae * C57BL/6 MGI:4948964
cn37
Rb1tm1Tyj/Rb1tm2Brn
Rbl1tm1Tyj/Rbl1tm1Tyj
Trp53tm1Brn/Trp53tm1Tyj
Tg(Chx10-EGFP/cre,-ALPP)2Clc/0
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL MGI:3710239
cn38
Brca2tm1Brn/Brca2tm1Brn
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL MGI:3831341
cn39
Trp53tm1Brn/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL MGI:3710323
cn40
Ddb1tm1Spg/Ddb1tm1Spg
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL MGI:3698834
cn41
Brca2tm1Brn/Brca2tm1Brn
Trp53tm1Tyj/Trp53+
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL MGI:3831340
cn42
Mdm4tm2Glo/Mdm4tm2.1Glo
Tg(Myh6-cre)2182Mds/0
Trp53tm1Tyj/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S/Sv * C57BL/6J * FVB/N MGI:5907135
cn43
Nf1tm1Par/Nf1+
Ptentm1Hwu/Pten+
Trp53tm1Tyj/Trp53+
Tg(GFAP-cre)25Mes/0
involves: 129S1/Sv * 129S2/SvPas * 129S4/SvJae * 129X1/SvJ * FVB/N MGI:4840094
cn44
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras2)12Hev/0
Trp53tm1Tyj/Trp53+
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6J * FVB/N MGI:5569005
cn45
Nf1tm1Par/Nf1+
Trp53tm1Tyj/Trp53+
Tg(GFAP-cre)25Mes/0
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * FVB/N MGI:4840090
cn46
Lig4tm1Pmc/Lig4tm1Pmc
Trp53tm1Tyj/Trp53tm1Tyj
Xrcc2tm2Pmc/Xrcc2tm2Pmc
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL MGI:3831351
cn47
Trp53tm1Tyj/Trp53tm1Tyj
Xrcc2tm2Pmc/Xrcc2tm2Pmc
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL MGI:3831338
cn48
Lig4tm1Pmc/Lig4tm1Pmc
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL MGI:3831348
cn49
Lig4tm1Pmc/Lig4tm1Pmc
Trp53tm1Tyj/Trp53+
Xrcc2tm2Pmc/Xrcc2tm2Pmc
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL MGI:3831355
cn50
Xrcc1tm1Pmc/Xrcc1tm1Pmc
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL MGI:4359666
cn51
Xrcc1tm1Pmc/Xrcc1tm1Pmc
Trp53tm1Tyj/Trp53+
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL MGI:4359665
cn52
Gt(ROSA)26Sortm1(cre/ERT2)Tyj/Gt(ROSA)26Sor+
Tacc3tm1.1Tno/Tacc3tm1.2Tno
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6 MGI:5305073
cn53
Gt(ROSA)26Sortm1(cre/ERT2)Tyj/Gt(ROSA)26Sor+
Tacc3tm1.1Tno/Tacc3+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6 MGI:5305074
cn54
Ptentm1Hwu/Ptentm1Hwu
Tg(Pdx1-cre)89.1Dam/0
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6 * CBA MGI:4836239
cn55
Rb1tm3Tyj/Rb1tm3Tyj
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Atp/0
involves: 129S2/SvPas * 129S4/SvJae * FVB/N MGI:3783529
cn56
Trp53tm1Elee/Trp53tm1Tyj
Tg(GFAP-cre)25Mes/0
involves: 129S2/SvPas * 129S4/SvJae * FVB/N MGI:3849178
cn57
Mdm4tm2Glo/Mdm4tm2.1Glo
Tg(Myh6-cre)2182Mds/0
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * 129S4/SvJaeSor * 129S7/SvEvBrd * C57BL/6J * FVB/N MGI:5907132
cn58
Trp53tm1Tyj/Trp53tm1Tyj
Usp7tm2Wgu/Usp7tm2Wgu
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 * SJL MGI:5526849
cn59
Mdm2tm1Glo/Mdm2tm2.1Glo
Tg(Myh6-cre)2182Mds/0
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S7/SvEvBrd * FVB/N MGI:3616710
cn60
Tg(Atoh1-sb11)1Mtay/0
TgTn(sb-T2/Onc3)12740Njen/0
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C3H * C57BL/6J * ICR MGI:5317026
cn61
Fbxw7tm1Kei/Fbxw7tm1Kei
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Lck-cre)1Cwi/?
involves: 129S2/SvPas * C57BL/6 MGI:3767597
cn62
Tg(EIIa-cre)C5379Lmgd/0
Tg(Rnu6-RNAi:Bccip)4Zshn/0
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 * FVB/N MGI:5292118
cn63
Tg(ACTB-NOTCH1)1Shn/0
Tg(Nes-cre)1Kln/0
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C57BL/6J MGI:3044602
cn64
Tg(ACTB-NOTCH1)1Shn/0
Tg(Nes-cre)1Kln/0
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6J MGI:3044601
cn65
Kdm6atm1Cdcn/Y
Tg(CAG-cre/Esr1*)5Amc/0
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6J * CBA * FVB/N MGI:6192377
cn66
Atrtm2Bal/Atrtm2Bal
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * C57BL/6 * SJL MGI:5316227
cx67
Rb1tm1.1Jyjw/Rb1tm1.1Jyjw
Trp53tm1Tyj/Trp53tm1Tyj
129S6.129-Trp53tm1Tyj Rb1tm1.1Jyjw MGI:3769498
cx68
Nf1tm1Tyj/Nf1+
Trp53tm1Tyj/Trp53+
B6.129S2-Trp53tm1Tyj Nf1tm1Tyj/+ + MGI:5286078
cx69
Espl1Gt(XL058)Byg/Espl1+
Trp53tm1Tyj/Trp53tm1Tyj
B6.129-Trp53tm1Tyj Espl1Gt(XL058)Byg MGI:5285700
cx70
Espl1Gt(XL058)Byg/Espl1+
Trp53tm1Tyj/Trp53+
B6.129-Trp53tm1Tyj Espl1Gt(XL058)Byg MGI:5285701
cx71
Rpl27aSfa/Rpl27a+
Trp53tm1Tyj/Trp53+
B6.Cg-Rpl27aSfa Trp53tm1Tyj MGI:5140357
cx72
Terttm1Rdp/Terttm1Rdp
Trp53tm1Tyj/Trp53+
B6.Cg-Trp53tm1Tyj Terttm1Rdp MGI:3639948
cx73
Nf1tm1Tyj/Nf1+
Trp53tm1Tyj/Trp53+
(C3H/HeJ x B6.129S2-Trp53tm1Tyj Nf1tm1Tyj/+ +)F1 MGI:5286079
cx74
Nf1tm1Tyj/Nf1+
Trp53tm1Tyj/Trp53+
(CAST/EiJ x B6.129S2-Trp53tm1Tyj Nf1tm1Tyj/+ +)F1 MGI:5286080
cx75
Nf1tm1Tyj/Nf1+
Trp53tm1Tyj/Trp53+
(CBA/J x B6.129S2-Trp53tm1Tyj Nf1tm1Tyj/+ +)F1 MGI:5286081
cx76
Lig4tm1Icrf/Lig4tm1Icrf
Trp53tm1Tyj/Trp53tm1Tyj
either: (involves: 129P2/OlaHsd * 129S2/SvPas) or (involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ) MGI:3655296
cx77
Lig4tm1Icrf/Lig4tm1Icrf
Trp53tm1Tyj/Trp53+
either: (involves: 129P2/OlaHsd * 129S2/SvPas) or (involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ) MGI:3655297
cx78
Ccne1tm1Jro/?
Trp53tm1Tyj/Trp53tm1Tyj
either: (involves: 129S2/SvPas * 129S4/SvJaeSor * C57BL/6J) or (involves: 129S2/SvPas * 129S4/SvJaeSor * C57BL/6 * C57BL/6J) MGI:3586556
cx79
Trp53tm1Tyj/Trp53tm1Tyj
Trp63tm1.1Elrf/Trp63tm1.1Elrf
either: (involves: 129S2/SvPas * C57BL/6 * FVB/N) or (involves: 129S2/SvPas * 129S4/SvJae * 129S6/SvEvTac * C57BL/6) MGI:4355557
cx80
Nhej1tm1Fwa/Nhej1tm1Fwa
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129 MGI:3809981
cx81
Ptch1tm1Mps/Ptch1+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129 * 129S2/SvPas * C57BL/6 MGI:3759458
cx82
Kat5tm1Jwl/Kat5+
Tg(IghMyc)22Bri/0
Trp53tm1Tyj/Trp53+
involves: 129 * C57BL * C57BL/6 * SJL MGI:3814381
cx83
Trp53tm1Tyj/Trp53+
Xpatm1Hvs/Xpatm1Hvs
involves: 129P2/OlaHsd * 129S2/SvPas MGI:4947935
cx84
Trp53tm1Tyj/Trp53tm1Tyj
Xrcc4tm1Fwa/Xrcc4tm1Fwa
involves: 129P2/OlaHsd * 129S2/SvPas MGI:2653516
cx85
Brca1tm1Mak/Brca1tm1Mak
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * 129S2/SvPas MGI:4420438
cx86
Tcrbetm1Che/Tcrbetm1Che
Tcrdtm1Mom/Tcrdtm1Mom
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae * C57BL/6 MGI:3620761
cx87
Ightm2Cgn/Ightm2Cgn
Igktm1Rsky/Igktm1Rsky
Lig4tm1Fwa/Lig4tm1Fwa
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * 129S2/SvPas * 129S6/SvEvTac MGI:4437910
cx88
Ightm2Cgn/Ightm2Cgn
Igktm1Rsky/Igktm1Rsky
Trp53tm1Tyj/Trp53tm1Tyj
Xrcc4tm1Fwa/Xrcc4tm1Fwa
involves: 129P2/OlaHsd * 129S2/SvPas * 129S6/SvEvTac MGI:4437907
cx89
Brca2tm1Kamc/Brca2tm1Kamc
Trp53tm1Tyj/Trp53+
involves: 129P2/OlaHsd * 129S2/SvPas * BALB/c * C57BL/6 MGI:3818475
cx90
LyarGt(RRG292)Byg/LyarGt(RRG292)Byg
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:6191737
cx91
Trp53tm1Tyj/?
Zfp148Gt(XB878)Byg/Zfp148Gt(XB878)Byg
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:5496437
cx92
Ightm1.1(Tag)Rwhe/Igh+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:3850824
cx93
SufuGt(XB699)Byg/Sufu+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:3759457
cx94
Rev3ltm1Ndew/Rev3ltm1Ndew
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:3840908
cx95
Cpt1cGt(XL823)Byg/Cpt1c+
Nf1tm1Tyj/Nf1+
Trp53tm1Tyj/Trp53+
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:5790202
cx96
LyarGt(RRG292)Byg/Lyar+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:6191738
cx97
Ightm2.1(Tag)Rwhe/Igh+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:3850823
cx98
Nf1tm1Tyj/Nf1+
Suz12Gt(Betageo)1Khe/Suz12+
Trp53tm1Tyj/Trp53+
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:5699874
cx99
Clp1tm1.1Pngr/Clp1tm1.1Pngr
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * C57BL/6J MGI:5554932
cx100
Cd44tm1Mak/Cd44tm1Mak
Trp53tm1Tyj/Trp53+
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * C57BL/6J MGI:4943188
cx101
Nop53tm2.1Asuz/Nop53tm2.1Asuz
Tg(Lck-cre)#Jxm/0
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * CBA MGI:5906184
cx102
Cul9tm1.2Yxi/Cul9tm1.2Yxi
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * FVB/N MGI:5007743
cx103
Cep63Gt(EUCE0251h11)Hmgu/Cep63Gt(EUCE0251h11)Hmgu
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6J MGI:5819195
cx104
Herc2Gt(AR0530)Wtsi/Herc2Gt(AR0530)Wtsi
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * C57BL/6 MGI:6286197
cx105
Sugt1Gt(RRS405)Byg/Sugt1+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * C57BL/6J MGI:5696984
cx106
Trp53tm1Tyj/Trp53tm1Tyj
Tsg101tm1Mak/Tsg101tm1Mak
involves: 129P3/J * 129S2/SvPas * C57BL/6 * CD-1 MGI:2450866
cx107
Emg1tm1Hdin/Emg1tm1Hdin
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S * 129S2/SvPas * 129X1/SvJ * CD-1 * ICR MGI:4839757
cx108
Rasal2Gt(463C12)Cmhd/Rasal2+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S * 129X1/SvJ * C57BL/6 * C57BL/6NCrl MGI:5554383
cx109
Rasal2Gt(463C12)Cmhd/Rasal2Gt(463C12)Cmhd
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S * 129X1/SvJ * C57BL/6 * C57BL/6NCrl MGI:5554381
cx110
Bard1tm1Thl/Bard1tm1Thl
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S1/Sv * 129S2/SvPas MGI:2675374
cx111
Ptch1tm1Mps/Ptch1+
Ptch2tm1Pmc/Ptch2+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6 MGI:3690370
cx112
Kat5tm1Jwl/Kat5+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6 MGI:3814378
cx113
Rtel1tm2.1Hdin/Rtel1tm2.1Hdin
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6 MGI:5559534
cx114
Trp53tm1Tyj/Trp53+
Xrcc2tm1Pmc/Xrcc2tm1Pmc
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 MGI:3655347
cx115
Cdkn2ctm1Bbd/Cdkn2c+
Trp53tm1Tyj/Trp53+
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 MGI:3710319
cx116
Cdkn2ctm1Bbd/Cdkn2c+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 MGI:3710320
cx117
Cdkn2ctm1Bbd/Cdkn2ctm1Bbd
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 MGI:3710321
cx118
Ptch2tm1Pmc/Ptch2tm1Pmc
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 MGI:3690369
cx119
Trp53tm1Tyj/Trp53tm1Tyj
Xrcc2tm1Pmc/Xrcc2tm1Pmc
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 MGI:3655298
cx120
Prmt6tm1.2Rchd/Prmt6tm1.2Rchd
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * C57BL/6J * FVB/N MGI:5509171
cx121
Terf1tm1Tdl/Terf1tm1Tdl
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas MGI:2677843
cx122
Nf1tm1Tyj/Nf1+
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas MGI:3776067
cx123
Rb1tm1Tyj/Rb1tm1Tyj
Tg(Rb1)1Blg/0
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas MGI:4420470
cx124
Ccnd3tm1Pisc/Ccnd3tm1Pisc
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas MGI:3819978
cx125
Atrtm1Ofc/Atrtm1Ofc
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas MGI:4355022
cx126
Mdm4tm1Glo/Mdm4tm1Glo
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas MGI:3850680
cx127
Mdm4tm1Glo/Mdm4tm1Glo
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas MGI:3850686
cx128
Gnl3Gt(W223E05)Wrst/Gnl3Gt(W223E05)Wrst
Trp53tm1Tyj/Trp53tm5Tyj
involves: 129S2/SvPas * 129S4/SvJae MGI:3702081
cx129
Trp53tm1Tyj/Trp53+
Trp63tm1Fmc/Trp63+
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6 MGI:5289961
cx130
Tcrbetm1Che/Tcrbetm1Che
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6 MGI:3620760
cx131
Trp53tm1Tyj/Trp53+
Trp73tm1Fmc/Trp73+
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6 MGI:5289964
cx132
Nf1tm1Tyj/?
Trp53tm1Tyj/?
Mastr129S4/SvJae/?
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6J MGI:3587059
cx133
Nf1tm1Tyj/?
Trp53tm1Tyj/?
MastrC57BL/6J/?
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6J MGI:3587060
cx134
Rad51btm1Kmic/Rad51btm1Kmic
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6J MGI:3623223
cx135
Mdm4tm2.1Glo/Mdm4tm2.1Glo
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S4/SvJaeSor * C57BL/6J MGI:3616708
cx136
Mdm4Gt(VICTR20)7Lex/Mdm4Gt(VICTR20)7Lex
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S5/SvEvBrd MGI:3700235
cx137
Pip4k2bGt(Betageo)1Lca/Pip4k2bGt(Betageo)1Lca
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S5/SvEvBrd MGI:5568932
cx138
Mdm4Gt(VICTR20)7Lex/Mdm4Gt(VICTR20)7Lex
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * 129S5/SvEvBrd MGI:3700236
cx139
Npm1Gt(VICTR37)704Lex/Npm1Gt(VICTR37)704Lex
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S5/SvEvBrd * C57BL/6 MGI:3608498
cx140
Rag2tm1.1Mss/Rag2tm1.1Mss
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S6/SvEvTac MGI:5002824
cx141
Rag1tm1Jsek/Rag1tm1Jsek
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S6/SvEvTac MGI:3840834
cx142
Rag1tm1Fwa/Rag1tm1Fwa
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S6/SvEvTac MGI:5002826
cx143
Mdm2tm1Glo/Mdm2+
Mdm4tm1Glo/Mdm4+
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 MGI:3850704
cx144
Mdm2tm1Glo/Mdm2+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 MGI:3850702
cx145
Rad50tm2Jpt/Rad50tm2Jpt
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 MGI:2450431
cx146
Arhgap1tm1Yizh/Arhgap1tm1Yizh
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 MGI:3762617
cx147
Hus1tm1Led/Hus1tm2Rsw
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 MGI:3702291
cx148
Mdm4tm1Glo/Mdm4+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 MGI:3850700
cx149
Bhlha15tm2(Kras)Skz/Bhlha15+
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 MGI:3618360
cx150
Metap2tm1.2Ccr/Metap2tm1.2Ccr
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:3663892
cx151
Trp53tm1Tyj/Trp53tm1Tyj
Trp53bp2tm1Xlu/Trp53bp2tm1Xlu
involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6J MGI:3629205
cx152
Trp53tm1Tyj/Trp53+
Trp53bp2tm1Xlu/Trp53bp2tm1Xlu
involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6J MGI:3629206
cx153
Trp53tm1Tyj/Trp53+
Trp53bp2tm1Xlu/Trp53bp2+
involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6J MGI:3629207
cx154
Rpl27aSfa/Rpl27a+
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6J MGI:5140356
cx155
Mdm2tm1Glo/Mdm2tm1Glo
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S7/SvEvBrd MGI:3850689
cx156
Mdm2tm1Glo/Mdm2tm1Glo
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * 129S7/SvEvBrd MGI:3850688
cx157
Nbntm1Jpt/Nbntm1Jpt
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S7/SvEvBrd MGI:3615887
cx158
Dclre1atm1Rleg/Dclre1atm1Rleg
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S7/SvEvBrd MGI:4941811
cx159
Dclre1atm1Rleg/Dclre1a+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S7/SvEvBrd MGI:4941812
cx160
Mdm2tm1Bay/Mdm2tm1Mep
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6 MGI:3715447
cx161
Pot1atm1Schg/Pot1atm1.1Schg
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6 MGI:3690106
cx162
Mdm2tm1Ypz/Mdm2tm1Ypz
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6 * FVB/N MGI:3763437
cx163
Mdm2tm1Ypz/Mdm2tm1Ypz
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6 * FVB/N MGI:3763436
cx164
Mtbptm1Glo/Mtbptm1Glo
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J MGI:3803626
cx165
Stk11tm1.1Mlfr/Stk11+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J MGI:3616344
cx166
Kat2atm1Roth/Kat2atm1Roth
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J MGI:3712154
cx167
Mtbptm1Glo/Mtbptm1Glo
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J MGI:3803625
cx168
Mdm2tm1Glo/Mdm2tm1Glo
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J MGI:2183201
cx169
Stk11tm1.1Mlfr/Stk11+
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J MGI:3616343
cx170
Mtbptm1Glo/Mtbp+
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J MGI:3803628
cx171
Trp53tm1Tyj/Trp53tm1Tyj
Xrcc1tm1Rpe/Xrcc1tm1Rpe
involves: 129S2/SvPas * 129X1/SvJ MGI:2653518
cx172
Grid2Lc-J/Grid2+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129X1/SvJ * BALB/cByJ * C57BL/6 MGI:4360675
cx173
Klf15tm1Jain/Klf15tm1Jain
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129X1/SvJ * C57BL/6 MGI:4888123
cx174
Cdkn2atm1Cjs/Cdkn2atm1Cjs
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129X1/SvJ * C57BL/6 MGI:3694644
cx175
Ubr5tm1Ckww/Ubr5tm1Ckww
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129X1/SvJ * C57BL/6 MGI:3606184
cx176
Rag2tm2.1Desi/Rag2tm2.1Desi
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129X1/SvJ * C57BL/6 MGI:4941323
cx177
Rag2tm1.1Desi/Rag2tm1.1Desi
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129X1/SvJ * C57BL/6 MGI:4941322
cx178
Dmbt1tm1Kumc/Dmbt1+
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * 129X1/SvJ * C57BL/6J MGI:3777616
cx179
Dmbt1tm1Kumc/Dmbt1tm1Kumc
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * 129X1/SvJ * C57BL/6J MGI:3777615
cx180
Nf1tm1Tyj/?
Nstr2A/J/?
Trp53tm1Tyj/?
involves: 129S2/SvPas * A/J * C57BL/6J MGI:3663692
cx181
Nf1tm1Tyj/?
Nstr1C57BL/6J/Nstr1C57BL/6J
Trp53tm1Tyj/?
involves: 129S2/SvPas * A/J * C57BL/6J MGI:3663691
cx182
Nf1tm1Tyj/?
Nstr1A/J/?
Trp53tm1Tyj/?
involves: 129S2/SvPas * A/J * C57BL/6J MGI:3663690
cx183
Trp53tm1Tyj/Trp53tm1Tyj
Wrntm1Lgu/Wrntm1Lgu
involves: 129S2/SvPas * BALB/c MGI:3700821
cx184
Rps7Zma/Rps7+
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * BALB/c * C3H/HeH * C57BL/6J MGI:5500165
cx185
Tg(Ela1-Tgfa)150Bri/0
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * BALB/c * C57BL/6 * SJL MGI:6192108
cx186
Tg(Ela1-Tgfa)150Bri/0
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * BALB/c * C57BL/6 * SJL MGI:6192107
cx187
Trp53tm1Tyj/Trp53tm1Tyj
Uimc1tm1.2Amj/Uimc1tm1.2Amj
involves: 129S2/SvPas * BALB/cJ * C57BL/6 MGI:5463922
cx188
Trp53tm1Tyj/Trp53+
Uimc1tm1.2Amj/Uimc1tm1.2Amj
involves: 129S2/SvPas * BALB/cJ * C57BL/6 MGI:5463923
cx189
Suprmam1BALB/cMed/Suprmam1BALB/cMed
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * BALB/cMed * C57BL/6 * C57BL/6J MGI:3715519
cx190
Tg(K6ODCtr)55Tgo/0
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C3H * C57BL/6 MGI:3799500
cx191
Rps19Mhdadsk3/Rps19+
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C3HeB/FeJ MGI:6260014
cx192
Rps20Mhdadsk4/Rps20+
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C3HeB/FeJ MGI:6260021
cx193
Exo1tm3.1Wed/Exo1tm3.1Wed
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 MGI:5523487
cx194
Exo1tm2Wed/Exo1tm2Wed
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 MGI:5523485
cx195
Fostm1Wag/Fostm1Wag
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C57BL/6 MGI:3700990
cx196
Tfdp1tm1Lili/Tfdp1+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 MGI:2653312
cx197
Pknox1tm1Fbla/Pknox1tm1Fbla
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 MGI:4839564
cx198
Tfdp1tm1Lili/Tfdp1tm1Lili
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 MGI:2653311
cx199
Rb1tm1Tyj/Rb1+
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C57BL/6 MGI:3582787
cx200
Krastm2Tyj/Kras+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 MGI:3770519
cx201
Pclaftm1.1Lkd/Pclaftm1.1Lkd
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C57BL/6 MGI:5302543
cx202
Krastm2Tyj/Kras+
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C57BL/6 MGI:3770520
cx203
Nhej1tm1.1Ics/Nhej1tm1.1Ics
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 MGI:5475167
cx204
Nf1tm1Tyj/Nf1+
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C57BL/6 MGI:5699872
cx205
Thbs1tm1Hyn/Thbs1tm1Hyn
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 MGI:3032769
cx206
Prdm2tm1Shg/Prdm2tm1Shg
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C57BL/6 MGI:3041266
cx207
Thbs1tm1Hyn/Thbs1tm1Hyn
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C57BL/6 MGI:3032768
cx208
Mdm4tm1Zmy/Mdm4tm1Zmy
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 MGI:5141752
cx209
Fostm1Wag/Fostm1Wag
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 MGI:3700989
cx210
Trp53tm1Tyj/Trp53tm1Tyj
Tg(CAG-EGFP/Map1lc3b)53Nmz/0
involves: 129S2/SvPas * C57BL/6 * C57BL/6NCrj MGI:5319199
cx211
Cenpjtm1d(EUCOMM)Wtsi/Cenpjtm1d(EUCOMM)Wtsi
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 * C57BL/6N * FVB/NJ MGI:5609812
cx212
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Prrx1-FUS/DDIT3)1Mete/0
involves: 129S2/SvPas * C57BL/6 * CBA MGI:5430234
cx213
Tg(Trp53)1Srn/0
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 * CBA MGI:5751688
cx214
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Ly6e-MALT1)#Isg/0
involves: 129S2/SvPas * C57BL/6 * CBA MGI:5432018
cx215
Tg(Pbsn-TAg)15Tvd/0
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 * DBA/2 MGI:4836242
cx216
Pum1tm1.2Hfl/Pum1tm1.2Hfl
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 * FVB MGI:5316383
cx217
Suds3tm1.1Rdp/Suds3+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 * FVB MGI:3698863
cx218
Suds3tm1.1Rdp/Suds3+
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C57BL/6 * FVB MGI:3698864
cx219
Sin3atm1.1Rdp/Sin3a+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 * FVB MGI:3698865
cx220
Rbm24tm1.1Xch/Rbm24tm1.1Xch
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C57BL/6 * FVB/N MGI:6152436
cx221
Tg(Scgb1a1-rtTA)1Jaw/0
Tg(tetO-Kras2)12Hev/0
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C57BL/6 * FVB/N MGI:5912344
cx222
Rbm24tm1.1Xch/Rbm24tm1.1Xch
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 * FVB/N MGI:6152435
cx223
Rbm38tm1.1Xch/Rbm38tm1.1Xch
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C57BL/6 * FVB/N MGI:5688515
cx224
Rbm38tm1.1Xch/Rbm38tm1.1Xch
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 * FVB/N MGI:5688514
cx225
Nabp2tm1.2Nfel/Nabp2tm1.2Nfel
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6 * FVB/N * SJL MGI:5448647
cx226
Prkdcscid/Prkdc+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6J MGI:2665138
cx227
Prkdcscid/Prkdcscid
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6J MGI:4456092
cx228
Rpl27aSfa/Rpl27aSfa
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6J MGI:5140355
cx229
Rpl27aSfa/Rpl27a+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6J MGI:5140354
cx230
Ino80tm1.1Schg/Ino80tm1.1Schg
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6J MGI:5898012
cx231
Ino80tm1.1Schg/Ino80+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6J MGI:5898013
cx232
Ercc6ltm1.2Ajlc/Y
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6J * C57BL/6N * SJL/J MGI:6283343
cx233
Ercc6ltm1.2Ajlc/Y
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C57BL/6J * C57BL/6N * SJL/J MGI:6283344
cx234
Ercc6ltm1.2Ajlc/Ercc6l+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6J * C57BL/6N * SJL/J MGI:6283345
cx235
Rps27lGt(IST11658B7)Tigm/Rps27lGt(IST11658B7)Tigm
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6N MGI:5707900
cx236
Rps27lGt(IST11658B7)Tigm/Rps27lGt(IST11658B7)Tigm
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C57BL/6N MGI:5707901
cx237
Pax3Sp/Pax3Sp
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C57BL * C57BL/6J * FVB MGI:3690111
cx238
Pax3Sp/Pax3Sp
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL * C57BL/6J * FVB MGI:3690112
cx239
Tg(TRP53*R72P)7Dgj/0
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * FVB MGI:4819640
cx240
Tg(TRP53)4Dgj/0
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * FVB MGI:4819639
cx241
Tg(MMTV-AURKA)#Cxd/?
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * FVB/N MGI:3836158
cx242
Pip4k2atm1.2Lca/Pip4k2atm1.2Lca
Pip4k2bGt(Betageo)1Lca/Pip4k2b+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S/SvEv * 129S2/SvPas * 129S5/SvEvBrd MGI:5568940
cx243
Ssbp2tm1Lana/Ssbp2tm1Lana
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S/SvEv * 129S2/SvPas * BALB/c * C57BL/6 MGI:4462851
cx244
Brca2tm1Arge/Brca2tm1Arge
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S/SvEv * 129S2/SvPas * C57BL/6 MGI:2177218
cx245
Nf1tm1Fcr/Nf1+
Trp53tm1Tyj/Trp53+
involves: 129S/SvEv * 129S2/SvPas * C57BL/6 MGI:3580069
cx246
Nf1tm1Fcr/Nf1+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S/SvEv * 129S2/SvPas * C57BL/6 MGI:3580070
cx247
Brca1tm1Arge/Brca1tm1Arge
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S/SvEv * 129S2/SvPas * C57BL/6 MGI:2177217
cx248
Rag2tm1Fwa/Rag2+
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S/SvEv * 129S2/SvPas * C57BL/6J MGI:2665119
cx249
Rag2tm1Fwa/Rag2tm1Fwa
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S/SvEv * 129S2/SvPas * C57BL/6J MGI:2665118
cx250
Cdkn2atm1.1Brn/Cdkn2atm1.1Brn
Pknox1tm1Fbla/Pknox1tm1Fbla
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129/Sv * 129P2/OlaHsd * 129S2/SvPas * C57BL/6 MGI:4839565
cx251
Tg(IghMyc)22Bri/0
Trp53tm1Tyj/Trp53+
involves: 129/Sv * 129X1/SvJ * C57BL * C57BL/6 * SJL MGI:3814379
cx252
Dph1tm2Bhr/Dph1tm2Bhr
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129/Sv * C57BL/6 MGI:3033460
cx253
Nf1tm1Tyj/Nf1+
Trp53tm1Tyj/Trp53+
involves: 129/Sv * C57BL/6 MGI:3580073
cx254
Dph1tm2Bhr/Dph1+
Trp53tm1Tyj/Trp53+
involves: 129/Sv * C57BL/6 MGI:3033461
cx255
Motp1CE/J/Motp1CE/J
Trp53tm1Tyj/Trp53+
involves: 129-Trp53tm1Tyj/J * CE/J MGI:3575575
cx256
Motp1CE/J/Motp1CE/J
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129-Trp53tm1Tyj/J * CE/J MGI:3575574
cx257
Susd6tm1.1Geno/Susd6+
Trp53tm1Tyj/Trp53tm1Tyj
involves: C57BL/6J MGI:5606044
cx258
Susd6tm1.1Geno/Susd6tm1.1Geno
Trp53tm1Tyj/Trp53tm1Tyj
involves: C57BL/6J MGI:5606045
cx259
Nf1tm1Tyj/Nf1+
Trp53tm1Tyj/Trp53+
(SJL/J x B6.129S2-Trp53tm1Tyj Nf1tm1Tyj/+ +)F1 MGI:5286082


Genotype
MGI:3769499
hm1
Allelic
Composition
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
129S6.129-Trp53tm1Tyj Rb1tm1.1Jyjw
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system

endocrine/exocrine glands

mortality/aging
• mice become moribund from lymphoma involving various tissues within >30 weeks; mice with aggressive lymphoma have a mean survival time of 18 weeks

neoplasm
• mice develop lymphomas
• median survival time of mice with teratomas is 7 weeks
• no mice living beyond median survival age show extratesticular teratomas

digestive/alimentary system
• after 7 days of dextran sodium sulfate treatment, mice develop large ulcers in the colon

growth/size/body
• with DSS treatment, double mutants have an average weight of 14% of body weight




Genotype
MGI:3849871
hm2
Allelic
Composition
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
129-Trp53tm1Tyj/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• Background Sensitivity: abnormally dilated peripheral retinal blood vessels, with some mice exhibiting thin blood vessels extending from the optic nerve head toward the lens, but few reach the lens surface

vision/eye
• Background Sensitivity: abnormally dilated peripheral retinal blood vessels, with some mice exhibiting thin blood vessels extending from the optic nerve head toward the lens, but few reach the lens surface




Genotype
MGI:3849876
hm3
Allelic
Composition
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
B6.129S2-Trp53tm1Tyj/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• Background Sensitivity: abnormal blood vessels are found to extend from the peripapillary inner retina through the posterior vitreous and into the retrolental membranes
• abnormally dilated peripheral retinal blood vessels

vision/eye
• Background Sensitivity: on the C57BL/6J background aberrant ocular phenotypes are observed as early as 14 days of age
• Background Sensitivity: the pial septae in many areas are disorganized on the C57BL/6J background but not the 129 or F1 backgrounds
• Background Sensitivity: degeneration is found to varying degrees on the C57BL/6J background, but not the 129 background
• Background Sensitivity: bilateral or unilateral optic nerve hypoplasia is found on the C57BL/6J background, but not on the 129 or F1 background
• Background Sensitivity: pigmented or nonpigmented fibrous retrolental tissue is commonly found in homozygotes on the C57BL/6J background
• Background Sensitivity: retinal folds are found in some homozygotes on the C57BL/6J background
• Background Sensitivity: abnormal blood vessels are found to extend from the peripapillary inner retina through the posterior vitreous and into the retrolental membranes
• abnormally dilated peripheral retinal blood vessels
• Background Sensitivity: fine snowflake-like vitreal opacities can be found on the C57BL/6J background by 21 days of age and may result from the accumulation of fibrous and vascular debris in the vitreous

nervous system
• Background Sensitivity: the pial septae in many areas are disorganized on the C57BL/6J background but not the 129 or F1 backgrounds
• Background Sensitivity: degeneration is found to varying degrees on the C57BL/6J background, but not the 129 background
• Background Sensitivity: bilateral or unilateral optic nerve hypoplasia is found on the C57BL/6J background, but not on the 129 or F1 background




Genotype
MGI:3584474
hm4
Allelic
Composition
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• animals die by about 26 weeks (J:88120)
• mean life span is 4.4 months (J:95316)
• majority of mice (82%) die before 9 months of age, or are euthanized due to occurrence of obvious tumor mass (J:132597)
• a slight decrease is seen in the number of females born

nervous system
• GNPs from mutants show ~50% levels of proliferation compared to Cdkn2c, Trp53-double null cells after 3 days in culture and levels of cells incorporating BrdU are still less in single mutants in tests where cells are stimulated with Shh after culture
• 13/19 (68%) of animals receiving 4 Gy radiation at P5 or 6 develop cerebellar tumors

neoplasm
• 32% have multiple tumors
• 3 of 10 mice develop lymphomas involving the spleen and lymph nodes
• mice start to develop T cell malignancies at 14-16 weeks (J:88120)
• 66% of homozygotes display hematological malignancies, primarily T cell lymphomas (J:95316)
• 6 of 10 mice develop thymic lymphomas (J:221224)
• 13/19 (68%) of animals receiving 4 Gy radiation at P5 or 6 develop cerebellar tumors
• the incidence of hemangiosarcomas is 32% compared to 62% in Trp53tm1Tyj/Trp53tm2.1Tyj mice

cellular
• after irradiation with UVC light, MEFs from null mice show higher levels of polyploidy than Trp53tm2Xu homozygotes
• gamma-irradiation fails to produce an increase in the relative number of cells in G1 compared to S phase (J:77907)
• mouse embryonic fibroblasts exposed to radiation fail to arrest at the G1/S transition unlike similarly treated wild-type cells (J:126920)
• thymocytes are essentially resistant to Trp53-mediated apoptosis
• rare following exposure to ionizing radiation (J:126920)
• in response to irradiation (J:158953)
• in irradiated thymocytes (J:195018)
• in irradiated spleen cells
• reduced sensitivity to UV-induced cell death in MEFs compared to wild-type cells
• GNPs from mutants show ~50% levels of proliferation compared to Cdkn2c, Trp53-double null cells after 3 days in culture and levels of cells incorporating BrdU are still less in single mutants in tests where cells are stimulated with Shh after culture

immune system
• thymocytes are essentially resistant to Trp53-mediated apoptosis
• rare following exposure to ionizing radiation (J:126920)
• in response to irradiation (J:158953)
• in irradiated thymocytes (J:195018)
• in irradiated spleen cells

cardiovascular system
• increased number of microvessels form 2 weeks after transverse aortic constriction
• increased hypertrophy as a result of transverse aortic restriction
• better systolic function than control

hematopoietic system
• thymocytes are essentially resistant to Trp53-mediated apoptosis
• rare following exposure to ionizing radiation (J:126920)
• in response to irradiation (J:158953)
• in irradiated thymocytes (J:195018)
• in irradiated spleen cells

endocrine/exocrine glands
• rare following exposure to ionizing radiation (J:126920)
• in response to irradiation (J:158953)
• in irradiated thymocytes (J:195018)
• mice start to develop T cell malignancies at 14-16 weeks (J:88120)
• 66% of homozygotes display hematological malignancies, primarily T cell lymphomas (J:95316)
• 6 of 10 mice develop thymic lymphomas (J:221224)

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Li-Fraumeni syndrome DOID:3012 OMIM:151623
OMIM:609265
J:95316




Genotype
MGI:3616345
hm5
Allelic
Composition
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• median age of survival is 17 months compared to 11 months in mice heterozygous for Stk11tm1.1Mlfr and Trp53tm1Tyj




Genotype
MGI:3695127
hm6
Allelic
Composition
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129S2/SvPas * BALB/c
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• at P10, pattern and extent of oocyte loss in ovaries of mutants after exposure to 0.45 Gy radiation on P5 is similar to wild-type and much more sever than Trp63tm2Fmc mutants




Genotype
MGI:2174782
hm7
Allelic
Composition
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
muscle

endocrine/exocrine glands
• most lymphomas are thymic lymphomas (J:17728)
• 75% of observed tumors are thymic lymphomas (J:87501)

skeleton
• 13% incidence (J:72391)

mortality/aging
• most die by 6 months of age (J:17728)
• average life span 160 days (J:72391)
• 90% succumb to tumors and die by 7 months of age (J:87501)
• homozygous mutants die between ~50 to 250 days after birth (J:95318)
• 16.6% rather than the expected 25% of mutants are observed at weaning, indicating partial lethality either during embryogenesis or after birth but before weaning

neoplasm
• predominantly lymphomas with sarcomas and teratomas (J:17728)
• 71% of mice develop lymphoma, usually affecting the thymus (J:17728)
• 70% incidence (J:72391)
• 56% of homozygous nulls developed lymphomas (J:95318)
• most lymphomas are thymic lymphomas (J:17728)
• 75% of observed tumors are thymic lymphomas (J:87501)
• 3.3% incidence
• 3.3% incidence of stomach squamous cell carcinoma
• 50% incidence (J:72391)
• 40% of homozygous nulls developed sarcomas (J:95318)
• 20% incidence (J:72391)
• 13% incidence (J:72391)

cellular
• irradiated E13.5 heterozygous embryos showed no evidence of apoptosis in the hypothalamus compared to wildtype and heterozygotes that showed a high number of apoptotic cells
• MEFs initially did not show any significant differences in growth rate but by day 4, grew more rapidly than wildtype or heterozygous MEFs
• in mouse embryonic fibroblasts treated with UV irradiation

digestive/alimentary system
• 6.7% incidence
• 3.3% incidence of stomach polyps




Genotype
MGI:5751693
hm8
Allelic
Composition
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• radiation-induced apoptosis in the thymus is decreased as compared to wild-type

endocrine/exocrine glands
• radiation-induced apoptosis in the thymus is decreased as compared to wild-type

hematopoietic system
• radiation-induced apoptosis in the thymus is decreased as compared to wild-type

immune system
• radiation-induced apoptosis in the thymus is decreased as compared to wild-type

mortality/aging
• average lifespan is 4.5 months




Genotype
MGI:5688516
hm9
Allelic
Composition
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival following exposure to 8 gray of whole body gamma-irradiation is 34 days
• longest lifespan is 34 weeks, median survival is 25 weeks

homeostasis/metabolism
• median survival following exposure to 8 gray of whole body gamma-irradiation is 34 days




Genotype
MGI:4420446
hm10
Allelic
Composition
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129S2/SvPas * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• following ionizing radiation treatment, hair follicles do not exhibit apoptosis unlike in similarly treated wild-type mice
• following ionizing radiation treatment, arrested cell growth in the epidermis is partially abrogated compared to in similarly treated wild-type mice

integument
• following ionizing radiation treatment, arrested cell growth in the epidermis is partially abrogated compared to in similarly treated wild-type mice




Genotype
MGI:3818474
ht11
Allelic
Composition
Trp53tm1Tyj/Trp53+
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * BALB/c * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 50% survival at 63 weeks




Genotype
MGI:3584473
ht12
Allelic
Composition
Trp53tm1Tyj/Trp53+
Genetic
Background
involves: 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• 12 of 45 mice treated with 2-AAF develop urinary bladder tumors

mortality/aging
• mean life span is 15.4 months

neoplasm
• 19% have multiple tumors compared to 44% of Trp53tm3.1Tyj heterozygotes
• 12 of 45 mice treated with 2-AAF develop urinary bladder tumors
• 4 of 37 develop low grade carcinomas including 1 with a well differentiated lung carcinoma
• 12 of 45 mice treated with 2-AAF develop urinary bladder tumors

cellular
• in response to irradiation
• a larger fraction of MEFs are in S phase compared to wild-type mice

hematopoietic system
• hematopoietic stem and progenitor cells (HSPC) from irradiated mice transplanted into irradiated mice reconstitute the HSPC population exhibit a competitive advantage over HSPC from untreated mice compared with cells from similarly irradiated wild-type mice
• however, no competitive advantage is observed over similarly treated Cdkn2atm2.1Rdp cells in irradiation chimera experiments
• in response to irradiation

immune system
• in response to irradiation

homeostasis/metabolism
• 12 of 45 mice treated with 2-AAF develop urinary bladder tumors

endocrine/exocrine glands
• in response to irradiation

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Li-Fraumeni syndrome DOID:3012 OMIM:151623
OMIM:609265
J:95316




Genotype
MGI:5463925
ht13
Allelic
Composition
Trp53tm1Tyj/Trp53+
Genetic
Background
involves: 129S2/SvPas * BALB/cJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 42.8% of mice (6 of 14) develop thymic lymphomas after exposure to ionizing radiation




Genotype
MGI:2174783
ht14
Allelic
Composition
Trp53tm1Tyj/Trp53+
Genetic
Background
involves: 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 28% of mutants die by 17 months of age due to tumors (J:17728)
• heterozygous mutants die between 150 to 750 days after birth (J:95318)
• less than 5% of mice live past two years due to cancerous tumors (J:135509)

endocrine/exocrine glands
• 2.9% incidence of pancreatic adenocarcinomas

integument

neoplasm
• tumors show loss of heterozygosity for Trp53
• age of onset 9 months (J:17728)
• over 95% of mice have tumors by 2 years of age (J:135509)
• 2.9% incidence of pancreatic adenocarcinomas
• 5.9% incidence
• is observed in 2.6% of mice by 24 months of age
• 25% of mutants exhibit lymphomas (J:17728)
• 32% incidence (J:72391)
• 32% of heterozygous mutants developed lymphomas (J:95318)
• is observed in 18.4% of mice by 24 months of age (J:135509)
• 35% incidence of carcinomas (J:72391)
• 2.9% incidence of pancreatic adenocarcinomas (J:72391)
• 12% of heterozygous mutants developed carcinomas, which are rare in homozygotes (J:95318)
• 18% incidence of ear squamous cell carcinoma
• 57% of mutants exhibit sarcomas (J:17728)
• 56% incidence of sarcomas (J:72391)
• 2.9% incidence of undifferentiated sarcomas (J:72391)
• 56% of heterozygous mutants developed sarcomas (J:95318)
• 8.8% incidence (J:72391)
• 29% incidence (J:72391)

digestive/alimentary system
• 2.9% incidence of small intestinal polyps
• 2.9% incidence of stomach polyps

muscle

respiratory system

skeleton
• 29% incidence (J:72391)

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Li-Fraumeni syndrome DOID:3012 OMIM:151623
OMIM:609265
J:17728




Genotype
MGI:5751694
ht15
Allelic
Composition
Trp53tm1Tyj/Trp53+
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• radiation-induced apoptosis in the thymus is increased as compared to homozygous Trp53tm1Tyj mice, but is decreased as compared to wild-type

endocrine/exocrine glands
• radiation-induced apoptosis in the thymus is increased as compared to homozygous Trp53tm1Tyj mice, but is decreased as compared to wild-type

hematopoietic system
• radiation-induced apoptosis in the thymus is increased as compared to homozygous Trp53tm1Tyj mice, but is decreased as compared to wild-type

immune system
• radiation-induced apoptosis in the thymus is increased as compared to homozygous Trp53tm1Tyj mice, but is decreased as compared to wild-type

mortality/aging
• average lifespan is 14 months




Genotype
MGI:5688517
ht16
Allelic
Composition
Trp53tm1Tyj/Trp53+
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival is 64 weeks




Genotype
MGI:3629208
ht17
Allelic
Composition
Trp53tm1Tyj/Trp53+
Genetic
Background
involves: 129S2/SvPas * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• compound mutants which are heterozygous for Trp53tm1Tyj and homozygous wild-type for Trp53bp2 show 7% tumor development over 72 weeks
• mice show a significant difference in tumor onset compared to Trp53bp2tm1Xlu/+ Trp53tm1Tyj homozygous mice




Genotype
MGI:3584471
ht18
Allelic
Composition
Trp53tm1Tyj/Trp53tm3.1Tyj
Genetic
Background
involves: 129S2/SvPas * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
Trp53tm3.1Tyj mutation (2 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• a slight decrease in hematological malignancies (primarily T cell lymphomas) is seen compared to Trp53tm1Tyj homozygotes (55% compared to 66%)

mortality/aging
• mean life span is 4.6 months
• a slight decrease is seen in the number of females born

neoplasm
• 43% have multiple tumors
• a slight decrease in hematological malignancies (primarily T cell lymphomas) is seen compared to Trp53tm1Tyj homozygotes (55% compared to 66%)
• carcinomas are seen in 18% of mice, with most carcinomas showing signs of invasion, metastasis, or other features of advanced human carcinomas
• most carcinomas are derived from epithelial cells

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Li-Fraumeni syndrome DOID:3012 OMIM:151623
OMIM:609265
J:95316




Genotype
MGI:3584464
ht19
Allelic
Composition
Trp53tm1Tyj/Trp53tm2.1Tyj
Genetic
Background
involves: 129S2/SvPas * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
Trp53tm2.1Tyj mutation (2 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• a slight decrease in hematological malignancies (primarily T cell lymphomas) is seen compared to Trp53tm1Tyj homozygotes (50% compared to 66%)

mortality/aging
• mean life span is 4.5 months
• a slight decrease is seen in the number of females born

neoplasm
• 57% have multiple tumors, significantly more than in Trp53tm1Tyj homozygotes (32%)
• a slight decrease in hematological malignancies (primarily T cell lymphomas) is seen compared to Trp53tm1Tyj homozygotes (50% compared to 66%)
• carcinomas are seen in 16% of mice, with most carcinomas showing signs of invasion, metastasis, or other features of advanced human carcinomas
• most carcinomas are derived from epithelial cells
• the incidence of hemangiosarcomas is increased to 62% compared to 32% in Trp53tm1Tyj homozygotes and these tumors are highly aggressive

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Li-Fraumeni syndrome DOID:3012 OMIM:151623
OMIM:609265
J:95316




Genotype
MGI:5790354
ht20
Allelic
Composition
Trp53tm1Tyj/Trp53tm1.1Umol
Genetic
Background
involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 * C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1.1Umol mutation (0 available); any Trp53 mutation (149 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• shortened survival compared to single Trp53tm1Tyj homozygotes

neoplasm
• T-lymphoma cell lines established from mutant mice develop into highly aggressive leukemias when tail vein injected into the circulation of nude mice
• lymphomas show a 2-fold increase in cell proliferation compared to lymphomas from Trp53tm1Tyj homozygotes and compound heterozygous Trp53tm2.1Umol/Trp53tm1Tyj mice
• accelerated tumor onset of T lymphomas compared to single Trp53tm1Tyj homozygotes
• accelerated tumor onset of B lymphomas compared to single Trp53tm1Tyj homozygotes
• mice show broadening of the tumor spectrum, showing more carcinomas compared with single Trp53tm1Tyj homozygotes
• mice show broadening of the tumor spectrum, showing a higher diversity of sarcoma subtypes compared with single Trp53tm1Tyj homozygotes
• mice show broadening of the tumor spectrum, showing more germ cell tumors compared with single Trp53tm1Tyj homozygotes
• accelerated tumor onset of T lymphomas, B lymphomas, and solid tumors compared to single Trp53tm1Tyj homozygotes

cellular
• thymocytes are resistant to apoptosis after gamma-irradiation

embryo
• mice show a similar expansion of mesenchymal stem cells as single Trp53tm1Tyj homozygotes

endocrine/exocrine glands
• accelerated tumor onset of T lymphomas compared to single Trp53tm1Tyj homozygotes

hematopoietic system
• mice show a greater increase in the number of hematopoietic Lin-Sca1+c-Kit+ (LSK) progenitor cells than single Trp53tm1Tyj homozygotes

reproductive system
• mice show broadening of the tumor spectrum, showing more germ cell tumors compared with single Trp53tm1Tyj homozygotes




Genotype
MGI:5790358
ht21
Allelic
Composition
Trp53tm1Tyj/Trp53tm2.1Umol
Genetic
Background
involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 * C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
Trp53tm2.1Umol mutation (0 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice show similar survival to single Trp53tm1Tyj homozygotes
• however, beyond 230 days, mice show a trend toward survival extension compared to single Trp53tm1Tyj homozygotes, most likely due to a reduction in very late appearing B lymphomas

neoplasm
• lymphomas show a decrease in cell proliferation compared to lymphomas from compound heterozygous Trp53tm1.1Umol/Trp53tm1Tyj mice
• mice show similar tumor latency as single Trp53tm1Tyj homozygotes
• mice show similar tumor latency as single Trp53tm1Tyj homozygotes
• mice show broadening of the tumor spectrum, showing more carcinomas compared with single Trp53tm1Tyj homozygotes
• mice show broadening of the tumor spectrum, showing a higher diversity of sarcoma subtypes compared with single Trp53tm1Tyj homozygotes
• mice show broadening of the tumor spectrum, showing more germ cell tumors compared with single Trp53tm1Tyj homozygotes

reproductive system
• mice show broadening of the tumor spectrum, showing more germ cell tumors compared with single Trp53tm1Tyj homozygotes

cellular
• thymocytes are resistant to apoptosis after gamma-irradiation

endocrine/exocrine glands
• mice show similar tumor latency as single Trp53tm1Tyj homozygotes

hematopoietic system
• mice show a similar increase in the number of hematopoietic Lin-Sca1+c-Kit+ (LSK) progenitor cells as single Trp53tm1Tyj homozygotes




Genotype
MGI:3722619
ht22
Allelic
Composition
Trp53tm1Tyj/Trp53tm3.1Glo
Genetic
Background
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
Trp53tm3.1Glo mutation (0 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice do not survive past 300 days compared to Trp53tm1Tyj heterozygotes and Trp53tm3.1Glo heterozygotes that live to 900 days




Genotype
MGI:5306614
cn23
Allelic
Composition
Trp53tm1Tyj/Trp53tm1.1Dgk
Genetic
Background
involves: 129S * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Trp53tm1.1Dgk mutation (1 available); any Trp53 mutation (149 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• in mouse embryonic fibroblasts transfected with a flpo-expressing adenovirus
• in mouse embryonic fibroblasts transfected with a flpo-expressing adenovirus




Genotype
MGI:3819400
cn24
Allelic
Composition
Telo2tm1Tdl/Telo2tm1.1Tdl
Trp53tm1Tyj/Trp53tm1Tyj
Gt(ROSA)26Sortm1(cre/ERT)Nat/Gt(ROSA)26Sor+
Genetic
Background
involves: 129 * 129P2/OlaHsd * 129S2/SvPas * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (492 available)
Telo2tm1.1Tdl mutation (0 available); any Telo2 mutation (6 available)
Telo2tm1Tdl mutation (0 available); any Telo2 mutation (6 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• tamoxifen-treated mouse embryonic fibroblasts exhibit cell cycle arrest after 6 days in culture unlike wild-type cells




Genotype
MGI:4443108
cn25
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz/Gt(ROSA)26Sortm1(cre/ERT)Nat
Trp53tm1Tyj/Trp53+
Genetic
Background
involves: 129 * 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz mutation (1 available); any Gt(ROSA)26Sor mutation (492 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (492 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• hematopoietic stem and progenitor cells of irradiated mice treated with tamoxifen do not exhibit a selective advantage over cells not expressing the modified cDNA




Genotype
MGI:4443109
cn26
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz/Gt(ROSA)26Sortm1(cre/ERT)Nat
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129 * 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-Trp53*,-EGFP)Medz mutation (1 available); any Gt(ROSA)26Sor mutation (492 available)
Gt(ROSA)26Sortm1(cre/ERT)Nat mutation (1 available); any Gt(ROSA)26Sor mutation (492 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• hematopoietic stem and progenitor cells of irradiated mice treated with tamoxifen do not exhibit a selective advantage over cells not expressing the modified cDNA




Genotype
MGI:5523425
cn27
Allelic
Composition
Gnl3tm2.1Rylt/Gnl3tm2.1Rylt
Trp53tm1Tyj/Trp53tm1Tyj
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129 * 129S2/SvPas * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gnl3tm2.1Rylt mutation (0 available); any Gnl3 mutation (35 available)
Tg(CAG-cre/Esr1*)5Amc mutation (6 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• increase in the percentage of MEFs showing signs of replication-induced DNA damage after tamoxifen treatment
• tamoxifen treatment shortens the lifespan of MEFs
• tamoxifen treatment impairs the long-term proliferative potential of MEFs




Genotype
MGI:4357787
cn28
Allelic
Composition
Terf1tm1.1Blas/Terf1tm1.1Blas
Tg(KRT5-cre)1Tak/0
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129 * C3H * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Terf1tm1.1Blas mutation (0 available); any Terf1 mutation (27 available)
Tg(KRT5-cre)1Tak mutation (0 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• perinatal and early postnatal lethality is normal

neoplasm
• in tail and ear skin of older mice

craniofacial

digestive/alimentary system

integument
N
• hair growth and skin pigmentation are normal
• in tail and ear skin of older mice

growth/size/body




Genotype
MGI:3783542
cn29
Allelic
Composition
Cops5tm1Rpar/Cops5tm1Rpar
Tg(Lck-cre)548Jxm/0
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129 * C57BL/6 * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cops5tm1Rpar mutation (0 available); any Cops5 mutation (7 available)
Tg(Lck-cre)548Jxm mutation (2 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• an 80-90% reduction compared to control showing no rescue of the reduced thymic cellularity resulting from Cops5 deficiency

immune system
• an 80-90% reduction compared to control showing no rescue of the reduced thymic cellularity resulting from Cops5 deficiency

endocrine/exocrine glands
• an 80-90% reduction compared to control showing no rescue of the reduced thymic cellularity resulting from Cops5 deficiency




Genotype
MGI:6260011
cn30
Allelic
Composition
Rps6tm1Gtho/Rps6+
Trp53tm1Tyj/Trp53tm1Tyj
Tg(KRT5-cre)5132Jlj/0
Genetic
Background
involves: 129 * C57BL/6J * DBA/2J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rps6tm1Gtho mutation (0 available); any Rps6 mutation (11 available)
Tg(KRT5-cre)5132Jlj mutation (1 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
N
• mice exhibit normal footpad pigmentation and normal Kitl mRNA levels in the footpad epidermis at P30, indicating complete reversal of the phenotype observed in mice that are only heterozygous for Rps6tm1Gtho and hemizygous for Tg(KRT5-cre)5132Jlj




Genotype
MGI:6260013
cn31
Allelic
Composition
Rps6tm1Gtho/Rps6+
Trp53tm1Tyj/Trp53+
Tg(KRT5-cre)5132Jlj/0
Genetic
Background
involves: 129 * C57BL/6J * DBA/2J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rps6tm1Gtho mutation (0 available); any Rps6 mutation (11 available)
Tg(KRT5-cre)5132Jlj mutation (1 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• mice exhibit an intermediate footpad pigmentation phenotype and reduced Kitl mRNA levels in the footpad epidermis at P30, indicating partial amelioration of the dark skin observed in mice that are only heterozygous for Rps6tm1Gtho and hemizygous for Tg(KRT5-cre)5132Jlj

integument
• mice exhibit an intermediate footpad pigmentation phenotype and reduced Kitl mRNA levels in the footpad epidermis at P30, indicating partial amelioration of the dark skin observed in mice that are only heterozygous for Rps6tm1Gtho and hemizygous for Tg(KRT5-cre)5132Jlj

limbs/digits/tail
• mice exhibit an intermediate footpad pigmentation phenotype and reduced Kitl mRNA levels in the footpad epidermis at P30, indicating partial amelioration of the dark skin observed in mice that are only heterozygous for Rps6tm1Gtho and hemizygous for Tg(KRT5-cre)5132Jlj




Genotype
MGI:3831342
cn32
Allelic
Composition
Brca2tm1Brn/Brca2tm1Brn
Ptch1tm1Mps/Ptch1+
Trp53tm1Tyj/Trp53+
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca2tm1Brn mutation (3 available); any Brca2 mutation (33 available)
Ptch1tm1Mps mutation (2 available); any Ptch1 mutation (23 available)
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 100% of mice develop medulloblastoma beginning at 10 weeks

neoplasm
• 100% of mice develop medulloblastoma beginning at 10 weeks




Genotype
MGI:3831343
cn33
Allelic
Composition
Brca2tm1Brn/Brca2tm1Brn
Ptch1tm1Mps/Ptch1+
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca2tm1Brn mutation (3 available); any Brca2 mutation (33 available)
Ptch1tm1Mps mutation (2 available); any Ptch1 mutation (23 available)
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 100% of mice develop medulloblastoma beginning at 5 weeks

neoplasm
• 100% of mice develop medulloblastoma beginning at 5 weeks




Genotype
MGI:3710322
cn34
Allelic
Composition
Cdkn2ctm1Bbd/Cdkn2ctm1Bbd
Trp53tm1Brn/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2ctm1Bbd mutation (1 available); any Cdkn2c mutation (6 available)
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Brn mutation (13 available); any Trp53 mutation (149 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 4/4 of mice receiving 4 Gy radiation at P5 develop cerebellar tumors by 5 months of age

neoplasm
• 4/4 of mice receiving 4 Gy radiation at P5 develop cerebellar tumors by 5 months of age

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
medulloblastoma DOID:0050902 OMIM:155255
J:102702




Genotype
MGI:5553372
cn35
Allelic
Composition
Nle1tm1Cba/Nle1tm1.1Cota
Gt(ROSA)26Sortm2(cre/ERT2)Brn/Gt(ROSA)26Sor+
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm2(cre/ERT2)Brn mutation (1 available); any Gt(ROSA)26Sor mutation (492 available)
Nle1tm1.1Cota mutation (0 available); any Nle1 mutation (2 available)
Nle1tm1Cba mutation (0 available); any Nle1 mutation (2 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
N
• tamoxifen-treated mice exhibit rescued total bone marrow and LSK cells




Genotype
MGI:4948964
cn36
Allelic
Composition
Krastm4Tyj/Kras+
Map2k7tm1.1Twad/Map2k7tm1.2Twad
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (6 available); any Kras mutation (35 available)
Map2k7tm1.1Twad mutation (0 available); any Map2k7 mutation (5 available)
Map2k7tm1.2Twad mutation (0 available); any Map2k7 mutation (5 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• following adenovirus cre infection, mice exhibit increased lung tumor burden compared with control mice
• however, tumorigenesis is the same as in Map2k7tm1.1Twad/Map2k7tm1.2Twad Krastm4Tyj/Kras+ mice
• following adenovirus cre infection, mice exhibit more adenocarcinomas than Map2k7tm1.1Twad/Map2k7tm1.2Twad Krastm4Tyj/Kras+ mice

neoplasm
• following adenovirus cre infection, mice exhibit increased lung tumor burden compared with control mice
• however, tumorigenesis is the same as in Map2k7tm1.1Twad/Map2k7tm1.2Twad Krastm4Tyj/Kras+ mice
• following adenovirus cre infection, mice exhibit more adenocarcinomas than Map2k7tm1.1Twad/Map2k7tm1.2Twad Krastm4Tyj/Kras+ mice




Genotype
MGI:3710239
cn37
Allelic
Composition
Rb1tm1Tyj/Rb1tm2Brn
Rbl1tm1Tyj/Rbl1tm1Tyj
Trp53tm1Brn/Trp53tm1Tyj
Tg(Chx10-EGFP/cre,-ALPP)2Clc/0
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rb1tm1Tyj mutation (5 available); any Rb1 mutation (80 available)
Rb1tm2Brn mutation (3 available); any Rb1 mutation (80 available)
Rbl1tm1Tyj mutation (1 available); any Rbl1 mutation (12 available)
Tg(Chx10-EGFP/cre,-ALPP)2Clc mutation (1 available)
Trp53tm1Brn mutation (13 available); any Trp53 mutation (149 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
• retinoblastoma cells that express amacrine/horizontal cell markers also extend processes and form synapses; some of these Golgi-Cox-labeled cells extend 1-3 long main processes with further neurite branching characteristic of horizontal or wide-field amacrine cells, while more (nearly half of ) labeled cells extend a main process with extensive neurite outgrowth characteristic of amacrine cells, and the remaining cells are less differentiated with short, unbranched neurites
• these labeled cells are mainly found near the tumor origin, while fewer are present toward the lens and anterior chamber
• tumor cells that invade the anterior eye chamber beneath the cornea are densely packed stage II cells surrounded by sparse regions of plexus with no synaptic densities or vesiclesin in the plexus or rosettes of these cells
• tumor cells have abundant mitochondria and mitotic figures; some rosettes have a central plexus made up of large, undifferentiated processes, with other rosettes having a central plexus containing neurons and synapses
• areas of the plexus within the posterior chamber are composed of neuron-like processes having synaptic structures similar to horizontal/amacrine cells; this is seen in extensive plexus areas of tumors

neoplasm
• retinoblastoma cells that express amacrine/horizontal cell markers also extend processes and form synapses; some of these Golgi-Cox-labeled cells extend 1-3 long main processes with further neurite branching characteristic of horizontal or wide-field amacrine cells, while more (nearly half of ) labeled cells extend a main process with extensive neurite outgrowth characteristic of amacrine cells, and the remaining cells are less differentiated with short, unbranched neurites
• these labeled cells are mainly found near the tumor origin, while fewer are present toward the lens and anterior chamber

cellular
• a substantial proportion of tumor cells expressing amacrine/horizontal cell markers are proliferating as shown by labeled thymidine incorporation




Genotype
MGI:3831341
cn38
Allelic
Composition
Brca2tm1Brn/Brca2tm1Brn
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca2tm1Brn mutation (3 available); any Brca2 mutation (33 available)
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 87% of mice develop medulloblastoma beginning at 13 weeks

neoplasm
• 87% of mice develop medulloblastoma beginning at 13 weeks

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
medulloblastoma DOID:0050902 OMIM:155255
J:144617




Genotype
MGI:3710323
cn39
Allelic
Composition
Trp53tm1Brn/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Brn mutation (13 available); any Trp53 mutation (149 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 2/5 (40%) of mice receiving 4 Gy radiation at P5 develop cerebellar tumors by 5 months of age

neoplasm
• 2/5 (40%) of mice receiving 4 Gy radiation at P5 develop cerebellar tumors by 5 months of age




Genotype
MGI:3698834
cn40
Allelic
Composition
Ddb1tm1Spg/Ddb1tm1Spg
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ddb1tm1Spg mutation (0 available); any Ddb1 mutation (9 available)
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants do not survive for more than a day

nervous system
• ventricular zone (VZ) and subventricular zone (SVZ) are irregularly enlarged with many abnormal cells; cells show high frequency of mitotic figures, apoptosis and irregularly shaped nuclei

vision/eye
• loss of lens epithelium cells is rescued compared to Ddb1tm1Spg;Tg(Nes-cre)1Kln mice; however, cells have abnormally large or small nuclei with irregular shapes and sporadic apoptosis




Genotype
MGI:3831340
cn41
Allelic
Composition
Brca2tm1Brn/Brca2tm1Brn
Trp53tm1Tyj/Trp53+
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca2tm1Brn mutation (3 available); any Brca2 mutation (33 available)
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 72% of mice develop medulloblastoma beginning at 21 weeks

neoplasm
• tumors exhibit a loss of heterozygosity at the Trp53 gene
• 72% of mice develop medulloblastoma beginning at 21 weeks

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
medulloblastoma DOID:0050902 OMIM:155255
J:144617




Genotype
MGI:5907135
cn42
Allelic
Composition
Mdm4tm2Glo/Mdm4tm2.1Glo
Tg(Myh6-cre)2182Mds/0
Trp53tm1Tyj/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S/Sv * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mdm4tm2.1Glo mutation (0 available); any Mdm4 mutation (155 available)
Mdm4tm2Glo mutation (1 available); any Mdm4 mutation (155 available)
Tg(Myh6-cre)2182Mds mutation (3 available)
Trp53tm1Brn mutation (13 available); any Trp53 mutation (149 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice show an extended mean survival of 403 days compared to compound heterozygous Mdm4tm2Glo/Mdm4tm2.1Glo conditional mutants
• mice die due to tumors not heart failure

cardiovascular system
N
• mice do not exhibit signs of heart failure such as edema and poor breathing and exhibit rescue of the dilated cardiomyopathy

neoplasm




Genotype
MGI:4840094
cn43
Allelic
Composition
Nf1tm1Par/Nf1+
Ptentm1Hwu/Pten+
Trp53tm1Tyj/Trp53+
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S1/Sv * 129S2/SvPas * 129S4/SvJae * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf1tm1Par mutation (4 available); any Nf1 mutation (22 available)
Ptentm1Hwu mutation (3 available); any Pten mutation (39 available)
Tg(GFAP-cre)25Mes mutation (2 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most die as early as 10 weeks of age, and usually within a week of showing signs of morbidity

behavior/neurological
• exaggerated startle response
• ataxic gait
• generalized motor seizures

nervous system
• generalized motor seizures
• gliomas from asymptomatic mutants are primarily classified as grade 3 astocytomas
• 5-fold higher growth rate of astrocytomas compared with tumors from transgenic mice heterozygous for Nf1tm1Par and Trp53tm1Tyj and hemizygous for Tg(GFAP-cre)25Mes

neoplasm
• gliomas from asymptomatic mutants are primarily classified as grade 3 astocytomas
• 5-fold higher growth rate of astrocytomas compared with tumors from transgenic mice heterozygous for Nf1tm1Par and Trp53tm1Tyj and hemizygous for Tg(GFAP-cre)25Mes

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
astrocytoma DOID:3069 J:134611




Genotype
MGI:5569005
cn44
Allelic
Composition
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(tetO-Kras2)12Hev/0
Trp53tm1Tyj/Trp53+
Genetic
Background
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (2 available); any Gt(ROSA)26Sor mutation (492 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (14 available)
Tg(tetO-Kras2)12Hev mutation (1 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mice develop invasive adenocarcinoma between 8 and 18 weeks after dox treatment, with some cases showing hemorrhagic ascites, with admixed poorly differentiated and well-differentiated areas and duodenal invasion
• mice in which dox is removed recover their health and show pancreatic tumor regression resulting in a small pancreatic remnant
• adult mice treated with dox 72 hours prior to injection with cholecystokinin analog cerulein to induce acute pancreatitis develop PanINs, dilated ducts with the presence of intracellular mucins, and extensive fibroinflammatory stroma

mortality/aging
• mice die between 8 and 18 weeks after doxycycline (dox) treatment to induce Kras2 expression due to pancreatic ductal adenocarinoma

neoplasm
• mice develop invasive adenocarcinoma between 8 and 18 weeks after dox treatment, with some cases showing hemorrhagic ascites, with admixed poorly differentiated and well-differentiated areas and duodenal invasion
• mice in which dox is removed recover their health and show pancreatic tumor regression resulting in a small pancreatic remnant
• adult mice treated with dox 72 hours prior to injection with cholecystokinin analog cerulein to induce acute pancreatitis develop PanINs, dilated ducts with the presence of intracellular mucins, and extensive fibroinflammatory stroma

homeostasis/metabolism
• adult mice treated with dox for 5 weeks prior to injection with cholecystokinin analog cerulein to induce acute pancreatitis exhibit a small, translucent remnant of pancreatic tissue, without fibrosis or PanIN lesions
• when dox is removed after pancreatitis induction, mice show show normal acini interspersed with dilated ducts and acinar-ductal metaplasia, fibrosis and occasional lipomatosis, but with minimal inflammatory infiltrate, and reduced proliferation

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:184378




Genotype
MGI:4840090
cn45
Allelic
Composition
Nf1tm1Par/Nf1+
Trp53tm1Tyj/Trp53+
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf1tm1Par mutation (4 available); any Nf1 mutation (22 available)
Tg(GFAP-cre)25Mes mutation (2 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• complete penetrance of malignant astrocytomas
• gliomas from asymptomatic mutants are primarily classified as grade 2 astocytomas
• neurospheres from mutant astrocytomas exhibit loss of heterozygosity at both Nf1 and Trp53 loci

mortality/aging
• mutants survive up to 8 weeks beyond initial appearance of symptoms

neoplasm
• complete penetrance of malignant astrocytomas
• gliomas from asymptomatic mutants are primarily classified as grade 2 astocytomas
• neurospheres from mutant astrocytomas exhibit loss of heterozygosity at both Nf1 and Trp53 loci

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
astrocytoma DOID:3069 J:134611




Genotype
MGI:3831351
cn46
Allelic
Composition
Lig4tm1Pmc/Lig4tm1Pmc
Trp53tm1Tyj/Trp53tm1Tyj
Xrcc2tm2Pmc/Xrcc2tm2Pmc
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lig4tm1Pmc mutation (0 available); any Lig4 mutation (10 available)
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
Xrcc2tm2Pmc mutation (0 available); any Xrcc2 mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 100% of mice develop medulloblastoma beginning at 14 weeks

mortality/aging
• mice die by 16 weeks

neoplasm
• 100% of mice develop medulloblastoma beginning at 14 weeks




Genotype
MGI:3831338
cn47
Allelic
Composition
Trp53tm1Tyj/Trp53tm1Tyj
Xrcc2tm2Pmc/Xrcc2tm2Pmc
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
Xrcc2tm2Pmc mutation (0 available); any Xrcc2 mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 100% of mice develop medulloblastoma beginning at 16 weeks

mortality/aging
• mice die by 28 weeks unlike Xrcc2tm2Pmc/Xrcc2tm2Pmc Tg(Nes-cre)1Kln mice with wild-type Trp53

neoplasm
• 100% of mice develop medulloblastoma beginning at 16 weeks




Genotype
MGI:3831348
cn48
Allelic
Composition
Lig4tm1Pmc/Lig4tm1Pmc
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lig4tm1Pmc mutation (0 available); any Lig4 mutation (10 available)
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 94% of mice develop medulloblastoma beginning at 16 weeks

mortality/aging
• mice die by 32 weeks unlike Lig4tm1Pmc/Lig4tm1Pmc Tg(Nes-cre)1Kln mice with wild-type Trp53

neoplasm
• 94% of mice develop medulloblastoma beginning at 16 weeks




Genotype
MGI:3831355
cn49
Allelic
Composition
Lig4tm1Pmc/Lig4tm1Pmc
Trp53tm1Tyj/Trp53+
Xrcc2tm2Pmc/Xrcc2tm2Pmc
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lig4tm1Pmc mutation (0 available); any Lig4 mutation (10 available)
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
Xrcc2tm2Pmc mutation (0 available); any Xrcc2 mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 75% of mice develop medulloblastoma beginning at 23 weeks

mortality/aging
• mice die by 32 weeks

neoplasm
• tumors exhibit a loss of heterozygosity at the Trp53 gene
• 75% of mice develop medulloblastoma beginning at 23 weeks




Genotype
MGI:4359666
cn50
Allelic
Composition
Xrcc1tm1Pmc/Xrcc1tm1Pmc
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
Xrcc1tm1Pmc mutation (0 available); any Xrcc1 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die by 4 months of age

nervous system
N
• loss of interneurons in the molecular layer of the cerebellum observed in Xrcc1tm1.1Pmc/Xrcc1tm1.1Pmc Tg(Nes-cre)1Kln is rescued with normal distribution of basket and stellate cells
• Golgi cells are only partially rescued compared to in Xrcc1tm1.1Pmc/Xrcc1tm1.1Pmc Tg(Nes-cre)1Kln

neoplasm

cellular
• Golgi cells are only partially rescued compared to in Xrcc1tm1.1Pmc/Xrcc1tm1.1Pmc Tg(Nes-cre)1Kln




Genotype
MGI:4359665
cn51
Allelic
Composition
Xrcc1tm1Pmc/Xrcc1tm1Pmc
Trp53tm1Tyj/Trp53+
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
Xrcc1tm1Pmc mutation (0 available); any Xrcc1 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system

mortality/aging
• mice die by 6 months of age

neoplasm




Genotype
MGI:5305073
cn52
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT2)Tyj/Gt(ROSA)26Sor+
Tacc3tm1.1Tno/Tacc3tm1.2Tno
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT2)Tyj mutation (3 available); any Gt(ROSA)26Sor mutation (492 available)
Tacc3tm1.1Tno mutation (0 available); any Tacc3 mutation (11 available)
Tacc3tm1.2Tno mutation (0 available); any Tacc3 mutation (11 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• in the absence of 4OHT, mutants develop thymic lymphoma tumors

neoplasm
• in the absence of 4OHT, mutants develop thymic lymphoma tumors
• administration of 4-hydroxytamoxifen (4OHT) to induce Cre recombination results in regression of autochthonous thymic lymphoma, with a reduction in tumor volume to 96% and 26% of original volume, over 3 and 10 days, respectively
• regression of tumors is due to apoptosis in thymic lymphoma
• 4OHT treatment of mutants results in massive apoptosis in thymic lymphomas but not in normal thymic tissue or other tissues
• lymphoma cells contain multi-polar spindles, indicating aberrant spindle formation, resulting in mitotic arrest and rapid cell death




Genotype
MGI:5305074
cn53
Allelic
Composition
Gt(ROSA)26Sortm1(cre/ERT2)Tyj/Gt(ROSA)26Sor+
Tacc3tm1.1Tno/Tacc3+
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT2)Tyj mutation (3 available); any Gt(ROSA)26Sor mutation (492 available)
Tacc3tm1.1Tno mutation (0 available); any Tacc3 mutation (11 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• administration of 4-hydroxytamoxifen (4OHT) to induce Cre recombination results in a rapid increase in tumor volume

neoplasm
• administration of 4-hydroxytamoxifen (4OHT) to induce Cre recombination results in a rapid increase in tumor volume




Genotype
MGI:4836239
cn54
Allelic
Composition
Ptentm1Hwu/Ptentm1Hwu
Tg(Pdx1-cre)89.1Dam/0
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Hwu mutation (3 available); any Pten mutation (39 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• 1 of 5 mutants develop a small acinar carcinoma
• 2 of 5 mutants develop papillary adenocarcionomas at 4 and 6 months of age

neoplasm
• 1 of 5 mutants develop a small acinar carcinoma
• 2 of 5 mutants develop papillary adenocarcionomas at 4 and 6 months of age




Genotype
MGI:3783529
cn55
Allelic
Composition
Rb1tm3Tyj/Rb1tm3Tyj
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Atp/0
Genetic
Background
involves: 129S2/SvPas * 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rb1tm3Tyj mutation (10 available); any Rb1 mutation (80 available)
Tg(Nes-cre)1Atp mutation (0 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mice with mosaic cre expression with maternal inheritance of Tg(Nes-cre)1Mrt exhibit pituitary tumors

mortality/aging
• mice with mosaic cre expression due to maternal inheritance of Tg(Nes-cre)1Mrt exhibit an average lifespan of 92+/-15 days and are moribund with pituitary tumors when euthanized

vision/eye
• retinal apoptosis levels are higher than in wild-type and Rb1tm3Tyj/Rb1tm3Tyj Tg(Nes-cre)1Mrt mice
• dysplasia in both eyes
• mice with mosaic cre expression due to maternal inheritance of Tg(Nes-cre)1Mrt exhibit focal retinal dysplasia
• in mice with mosaic cre expression when Tg(Nes-cre)1Mrt is maternally inherited

neoplasm
• mice with mosaic cre expression with maternal inheritance of Tg(Nes-cre)1Mrt exhibit pituitary tumors

nervous system
• mice with mosaic cre expression with maternal inheritance of Tg(Nes-cre)1Mrt exhibit pituitary tumors

cellular
• retinal apoptosis levels are higher than in wild-type and Rb1tm3Tyj/Rb1tm3Tyj Tg(Nes-cre)1Mrt mice




Genotype
MGI:3849178
cn56
Allelic
Composition
Trp53tm1Elee/Trp53tm1Tyj
Tg(GFAP-cre)25Mes/0
Genetic
Background
involves: 129S2/SvPas * 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(GFAP-cre)25Mes mutation (2 available)
Trp53tm1Elee mutation (0 available); any Trp53 mutation (149 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice die prior to 500 days

behavior/neurological
• 85% of mice
• 85% of mice
• 85% of mice
• 85% of mice

neoplasm
• 90% of mice develop medulloblastomas
• mice develop tumors outside of the central nervous system consisting of soft-tissue sarcomas
• 90% of mice develop malignant gliomas with astrocytic characteristics
• 40% of high-grade astrocytic gliomas exhibit necrosis, pseudopalisading tumors cells, high degree of nuclear atypia, and microvascular proliferation similar to human glioblastoma multiforme
• tumors are relatively heterogeneous histological and in lineage marker expression

nervous system
N
• at 2 months of age, brain cells in the subventricular zone and progenitor cells exhibit normal growth rates
• 85% of mice
• 90% of mice develop medulloblastomas
• 90% of mice develop malignant gliomas with astrocytic characteristics
• 40% of high-grade astrocytic gliomas exhibit necrosis, pseudopalisading tumors cells, high degree of nuclear atypia, and microvascular proliferation similar to human glioblastoma multiforme
• tumors are relatively heterogeneous histological and in lineage marker expression
• in mice with neurological defects

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
glioblastoma multiforme DOID:3068 J:149662




Genotype
MGI:5907132
cn57
Allelic
Composition
Mdm4tm2Glo/Mdm4tm2.1Glo
Tg(Myh6-cre)2182Mds/0
Trp53tm1Tyj/Trp53+
Genetic
Background
involves: 129S2/SvPas * 129S4/SvJaeSor * 129S7/SvEvBrd * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mdm4tm2.1Glo mutation (0 available); any Mdm4 mutation (155 available)
Mdm4tm2Glo mutation (1 available); any Mdm4 mutation (155 available)
Tg(Myh6-cre)2182Mds mutation (3 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice show an extended median survival of 274 days compared to compound heterozygous Mdm4tm2Glo/Mdm4tm2.1Glo conditional mutants




Genotype
MGI:5526849
cn58
Allelic
Composition
Trp53tm1Tyj/Trp53tm1Tyj
Usp7tm2Wgu/Usp7tm2Wgu
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
Usp7tm2Wgu mutation (0 available); any Usp7 mutation (58 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

nervous system
N
• mice exhibit normal forebrain, midbrain and cerebellum size, cerebellum thickness and neural cell density
• in some mice

embryo
• in some mice




Genotype
MGI:3616710
cn59
Allelic
Composition
Mdm2tm1Glo/Mdm2tm2.1Glo
Tg(Myh6-cre)2182Mds/0
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129S2/SvPas * 129S7/SvEvBrd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mdm2tm1Glo mutation (0 available); any Mdm2 mutation (25 available)
Mdm2tm2.1Glo mutation (1 available); any Mdm2 mutation (25 available)
Tg(Myh6-cre)2182Mds mutation (3 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
N
• exhibit rescue of the heart lethality seen in conditional Mdm2 mice and have the same life span as single homozygous Trp53 mice




Genotype
MGI:5317026
cn60
Allelic
Composition
Tg(Atoh1-sb11)1Mtay/0
TgTn(sb-T2/Onc3)12740Njen/0
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129S2/SvPas * C3H * C57BL/6J * ICR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Atoh1-sb11)1Mtay mutation (0 available)
TgTn(sb-T2/Onc3)12740Njen mutation (1 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• in some mice with large cells, nuclear atypia and nuclear moulding typical of large cell/anaplastic histology

neoplasm
• in some mice with large cells, nuclear atypia and nuclear moulding typical of large cell/anaplastic histology




Genotype
MGI:3767597
cn61
Allelic
Composition
Fbxw7tm1Kei/Fbxw7tm1Kei
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Lck-cre)1Cwi/?
Genetic
Background
involves: 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fbxw7tm1Kei mutation (1 available); any Fbxw7 mutation (38 available)
Tg(Lck-cre)1Cwi mutation (2 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (149 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice develop double positive lymphomas at increased frequency and decreased latency compared to Fbxw7tm1Kei/Fbxw7tm1Kei Tg(Lck-cre)1Cwi mice
• at 8 weeks of age 2 mice develop thymic lymphoma

endocrine/exocrine glands
• at 8 weeks of age 2 mice develop thymic lymphoma

immune system
N
• unlike in Fbxw7tm1Kei/Fbxw7tm1Kei Tg(Lck-cre)1Cwi mice, T cells do not arrest in S phase or undergo increased apoptosis




Genotype
MGI:5292118
cn62
Allelic
Composition
Tg(EIIa-cre)C5379Lmgd/0
Tg(Rnu6-RNAi:Bccip)4Zshn/0
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(EIIa-cre)C5379Lmgd mutation (4 available)
Tg(Rnu6-RNAi:Bccip)4Zshn mutation (0 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (