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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Nes-cre)1Kln
transgene insertion 1, Rudiger Klein
MGI:2176173
Summary 291 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Ccm2tm1Etl/Ccm2tm1Etl
Tg(Nes-cre)1Kln/?
B6.Cg-Ccm2tm1Etl Tg(Nes-cre)1Kln MGI:3837691
cn2
Foxa2tm1.1Stf/Foxa2tm1.1Stf
Tg(Nes-cre)1Kln/0
B6.Cg-Foxa2tm1.1Stf Tg(Nes-cre)1Kln MGI:4417949
cn3
Kalrntm2Npl/Kalrntm2Npl
Tg(Nes-cre)1Kln/0
B6.Cg-Kalrntm2Npl Tg(Nes-cre)1Kln MGI:5551312
cn4
Mc3rtm1Butl/Mc3rtm1Butl
Tg(Nes-cre)1Kln/0
B6.Cg-Mc3rtm1Butl Tg(Nes-Cre)1Kln MGI:5302397
cn5
Myd88tm1Jcbr/Myd88tm1Jcbr
Tg(Nes-cre)1Kln/0
B6.Cg-Myd88tm1Jcbr Tg(Nes-cre)1Kln MGI:4367075
cn6
Prmt5tm2c(EUCOMM)Wtsi/Prmt5tm2c(EUCOMM)Wtsi
Tg(Nes-cre)1Kln/0
B6.Cg-Prmt5tm2c(EUCOMM)Wtsi Tg(Nes-cre)1Kln MGI:5546601
cn7
Slc1a2tm1.1Ncd/Slc1a2tm1.1Ncd
Tg(Nes-cre)1Kln/0
B6.Cg-Slc1a2tm1.1Ncd Tg(Nes-cre)1Kln MGI:5576464
cn8
Slc6a12tm1.1Ncd/Slc6a12tm1.1Ncd
Tg(Nes-cre)1Kln/0
B6.Cg-Slc6a12tm1.1Ncd Tg(Nes-cre)1Kln MGI:5306259
cn9
Ndufs4tm1Rpa/Ndufs4tm1Rpa
Tg(Nes-cre)1Kln/0
B6.Cg-Tg(Nes-cre)1Kln Ndufs4tm1Rpa MGI:5451025
cn10
Tg(ACTB-NOTCH1)1Shn/0
Tg(Nes-cre)1Kln/0
B6.Cg-Tg(Nes-cre)1Kln Tg(ACTB-NOTCH1)1Shn MGI:3044595
cn11
Uba6tm1Whpr/Uba6tm1Whpr
Tg(Nes-cre)1Kln/0
B6.Cg-Uba6tm1Whpr Tg(Nes-cre)1Kln MGI:5511126
cn12
Tg(CAG-Ppard*E411P)#Als/0
Tg(Nes-cre)1Kln/0
B6J.Cg-Tg(Nes-cre)1Kln Tg(CAG-Ppard*E411P)#Als MGI:5897176
cn13
Abcb7tm1Mdf/Y
Tg(Nes-cre)1Kln/0
either: B6.Cg-Tg(Nes-cre)1Kln Abcb7tm1Mdf or (involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * SJL) MGI:3629065
cn14
Rai1tm2.1Luo/Rai1+
Tg(Nes-cre)1Kln/?
either: (involves: 129S1/Sv * C57BL/6 * SJL) or (involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL) MGI:5817609
cn15
Rai1tm2.2Luo/Rai1tm2.1Luo
Tg(Nes-cre)1Kln/?
either: (involves: 129S1/Sv * C57BL/6 * SJL) or (involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL) MGI:5817614
cn16
Rai1tm2.1Luo/Rai1tm2.1Luo
Tg(Nes-cre)1Kln/?
either: (involves: 129S1/Sv * C57BL/6 * SJL) or (involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL) MGI:5817471
cn17
Sox2tm2Skn/Sox2tm4.1Skn
Tg(Nes-cre)1Kln/0
either: (involves: 129S/Sv * C57BL/6 * SJL) or (involves: 129S/Sv * C57BL/6 * DBA/2 * SJL) MGI:4398746
cn18
Stat5atm2Mam/Stat5atm2Mam
Stat5btm1Mam/Stat5btm1Mam
Tg(Nes-cre)1Kln/0
involves: 129 * 129S6/SvEvTac * C57BL/6 * SJL MGI:4840275
cn19
Stat5btm1Mam/Stat5btm1Mam
Tg(Nes-cre)1Kln/0
involves: 129 * 129S6/SvEvTac * C57BL/6 * SJL MGI:4840276
cn20
Cfl1tm1.1Wit/Cfl1+
Dstntm1.1Wit/Dstntm1.1Wit
Tg(Nes-cre)1Kln/0
involves: 129 * BALB/cJ * C57BL/6 * SJL MGI:4943294
cn21
Socs3tm1Ayos/Socs3tm1Ayos
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 MGI:3051638
cn22
Slc6a8tm1.1Lbar/Y
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * C57BL/6J * C57BL/6N * SJL MGI:5825029
cn23
Abl1tm2.1Goff/Abl1tm2.1Goff
Abl2tm1Ajk/Abl2tm1Ajk
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * C57BL/6J * SJL MGI:4850044
cn24
Tnfrsf11atm1.1Pngr/Tnfrsf11atm1.2Pngr
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * C57BL/6NTac * SJL MGI:4415816
cn25
Gnl3tm2.1Rylt/Gnl3tm2.1Rylt
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * CBA MGI:5523421
cn26
Ahi1tm1Jgg/Ahi1tm2.1Jgg
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * FVB/N * SJL MGI:4437796
cn27
Gt(ROSA)26Sortm1(SNCA*A53T)Djmo/Gt(ROSA)26Sor+
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:4353815
cn28
Tg(EEF1A1-SHC1*)1Ravi/0
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:3851591
cn29
Shc1tm1Ravi/Shc1tm1Ravi
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:3851590
cn30
Mycntm1Psk/Mycntm1Psk
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:3836814
cn31
Brca2tm1Brn/Brca2tm1Brn
Ptch1tm1Mps/Ptch1+
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:3831343
cn32
Brca2tm1Brn/Brca2tm1Brn
Ptch1tm1Mps/Ptch1+
Trp53tm1Tyj/Trp53+
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:3831342
cn33
Deaf1tm1.1Mico/Deaf1tm1.1Mico
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:5576197
cn34
Hsd17b4tm2Baes/Hsd17b4tm2Baes
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:5523950
cn35
Braftm2Urr/Braftm2Urr
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:5512711
cn36
Braftm2.1Urr/Braftm2.1Urr
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:5512710
cn37
Asic1tm1.1Ccli/Asic1tm1.1Ccli
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:5490900
cn38
Sp2tm1.1Htg/Sp2+
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:5471311
cn39
Sp2tm1.1Htg/Sp2tm1.1Htg
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:5471309
cn40
Ccdc88atm4.1Mat/Ccdc88a+
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:5449209
cn41
Ccdc88atm4.1Mat/Ccdc88atm4.1Mat
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:5449208
cn42
Pdcd10tm1Wami/Pdcd10tm1Wami
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:5002665
cn43
Fbxw7tm1.1Axbe/Fbxw7tm1.1Axbe
Notch1tm1Agt/Notch1+
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:4867645
cn44
Ahi1tm1Xjl/Ahi1tm1Xjl
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:4849288
cn45
Gt(ROSA)26Sortm2(SNCA*119)Djmo/Gt(ROSA)26Sor+
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * SJL MGI:4353817
cn46
Fostm7Wag/Fostm7Wag
Tg(Nes-cre)1Kln/?
involves: 129P2/OlaHsd MGI:2679378
cn47
Cdkn2ctm1Bbd/Cdkn2ctm1Bbd
Trp53tm1Brn/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL MGI:3710322
cn48
Mettm1Cpo/Mettm1Sst
Tg(Nes-cre)1Kln/?
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1 * SJL MGI:5052134
cn49
Braftm1Sva/Braftm1.1Sva
Raf1tm1Bacc/Raf1tm2Bacc
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3713581
cn50
Braftm1Wds/Braftm1.1Wds
Raf1tm1Bacc/Raf1tm2Bacc
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3713654
cn51
Mettm1Cpo/Mettm1Sst
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5285657
cn52
Pitx2tm1.1Dmm/Pitx2tm1.1Sac
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5308810
cn53
Braftm1Sva/Braftm1Sva
Raf1tm2Bacc/Raf1+
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3713555
cn54
Brca2tm1Brn/Brca2tm1Brn
Trp53tm1Tyj/Trp53+
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL MGI:3831340
cn55
Brca2tm1Brn/Brca2tm1Brn
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL MGI:3831341
cn56
Ddb1tm1Spg/Ddb1tm1Spg
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL MGI:3698834
cn57
Trp53tm1Brn/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL MGI:3710323
cn58
Atrtm2Bal/Atrtm2Bal
Cdkn2atm2Brn/Cdkn2atm2Brn
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL MGI:5316228
cn59
Itgavtm2Hyn/Itgavtm2.1Hyn
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB * SJL MGI:5306156
cn60
Ftotm1.1Pzg/Ftotm1.1Pzg
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * SJL MGI:4868751
cn61
Tbxa2rtm1Cof/Tbxa2rtm1.1Bhk
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S/SvEv * C57BL/6 * SJL MGI:5319079
cn62
Plectm4Gwi/Plectm4.1Gwi
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * BALB/cJ * C57BL/6 * SJL MGI:4414792
cn63
Gjc1tm1Kwi/Gjc1tm1Weil
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 MGI:3582061
cn64
Gjc1tm1Weil/Gjc1tm1Weil
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 MGI:3582060
cn65
Efnb2tm4Kln/Efnb2tm4Kln
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 MGI:3026784
cn66
Plxnb2tm1c(EUCOMM)Wtsi/Plxnb2tm1Matl
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * C57BL/6N * SJL MGI:5811236
cn67
Plxnb1tm1Matl/Plxnb1tm1Matl
Plxnb2tm1c(EUCOMM)Wtsi/Plxnb2tm1Matl
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * C57BL/6N * SJL MGI:5811146
cn68
Mapk8ip3tm1Ysok/Mapk8ip3tm1Ysok
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * SJL MGI:3818511
cn69
Tg(Nes-cre)1Kln/0
Zfp568tm1Ckjs/Zfp568tm1Ckjs
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * SJL MGI:5466414
cn70
Dab1tm1.1Mull/Dab1tm1.1Mull
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * SJL MGI:5141431
cn71
Cdc42tm1.1Rac/Cdc42tm1.1Rac
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N * SJL MGI:5495326
cn72
Pdha1tm1Ptl/Pdha1tm1Ptl
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N * SJL MGI:3843824
cn73
Pdha1tm1Ptl/Y
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * FVB/N * SJL MGI:3843822
cn74
Nr3c1tm2Gsc/Nr3c1tm2Gsc
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6J * SJL MGI:2176972
cn75
Ugcgtm1Hjg/Ugcgtm1.1Hjg
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3604768
cn76
Mecp2tm1Bird/Y
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3624719
cn77
Ddb1tm1Spg/Ddb1tm1Spg
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3698831
cn78
Braftm1Wds/Braftm1.1Wds
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3713535
cn79
Braftm1Wds/Braftm1Wds
Raf1tm2Bacc/Raf1+
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3713536
cn80
Braftm1Wds/Braf+
Raf1tm2Bacc/Raf1tm2Bacc
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3713540
cn81
Braftm1Sva/Braf+
Raf1tm2Bacc/Raf1tm2Bacc
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3713653
cn82
Dbx1tm1(DTA)Apie/Dbx1+
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3770261
cn83
Txnrd1tm1Marc/Txnrd1tm1Marc
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3778634
cn84
Txnrd2tm1Marc/Txnrd2tm1Marc
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3778635
cn85
Brca2tm1Brn/Brca2tm1Brn
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3831339
cn86
Nrg1tm1Fej/Nrg1tm1Fej
Tg(Nes-cre)1Kln/?
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3835561
cn87
Nr3c1tm2Gsc/Nr3c1tm2Gsc
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3852117
cn88
Nf2tm2Gth/Nf2tm2Gth
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:4819847
cn89
Adam10tm2Psa/Adam10tm2Psa
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:4838242
cn90
Fbxw7tm1.1Axbe/Fbxw7tm1.1Axbe
Juntm4Wag/Jun+
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:4867644
cn91
Mettm1Ics/Mettm1Sst
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:5285658
cn92
Juntm4Wag/Juntm4Wag
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:5294554
cn93
Gjc1tm1.1(Gjd2)Kwi/Gjc1tm1.1(Gjd2)Kwi
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:5317173
cn94
Map2k1tm1Bacc/Map2k1tm1.1Bacc
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:5504405
cn95
Adktm2Bois/Adktm2Bois
Adora1tm1Bbf/Adora1tm1Bbf
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:5816716
cn96
Xrcc1tm1Pmc/Xrcc1tm1Pmc
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL MGI:4359666
cn97
Lig4tm1Pmc/Lig4tm1Pmc
Trp53tm1Tyj/Trp53+
Xrcc2tm2Pmc/Xrcc2tm2Pmc
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL MGI:3831355
cn98
Trp53tm1Tyj/Trp53tm1Tyj
Xrcc2tm2Pmc/Xrcc2tm2Pmc
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL MGI:3831338
cn99
Lig4tm1Pmc/Lig4tm1Pmc
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL MGI:3831348
cn100
Lig4tm1Pmc/Lig4tm1Pmc
Trp53tm1Tyj/Trp53tm1Tyj
Xrcc2tm2Pmc/Xrcc2tm2Pmc
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL MGI:3831351
cn101
Xrcc1tm1Pmc/Xrcc1tm1Pmc
Trp53tm1Tyj/Trp53+
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 * SJL MGI:4359665
cn102
Actbtm1(INSR)Dac/Actbtm1(INSR)Dac
Insrtm1Dac/Insrtm1Dac
Tg(Nes-cre)1Kln/?
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * SJL MGI:4831154
cn103
Tg(Nes-cre)1Kln/0
Tor1atm1Wtd/Tor1atm3.1Wtd
involves: 129S1/Sv * 129S6/SvEvTac * C57BL/6J * SJL MGI:5605973
cn104
Tg(Nes-cre)1Kln/0
Tor1atm2Wtd/Tor1atm3.1Wtd
involves: 129S1/Sv * 129S6/SvEvTac * C57BL/6J * SJL MGI:5605976
cn105
Vegfatm2Gne/Vegfatm2.1Nagy
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1 * SJL MGI:4422207
cn106
Vegfatm2Gne/Vegfa+
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CD-1 * SJL MGI:4422199
cn107
Lhx1tm4Bhr/Lhx1tm4Bhr
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3719686
cn108
Tg(Nes-cre)1Kln/0
Wnt7atm1Amc/Wnt7atm1Amc
Wnt7btm1Parr/Wnt7btm2Amc
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3831188
cn109
Irs2tm2Mfw/Irs2tm2Mfw
Irs4tm1.1Mfw/Y
Tg(Nes-cre)1Kln/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5705238
cn110
Irs2tm2Mfw/Irs2tm2Mfw
Tg(Nes-cre)1Kln/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5705240
cn111
Shhtm2Amc/Shhtm2Amc
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3617985
cn112
Ei24tm1Hzha/Ei24tm1Hzha
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5475097
cn113
Dag1tm2Kcam/Dag1tm2Kcam
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:4440460
cn114
Gt(ROSA)26Sortm1(Actb-Met)Fmai/?
Tg(Nes-cre)1Kln/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5052135
cn115
Gbatm1Karl/Gbatm1Karl
Tg(Nes-cre)1Kln/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3764516
cn116
Braftm1Sva/Braftm1.1Sva
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3713552
cn117
Edn2tm1.1Nat/Edn2tm1.1Nat
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5519893
cn118
Kdrtm1Wag/Kdrtm1Wag
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:4422209
cn119
Lhx1tm1Tmj/Lhx1tm4Bhr
Lhx5tm1Lmgd/Lhx5tm1Lmgd
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3719689
cn120
Nlgn3tm4.1Sud/Y
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5660861
cn121
Hsd11b1tm1.2Awhi/Hsd11b1tm1.2Awhi
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5566781
cn122
Gt(ROSA)26Sortm1(HD*103Q)Xwy/?
Tg(Nes-cre)1Kln/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3584455
cn123
Smotm1Amc/Smotm2Amc
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL * Swiss Webster MGI:3665560
cn124
Xrcc1tm1Pmc/Xrcc1tm1Pmc
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * C57BL/6 * SJL MGI:4359667
cn125
Smarcb1tm2Sho/Smarcb1tm2Sho
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * C57BL/6 * SJL MGI:5771799
cn126
Smarcb1tm2Sho/Smarcb1+
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * C57BL/6 * SJL MGI:5771800
cn127
Pnkptm1.1Pmc/Pnkptm1.1Pmc
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * C57BL/6 * SJL MGI:5795748
cn128
Atmtm2Pmc/Atmtm2Pmc
Pnkptm1.1Pmc/Pnkptm1.1Pmc
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * C57BL/6 * SJL MGI:5795758
cn129
Xrcc2tm2Pmc/Xrcc2tm2Pmc
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * C57BL/6 * SJL MGI:3831335
cn130
Lig4tm1Pmc/Lig4tm1Pmc
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * C57BL/6 * SJL MGI:3831346
cn131
Xrcc1tm1Pmc/Xrcc1tm1Pmc
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * FVB/N MGI:4946938
cn132
Lig4tm1Pmc/Lig4tm1Pmc
Mre11atm1Jpt/Mre11atm1Jpt
Tg(Nes-cre)1Kln/0
involves: 129S1/SvImJ * 129S7/SvEvBrd * C57BL/6 * SJL MGI:3831179
cn133
Lig4tm1Pmc/Lig4tm1Pmc
Nbntm1Jpt/Nbntm1Jpt
Tg(Nes-cre)1Kln/0
involves: 129S1/SvImJ * 129S7/SvEvBrd * C57BL/6 * SJL MGI:3831185
cn134
Lig4tm1Pmc/Lig4tm1Pmc
Tg(Nes-cre)1Kln/0
involves: 129S1/SvImJ * C57BL/6 * SJL MGI:3831178
cn135
Atmtm1Pmc/Atmtm1Pmc
Lig4tm1Pmc/Lig4tm1Pmc
Tg(Nes-cre)1Kln/0
involves: 129S1/SvImJ * C57BL/6 * SJL MGI:3831182
cn136
Rbfox1tm1.1Dblk/Rbfox1tm1.1Dblk
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * 129S4/SvJaeSor * C57BL/6 * C57BL/6J * SJL MGI:5291908
cn137
Rbfox1tm1.1Dblk/Rbfox1+
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * 129S4/SvJaeSor * C57BL/6 * C57BL/6J * SJL MGI:5291909
cn138
Ext1tm1Yama/Ext1+
Slit2tm1Matl/Slit2tm1Matl
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * 129S5/SvEvBrd * C57BL/6 * SJL MGI:2682063
cn139
Trp53tm1Tyj/Trp53tm1Tyj
Usp7tm2Wgu/Usp7tm2Wgu
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * 129S6/SvEvTac * C57BL/6 * SJL MGI:5526849
cn140
Rbfox2tm1.1Dblk/Rbfox2tm1.1Dblk
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * C57BL/6 * C57BL/6J * SJL MGI:5291910
cn141
Rbfox1tm1.1Dblk/Rbfox1tm1.1Dblk
Rbfox2tm1.1Dblk/Rbfox2tm1.1Dblk
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * C57BL/6 * C57BL/6J * SJL MGI:5318255
cn142
Rbfox1tm1.1Dblk/Rbfox1+
Rbfox2tm1.1Dblk/Rbfox2tm1.1Dblk
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * C57BL/6 * C57BL/6J * SJL MGI:5318256
cn143
Crhr1tm2Wrst/Crhr1tm2Wrst
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * C57BL/6 * C57BL/6J * SJL MGI:5294457
cn144
Mbd5tm1.1Gxu/Mbd5tm1.1Gxu
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * C57BL/6 * C57BL/6J * SJL MGI:5466593
cn145
Pkd1tm2.2Bol/Pkd1tm3.1Bol
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * C57BL/6 * C57BL/6NTac * SJL MGI:4366028
cn146
Tg(ACTB-NOTCH1)1Shn/0
Tg(Nes-cre)1Kln/0
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129S2/SvPas * C57BL/6J MGI:3044601
cn147
Tg(ACTB-NOTCH1)1Shn/0
Tg(Nes-cre)1Kln/0
Trp53tm1Tyj/Trp53+
involves: 129S2/SvPas * C57BL/6J MGI:3044602
cn148
Atrtm2Bal/Atrtm2Bal
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * C57BL/6 * SJL MGI:5316221
cn149
Ccne1tm3.1Pisc/Ccne1tm3.1Pisc
Ccne2tm1Pisc/Ccne2tm1Pisc
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * C57BL/6 * SJL MGI:5304330
cn150
Atrtm2Bal/Atrtm2Bal
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * C57BL/6 * SJL MGI:5316227
cn151
Atmtm2Pmc/Atmtm2Pmc
Atrtm2Bal/Atrtm2Bal
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * C57BL/6 * SJL MGI:5316230
cn152
Ntrk2tm2Kln/Ntrk2tm2Kln
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * C57BL/6 * SJL MGI:4840349
cn153
Gja1tm8Kwi/Gja1+
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * C57BL/6 * SJL MGI:3807708
cn154
Ptbp2tm1.1Dblk/Ptbp2tm1.1Dblk
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * C57BL/6 * SJL MGI:5608593
cn155
Gt(ROSA)26Sortm1(Crh)Jde/Gt(ROSA)26Sortm1(Crh)Jde
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * C57BL/6 * SJL MGI:3815323
cn156
Ptpn1tm2Bbk/Ptpn1tm2Bbk
Ptpn2tm1.1Ttig/Ptpn2tm1.1Ttig
Tg(Nes-cre)1Kln/0
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL MGI:5304839
cn157
Insrtm1Khn/Insrtm1Khn
Tg(Nes-cre)1Kln/0
involves: 129S4/SvJae * C57BL/6J * SJL MGI:3583775
cn158
Akt1tm2Mbb/Akt1tm2Mbb
Tg(Nes-cre)1Kln/0
involves: 129S4/SvJae * C57BL/6J * SJL MGI:5317892
cn159
Ptger3tm1Csml/Ptger3tm1Csml
Tg(Nes-cre)1Kln/?
involves: 129S4/SvJae * C57BL/6 * SJL MGI:3764896
cn160
Gt(ROSA)26Sortm1(Kcnj11*V59M)Fmas/Gt(ROSA)26Sor+
Tg(Nes-cre)1Kln/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:4819394
cn161
Insrtm1Khn/Insrtm1Khn
Tg(Nes-cre)1Kln/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:3629045
cn162
Mapk8tm1Jcbr/Mapk8tm1Jcbr
Tg(Nes-cre)1Kln/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:4441341
cn163
Adktm2Bois/Adktm2Bois
Adora2atm1Jfc/Adora2atm1Jfc
Tg(Nes-cre)1Kln/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:5816717
cn164
Drd2tm1.1Mrub/Drd2tm1.1Mrub
Tg(Nes-cre)1Kln/?
involves: 129S4/SvJae * C57BL/6 * SJL MGI:5471750
cn165
Ptpn1tm2Bbk/Ptpn1tm2Bbk
Tg(Nes-cre)1Kln/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:3664097
cn166
Ptpn1tm2Bbk/Ptpn1+
Tg(Nes-cre)1Kln/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:3664098
cn167
Mc4rtm1Lowl/Mc4rtm1Lowl
Tg(Nes-cre)1Kln/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:3692537
cn168
Vps18tm1.1Wtao/Vps18tm1.1Wtao
Tg(Nes-cre)1Kln/0
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 * SJL MGI:5431979
cn169
Dab1tm1Cpr/Dab1+
Rnf7tm1c(EUCOMM)Wtsi/Rnf7tm1c(EUCOMM)Wtsi
Tg(Nes-cre)1Kln/0
involves: 129S4/SvJaeSor * C57BL/6 * C57BL/6N * SJL MGI:5545907
cn170
Dab1tm1Cpr/Dab1tm1Cpr
Rnf7tm1c(EUCOMM)Wtsi/Rnf7tm1c(EUCOMM)Wtsi
Tg(Nes-cre)1Kln/0
involves: 129S4/SvJaeSor * C57BL/6 * C57BL/6N * SJL MGI:5545906
cn171
Id1tm3Bene/Id1tm3Bene
Id2tm1Xdz/Id2tm1Xdz
Id3tm1Zhu/Id3tm1Zhu
Tg(Nes-cre)1Kln/0
involves: 129S4/SvJaeSor * C57BL/6 * SJL MGI:5428946
cn172
Ndufs4tm1Rpa/Ndufs4tm1Rpa
Tg(Nes-cre)1Kln/0
involves: 129S4/SvJaeSor * C57BL/6 * SJL MGI:4818648
cn173
Rasgrf1tm4.1Pds/Rasgrf1+
Tg(Nes-cre)1Kln/0
involves: 129S4/SvJaeSor * C57BL/6 * SJL MGI:3698137
cn174
Id1tm3Bene/Id1tm3Bene
Id2tm1Xdz/Id2+
Id3tm1Zhu/Id3tm1Zhu
Tg(Nes-cre)1Kln/0
involves: 129S4/SvJaeSor * C57BL/6 * SJL MGI:5428947
cn175
Ext1tm1Yama/Ext1tm1Yama
Tg(Nes-cre)1Kln/0
involves: 129S5/SvEvBrd * C57BL/6 * SJL MGI:2682062
cn176
Trp53tm1Brd/Trp53tm1Brd
Xrcc4tm2.1Fwa/Xrcc4tm2Fwa
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * SJL MGI:3652717
cn177
Trp53tm1Brd/Trp53+
Xrcc4tm2.1Fwa/Xrcc4tm2Fwa
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * SJL MGI:3652715
cn178
Stk11tm1.1Rdp/Stk11tm1.1Rdp
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * SJL MGI:5524151
cn179
Baxtm2Sjk/Baxtm2Sjk
Scyl2tm1.1Spel/Scyl2tm1.1Spel
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * 129X1/SvJ * C57BL/6 * SJL MGI:5752574
cn180
Usp7tm2Wgu/Usp7tm2Wgu
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * SJL MGI:5526848
cn181
Scyl1tm1Spel/Scyl1tm1Spel
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * SJL MGI:5469975
cn182
Macf1tm2.1Liem/Macf1tm2.2Liem
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * C57BL/6 * FVB/N * SJL MGI:4831040
cn183
Irs2tm1With/Irs2tm1With
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * C57BL/6J MGI:3576500
cn184
Gad1tm1.1Bgc/Gad1tm1Rpa
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:4442419
cn185
Scyl2tm1.1Spel/Scyl2tm1.1Spel
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:5752573
cn186
Ugcgtm4Rlp/Ugcgtm4Rlp
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:4442808
cn187
Ugcgtm1Rlp/Ugcgtm4Rlp
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:4442809
cn188
Tg(Nes-cre)1Kln/0
Triotm1Mzhu/Triotm1Mzhu
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:4839271
cn189
Gt(ROSA)26Sortm3(RNAi:Map2k1,Map2k2)Rkuhn/Gt(ROSA)26Sor+
Tg(Nes-cre)1Kln/?
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:3785815
cn190
Zfxtm1.1Reiz/Y
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:3848803
cn191
Zfxtm1.1Reiz/Zfxtm1.1Reiz
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:3848809
cn192
Sirt1tm3Fwa/Sirt1tm3Fwa
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:4881924
cn193
Esrrbtm1.1Nat/Esrrbtm1.2Nat
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:3723507
cn194
Gaktm2Legr/Gaktm2Legr
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:5305777
cn195
Irs2tm1With/Irs2tm1With
Tg(Nes-cre)1Kln/?
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:3713798
cn196
Xbp1tm2Glm/Xbp1tm2Glm
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:3811309
cn197
Eif2ak4tm1.1Dron/Eif2ak4tm1.1Dron
Tg(Nes-cre)1Kln/0
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:3806277
cn198
Gli3tm1Alj/Gli3tm1Alj
Tg(Nes-cre)1Kln/?
involves: 129S6/SvEvTac * C57BL/6 * SJL MGI:3803099
cn199
Ank3tm3Bnt/Ank3tm3Bnt
Tg(Nes-cre)1Kln/?
involves: 129S6/SvEvTac * C57BL/6 * SJL/J MGI:5829751
cn200
Aplp2tm1Dbo/Aplp2tm1Dbo
Apptm1.1Zhe/Apptm1.1Zhe
Tg(Nes-cre)1Kln/0
involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6J * SJL MGI:4359070
cn201
Sptbn1tm1.1Mnr/Sptbn1tm1.1Mnr
Tg(Nes-cre)1Kln/0
involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6J * SJL MGI:5431704
cn202
Crktm1Cur/Crktm1Cur
Crkltm1Cur/Crkltm1Cur
Tg(Nes-cre)1Kln/0
involves: 129S/SvEv * C57BL/6 * SJL MGI:3830069
cn203
Crkltm1Cur/Crkltm1Cur
Tg(Nes-cre)1Kln/0
involves: 129S/SvEv * C57BL/6 * SJL MGI:3830068
cn204
Crktm1Cur/Crktm1Cur
Tg(Nes-cre)1Kln/0
involves: 129S/SvEv * C57BL/6 * SJL MGI:3830067
cn205
Atg5tm1Myok/Atg5tm1Myok
Tg(Nes-cre)1Kln/?
involves: 129S/SvEv * C57BL/6 * SJL MGI:3713123
cn206
Tbptm1Xjl/Tbptm1Xjl
Tg(Nes-cre)1Kln/?
involves: 129S/SvEv * C57BL/6 * SJL MGI:5691953
cn207
Itgb8tm1Lfr/Itgb8tm2Lfr
Tg(Nes-cre)1Kln/0
involves: 129/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:3609116
cn208
Rettm1Kln/Rettm1Kln
Tg(Nes-cre)1Kln/0
involves: 129/Sv * BALB/c * C57BL/6 * CBA/J * SJL MGI:3662906
cn209
Lhx1tm1Tmj/Lhx1+
Rettm1Kln/Rettm1Kln
Tg(Nes-cre)1Kln/0
involves: 129/Sv * BALB/c * C57BL/6 * CBA/J * SJL MGI:3662908
cn210
Gmnntm1Tjm/Gmnntm1Tjm
Tg(Nes-cre)1Kln/0
involves: 129/Sv * C57BL/6 * SJL MGI:4999656
cn211
Gmnntm1Tjm/Gmnn+
Tg(Nes-cre)1Kln/0
involves: 129/Sv * C57BL/6 * SJL MGI:4999657
cn212
Bhlhe22tm2.1Meg/Bhlhe22tm2.1Meg
Tg(Nes-cre)1Kln/0
involves: 129/Sv * C57BL/6 * SJL MGI:4440899
cn213
Gli2tm1Alj/Gli2tm6Alj
Tg(Nes-cre)1Kln/0
involves: 129/Sv * C57BL/6 * SJL * Swiss Webster MGI:3665562
cn214
Pex13tm1Crne/Pex13tm1.1Crne
Tg(Nes-cre)1Kln/0
involves: 129T2/SvEms * C57BL/6 * C57BL/6J * SJL MGI:5636606
cn215
Notch1tm2Rko/Notch1tm2Rko
Tg(Nes-cre)1Kln/0
involves: 129X1/SvJ * C57BL/6J * SJL MGI:3044600
cn216
Itgb1tm1Lscd/Itgb1tm1Mll
Tg(Nes-cre)1Kln/0
involves: 129X1/SvJ * C57BL/6 * SJL MGI:3703619
cn217
Ctnna1tm1Efu/Ctnna1tm1Efu
Tg(Nes-cre)1Kln/?
involves: 129X1/SvJ * C57BL/6 * SJL MGI:3720627
cn218
Smotm2Amc/Smotm2Amc
Tg(Nes-cre)1Kln/0
involves: 129X1/SvJ * C57BL/6 * SJL MGI:3844949
cn219
Gt(ROSA)26Sortm1(Smo/EYFP)Amc/Gt(ROSA)26Sor+
Tg(Nes-cre)1Kln/0
involves: 129X1/SvJ * C57BL/6 * SJL MGI:3844934
cn220
Itgb1tm1Mll/Itgb1tm1Mll
Tg(Nes-cre)1Kln/0
involves: 129X1/SvJ * C57BL/6 * SJL MGI:3789472
cn221
Ank3tm2.1Bnt/Ank3tm2.1Bnt
Tg(Nes-cre)1Kln/?
involves: 129X1/SvJ * C57BL/6 * SJL/J MGI:5829760
cn222
Kitltm2.1Sjm/Kitltm2.2Sjm
Tg(Nes-cre)1Kln/0
involves: BALB/cJ * C57BL/6 * C57BL/Ka * SJL MGI:5306353
cn223
Foxj1tm1.1Ctk/Foxj1tm1.2Ctk
Tg(FOXJ1-EGFP)85Leo/0
Tg(Nes-cre)1Kln/0
involves: C3H * C57BL/6 * C57BL/6J * SJL MGI:5285556
cn224
Gys1tm1c(EUCOMM)Wtsi/Gys1tm1c(EUCOMM)Wtsi
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * C57BL/6J * C57BL/6N * SJL MGI:5770262
cn225
Ren1tm1.1Sig/Ren1tm1.1Sig
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * C57BL/6J * SJL MGI:4939887
cn226
Dnm1ltm1.1Miha/Dnm1ltm1.1Miha
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * C57BL/6J * SJL MGI:4438714
cn227
Smc2tm1.1Itl/Smc2tm1.2Itl
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * C57BL/6J * SJL MGI:5703894
cn228
Ncaphtm1.1Itl/Ncaphtm1.2Itl
Ncaph2tm1.1Itl/Ncaph2tm1.2Itl
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * C57BL/6J * SJL MGI:5703890
cn229
Ncaph2tm1.1Itl/Ncaph2tm1.2Itl
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * C57BL/6J * SJL MGI:5703889
cn230
Ncaphtm1.1Itl/Ncaphtm1.2Itl
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * C57BL/6J * SJL MGI:5703887
cn231
Prlhtm2Smln/Prlhtm2Smln
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * C57BL/6J * SJL MGI:5634286
cn232
Ptpn2tm1.1Ttig/Ptpn2tm1.1Ttig
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * C57BL/6J * SJL MGI:5304838
cn233
Cpeb2tm1.1Yshu/Cpeb2tm1.1Yshu
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * C57BL/6J * SJL/J MGI:5882503
cn234
Rcor2tm1c(EUCOMM)Wtsi/Rcor2tm1c(EUCOMM)Wtsi
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * C57BL/6N * SJL MGI:5897781
cn235
Socs7tm1c(EUCOMM)Wtsi/Socs7tm1c(EUCOMM)Wtsi
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * C57BL/6N * SJL MGI:5545908
cn236
Rnf7tm1c(EUCOMM)Wtsi/Rnf7tm1c(EUCOMM)Wtsi
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * C57BL/6N * SJL MGI:5545905
cn237
Ctsdtm1.1Thre/Ctsdtm1.1Thre
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * C57BL/6N * SJL MGI:5702324
cn238
Taok2tm1.1Dkap/Taok2tm1.1Dkap
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * C57BL/6NTac * SJL MGI:5554943
cn239
Psmg1tm1.1Smta/Psmg1tm1.1Smta
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * CBA * SJL MGI:4820735
cn240
Sqstm1tm2.1Jmos/Sqstm1tm2.1Jmos
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * DBA MGI:5487466
cn241
Ldb1tm2Lmgd/Ldb1tm2Lmgd
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * FVB/N * SJL MGI:3719691
cn242
Htra2tm1.1Hohj/Htra2tm1.1Hohj
Tg(Nes-cre)1Kln/0
involves: C57BL/6J MGI:5760304
cn243
Tg(Actb-NOTCH1)2Shn/0
Tg(Nes-cre)1Kln/0
involves: C57BL/6J * SJL MGI:3044597
cn244
S1pr1tm1Jch/S1pr1tm1Jch
Tg(Nes-cre)1Kln/0
involves: C57BL/6J * SJL MGI:4939153
cn245
Tg(ACTB-eGFP,-RAMP1)#Afru/0
Tg(Nes-cre)1Kln/0
involves: C57BL/6J * SJL/J MGI:5306399
cn246
Ndfip1tm1Sest/Ndfip1tm1Sest
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:5313247
cn247
Ccm2tm1Kwhi/Ccm2tm1.1Kwhi
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:3838804
cn248
Gt(ROSA)26Sortm2(GFP/tetX)Gld/Gt(ROSA)26Sor+
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:3839916
cn249
Use1tm1.1Aha/Use1tm1.1Aha
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:3842575
cn250
Lhx2tm1.1Ddmo/Lhx2tm1.1Ddmo
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:4399058
cn251
Pnpla6tm1Mvc/Pnpla6tm1Mvc
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:3041706
cn252
Stat3tm1Flv/Stat3tm1Flv
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:3783343
cn253
Nr2e1tm1Rev/Nr2e1tm1Rev
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:3777346
cn254
Fbxw7tm1.1Axbe/Fbxw7tm1.1Axbe
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:4867643
cn255
Nck1tm1Paw/Nck1tm1Paw
Nck2tm1Paw/Nck2tm3Paw
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:3769794
cn256
Map2k4tm1Ctr/Map2k4tm1Ctr
Tg(Nes-cre)1Kln/?
involves: C57BL/6 * SJL MGI:3769122
cn257
Atmintm1Axbe/Atmintm1Axbe
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:4868763
cn258
Rhebtm1Pfw/Rhebtm1Pfw
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:4939480
cn259
Gt(ROSA)26Sortm1(CAG-Rheb*)Pfw/Gt(ROSA)26Sor+
Rhebtm1Pfw/Rhebtm1Pfw
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:4939481
cn260
Gt(ROSA)26Sortm1(CAG-Rheb*)Pfw/Gt(ROSA)26Sortm1(CAG-Rheb*)Pfw
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:4939482
cn261
Mycbp2tm1.1Klsc/Mycbp2tm1.1Klsc
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:4939605
cn262
Srgap3tm1Ssod/Srgap3tm1Ssod
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:4941467
cn263
Lig3tm1.1Pmc/Lig3tm1.1Pmc
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:4946935
cn264
Ccl2tm1.1Pame/Ccl2tm1.1Pame
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:4950280
cn265
Pdcd10tm1Kwhi/Pdcd10tm1Kwhi
Tg(Nes-cre)1Kln/?
involves: C57BL/6 * SJL MGI:5052327
cn266
Ccm2tm1Kwhi/Ccm2tm1Kwhi
Tg(Nes-cre)1Kln/?
involves: C57BL/6 * SJL MGI:5052329
cn267
Smad2tm1.1Nomu/Smad2tm1.1Nomu
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:5085298
cn268
Foxj1tm1.1Ctk/Foxj1tm1.2Ctk
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:5285555
cn269
Ptgs2tm1Wlf/Ptgs2tm1Wlf
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:3837439
cn270
Zbtb18tm1.1Nda/Zbtb18tm1.1Nda
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:5425229
cn271
Ric8atm1Zhua/Ric8atm1Zhua
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:5467518
cn272
Cxcl12tm1.1Sjm/Cxcl12tm1.1Sjm
Tg(Nes-cre)1Kln/?
involves: C57BL/6 * SJL MGI:5488608
cn273
Prkar2btm3Gsm/Prkar2btm2Gsm
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:5515334
cn274
Nr2c2tm1Bbm/Nr2c2tm1Bbm
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:5517371
cn275
Fgfr1tm1Upir/Fgfr1tm1Upir
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:3641104
cn276
Acot7tm1.1Mwol/Acot7tm1.1Mwol
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:5528849
cn277
Tg(CAG-EGFP,-dsRed2/RNAi:Tardbp)6Zxu/0
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:5563084
cn278
Mirc31tm1.1Sjm/Mirc31tm1.1Sjm
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:5569526
cn279
Ncdntm2Afu/Ncdntm2Afu
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:3605043
cn280
Gt(ROSA)26Sortm2(CAG-Lancl1)Pfw/Gt(ROSA)26Sortm2(CAG-Lancl1)Pfw
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:5646277
cn281
Camta1tm1.1Eno/Camta1tm1.1Eno
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:5762853
cn282
Adktm2Bois/Adktm2Bois
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:5816712
cn283
Gt(ROSA)26Sortm4(Wnt7a)Amc/?
Tg(Nes-cre)1Kln/0
involves: C57BL/6 * SJL MGI:3831434
cn284
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Nes-cre)1Kln/0
Tg(tetO-Vegfa)90Ala/0
mixed MGI:3587022
cn285
Auts2tm1.1Dare/Auts2tm1.1Dare
Tg(Nes-cre)1Kln/0
Not Specified MGI:5697531
cn286
Fgfr1tm1Upir/Fgfr1tm1Upir
Tg(Mnx1-GFP)1Slp/?
Tg(Nes-cre)1Kln/?
Not Specified MGI:3767836
cn287
Auts2tm1.1Dare/Auts2+
Tg(Nes-cre)1Kln/0
Not Specified MGI:5697533
cx288
Rai1tm2.2Luo/Rai1+
Tg(Nes-cre)1Kln/?
either: (involves: 129S1/Sv * C57BL/6 * SJL) or (involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL) MGI:5817608
cx289
Tg(Nes-cre)1Kln/0
Trp53tm1Brd/Trp53tm1Brd
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6 * SJL MGI:3652719
cx290
Tg(Nes-cre)1Kln/?
Tshz1tm1Garr/Tshz1tm2.1Garr
mixed MGI:5588820
tg291
Tg(Nes-cre)1Kln/0 involves: C57BL/6 * SJL MGI:5004891


Genotype
MGI:3837691
cn1
Allelic
Composition
Ccm2tm1Etl/Ccm2tm1Etl
Tg(Nes-cre)1Kln/?
Genetic
Background
B6.Cg-Ccm2tm1Etl Tg(Nes-cre)1Kln
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ccm2tm1Etl mutation (0 available); any Ccm2 mutation (39 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
NOT cerebral cavernous malformation 2 DOID:0060670 OMIM:603284
J:146210




Genotype
MGI:4417949
cn2
Allelic
Composition
Foxa2tm1.1Stf/Foxa2tm1.1Stf
Tg(Nes-cre)1Kln/0
Genetic
Background
B6.Cg-Foxa2tm1.1Stf Tg(Nes-cre)1Kln
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxa2tm1.1Stf mutation (0 available); any Foxa2 mutation (16 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• in fed mice and mice fed a high fat diet
• in fasting mice and mice fed a high fat diet
• in mice fed regular chow or a high fat diet
• glucose clearance is modestly increased compared to in wild-type mice
• indicated by reduced fasting plasma insulin and free fatty acid

behavior/neurological
• in mice fed a high fat diet
• in mice fed regular chow or a high fat diet

adipose tissue
• in mice fed regular chow or a high fat diet

growth/size/body
• in mice fed regular chow or a high fat diet




Genotype
MGI:5551312
cn3
Allelic
Composition
Kalrntm2Npl/Kalrntm2Npl
Tg(Nes-cre)1Kln/0
Genetic
Background
B6.Cg-Kalrntm2Npl Tg(Nes-cre)1Kln
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kalrntm2Npl mutation (0 available); any Kalrn mutation (104 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• on a rotarod




Genotype
MGI:5302397
cn4
Allelic
Composition
Mc3rtm1Butl/Mc3rtm1Butl
Tg(Nes-cre)1Kln/0
Genetic
Background
B6.Cg-Mc3rtm1Butl Tg(Nes-Cre)1Kln
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mc3rtm1Butl mutation (1 available); any Mc3r mutation (15 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• increase in fat mass in mice on a standard diet is attenuated compared to homozygous mice not expressing the cre transgene
• on a standard chow diet

adipose tissue
• increase in fat mass in mice on a standard diet is attenuated compared to homozygous mice not expressing the cre transgene

homeostasis/metabolism




Genotype
MGI:4367075
cn5
Allelic
Composition
Myd88tm1Jcbr/Myd88tm1Jcbr
Tg(Nes-cre)1Kln/0
Genetic
Background
B6.Cg-Myd88tm1Jcbr Tg(Nes-cre)1Kln
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Myd88tm1Jcbr mutation (0 available); any Myd88 mutation (30 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• at 12 weeks, male mice fed a high fat diet exhibit increased energy expenditure during the nighttime compared with similarly treated wild-type mice
• when fed a high fat diet, mice exhibit reduced weight gain and female mice exhibit no weight gain unlike similarly treated wild-type mice
• mice fed a high fat diet exhibit a blunted impairment of glucose and insulin tolerance and insulin serum levels compared with similarly treated wild-type mice
• in male mice fed a high fat diet compared with similarly treated wild-type mice
• when fed a high fat diet, male mice exhibit improved insulin sensitivity compared with similarly treated wild-type mice
• when fed a high fat diet and treated with palmitate, mice exhibit a blunted insulin resistance compared with similarly treated wild-type mice

adipose tissue
• when fed a high fat diet, female mice exhibit a 24% in total fat mass compared with similarly treated wild-type mice
• when fed a high fat diet compared with similarly treated wild-type mice
• slightly in male mice fed a high fat diet compared with similarly treated wild-type mice
• when fed a high fat diet, female mice exhibit a 60% reduction in parametiral fat mass compared with similarly treated wild-type mice

behavior/neurological
• at 12 weeks, male mice fed a high fat diet exhibit reduced food intake compared with similarly treated wild-type mice
• female mice fed a high fat diet and treated with leptin exhibit decreased food intake unlike similarly treated wild-type mice
• male mice fed a high fat diet and treated with leptin exhibit a greater decrease in eating compared with similarly treated wild-type mice
• male mice fed a high fat diet exhibit decreased activity during the nighttime compared with similarly treated wild-type mice

growth/size/body
• when fed a high fat diet, mice fail to exhibit an increase in length unlike similarly treated wild-type mice
• when fed a high fat diet, mice exhibit reduced weight gain and female mice exhibit no weight gain unlike similarly treated wild-type mice




Genotype
MGI:5546601
cn6
Allelic
Composition
Prmt5tm2c(EUCOMM)Wtsi/Prmt5tm2c(EUCOMM)Wtsi
Tg(Nes-cre)1Kln/0
Genetic
Background
B6.Cg-Prmt5tm2c(EUCOMM)Wtsi Tg(Nes-cre)1Kln
Cell Lines EPD0160_2_A08
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Prmt5tm2c(EUCOMM)Wtsi mutation (1 available); any Prmt5 mutation (27 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

nervous system
• apoptotic cells are detected at E15.5 in the ventricular/subventricular zone and ganglionic eminence
• decrease in the number of proliferating neuronal precursor cells at P0
• decrease in the number of primary neurospheres and the number of cells in the neurospheres produced by cultured neuronal precursor cells from E14.5 mice
• self renewal potential of neuronal precursor cells is impaired
• reduced cellularity at P0
• reduced cellularity at P0
• detectable at E17.5
• enlarged and disrupted at P10

behavior/neurological
• balance disorders

cellular
• apoptotic cells are detected at E15.5 in the ventricular/subventricular zone and ganglionic eminence
• decrease in the number of proliferating neuronal precursor cells at P0
• decrease in the number of primary neurospheres and the number of cells in the neurospheres produced by cultured neuronal precursor cells from E14.5 mice
• self renewal potential of neuronal precursor cells is impaired




Genotype
MGI:5576464
cn7
Allelic
Composition
Slc1a2tm1.1Ncd/Slc1a2tm1.1Ncd
Tg(Nes-cre)1Kln/0
Genetic
Background
B6.Cg-Slc1a2tm1.1Ncd Tg(Nes-cre)1Kln
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc1a2tm1.1Ncd mutation (1 available); any Slc1a2 mutation (18 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 50% survival after 8 weeks
• higher mortality rate after 3 weeks, with only 50% survival after 8 weeks

growth/size/body

behavior/neurological
• mice become hyperactive after about 2 weeks
• spontaneous seizures are seen after about 2 weeks

nervous system
• spontaneous seizures are seen after about 2 weeks




Genotype
MGI:5306259
cn8
Allelic
Composition
Slc6a12tm1.1Ncd/Slc6a12tm1.1Ncd
Tg(Nes-cre)1Kln/0
Genetic
Background
B6.Cg-Slc6a12tm1.1Ncd Tg(Nes-cre)1Kln
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc6a12tm1.1Ncd mutation (1 available); any Slc6a12 mutation (27 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• mice exhibit normal seizure threshold (corneal kindling, the minimal clonic and minimal tonic extension seizure threshold tests, the 6 Hz seizure threshold test, and the i.v. pentylenetetrazol threshold test)




Genotype
MGI:5451025
cn9
Allelic
Composition
Ndufs4tm1Rpa/Ndufs4tm1Rpa
Tg(Nes-cre)1Kln/0
Genetic
Background
B6.Cg-Tg(Nes-cre)1Kln Ndufs4tm1Rpa
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ndufs4tm1Rpa mutation (1 available); any Ndufs4 mutation (22 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• more than 90% mortality by P50

growth/size/body
• mutants show growth retardation and fail to thrive

respiratory system
• intermittent breathing irregularities, including hypo- or hyperventilation and gasping
• breathing rate is variable and lower in restrained mutants than in controls
• mutants exhibit intermittent episodes of apnea and periods during which respiratory frequency is very irregular; number of apnea episodes increases with age
• gasping-like episodes that occur more commonly under stressful conditions, such as when being handled
• under normoxic conditions, mice at P8-P12 and those older than P30 have normal respiratory frequency, however they have higher tidal volume and minute ventilation
• in response to hypoxia, mutants show an initial augmentation of breathing, followed by a depression
• some mutants exhibit an abnormal response to excess CO2 (hypercapnia), with 6 of 13 mice failing to show the hyperventilation response seen in control mice, while the rest show an exaggerated response

nervous system
• edematous regions/lesions in the dorsal medulla (in the vestibular nucleus)
• extensive bilateral neuroinflammation in the vestibular nucleus
• edematous regions/lesions in the external plexiform layer of the olfactory bulb
• edematous regions/lesions in the cerebellar lobes
• edematous regions/lesions in the deep cerebellar fastigial nucleus
• neurons with cytoplasmic vacuoles are seen in the brain
• progressive gliosis in the brain
• microglial activation is rarely seen in respiratory centers such as the medial parabrachial nucleus, nucleus of the solitary tract or preBotzinger complex, however it is seen in late-stage mutants around serotonergic cell bodies in the medullary raphe
• mutants develop a fatal progressive encephalopathy
• neurons with cytoplasmic vacuoles and aberrant mitochondria containing condensed cristae and microglia engorged with cytoplasmic remnants in the brain
• mutants exhibit abnormal responses of the Botzinger complex in the ventral medulla under hypoxic conditions; the initial augmentation phase is normal but during depression, the amplitude of fictive gasping is decreased
• intracellular recordings of preBotzinger complex inspiratory neurons show that under control conditions, the depolarization in phase with the network burst is reduced in mutants and the number and frequency of action potentials per burst and firing frequency is lower
• upon transition from control to hypoxic conditions, mutants have a severe reduction of the underlying depolarization when challenged by hypoxia, the number and frequency of action potentials per burst drops dramatically compared to a mild reduction in controls

behavior/neurological

cardiovascular system
• lower heart rate, especially in late stages of disease

homeostasis/metabolism
• percentage of oxygen saturation of arterial blood in late-stage mutants is often less than 99% which is not seen in controls

immune system
• microglial activation is rarely seen in respiratory centers such as the medial parabrachial nucleus, nucleus of the solitary tract or preBotzinger complex, however it is seen in late-stage mutants around serotonergic cell bodies in the medullary raphe

integument
• mutants lose most of their hair at around P20

muscle

hematopoietic system
• microglial activation is rarely seen in respiratory centers such as the medial parabrachial nucleus, nucleus of the solitary tract or preBotzinger complex, however it is seen in late-stage mutants around serotonergic cell bodies in the medullary raphe

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Leigh disease DOID:3652 OMIM:220111
OMIM:256000
J:190475




Genotype
MGI:3044595
cn10
Allelic
Composition
Tg(ACTB-NOTCH1)1Shn/0
Tg(Nes-cre)1Kln/0
Genetic
Background
B6.Cg-Tg(Nes-cre)1Kln Tg(ACTB-NOTCH1)1Shn
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(ACTB-NOTCH1)1Shn mutation (1 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• some of the mutants die before birth; however, most survive to the perinatal stage

nervous system
• at E10 the number of apoptotic cells in the forebrain-midbrain junction is increased
• by E11.5 apoptosis is more widespread in the telencephalon with about 30% of all cells being TUNEL positive
• at E12 - 13.5 the ventricular zone harboring neural progenitors is thinner
• at E12 - 13.5 the telencephalon is smaller compared to wild-type or single transgenic littermates
• at E12 - 13.5 all brain subregions are smaller compared to wild-type or single transgenic littermates
• at P0 the brain especially the cerebral cortex is much smaller in double transgenic mice compared to wild-type or single transgenic littermates
• the number of postmitotic neurons is decreased at E12 - 13.5 in the telencephalon and diencephalon

cellular
• at E10 the number of apoptotic cells in the forebrain-midbrain junction is increased
• by E11.5 apoptosis is more widespread in the telencephalon with about 30% of all cells being TUNEL positive




Genotype
MGI:5511126
cn11
Allelic
Composition
Uba6tm1Whpr/Uba6tm1Whpr
Tg(Nes-cre)1Kln/0
Genetic
Background
B6.Cg-Uba6tm1Whpr Tg(Nes-cre)1Kln
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Nes-cre)1Kln mutation (4 available)
Uba6tm1Whpr mutation (1 available); any Uba6 mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• half of mice die between P5 and P21
• a quarter of mice that survive to P21 die within 2 months
• however, lethality is partially rescued by making food more accessible

behavior/neurological
• with altered response to an aversive stimulus
• in the Y-maze test
• absence of stomach content in several mice at death
• in a forced swim test, mice spend less time immobilized compared with wild-type mice
• constitutive without an alteration in body temperature
• slightly better performance on a rotarod
• in a novel environment with a lack of habituation
• pronounced in the dark phase
• aversion to nesting
• mice prefer to explore an empty chamber rather than a stranger mouse

nervous system
N
• neuronal apoptosis at E14.5 and P5 is normal
• reduced density in the CA3 region and amygdala
• in the CA3 region as early as P5, the basolateral amygdala and piriform cortex
• however, the number of neurons is normal in the CA1, dentate gyrus, cortex and cerebellar regions

homeostasis/metabolism
N
• mice exhibit normal body temperature and constant respiratory exchange ratio throughout the diurnal cycle
• hypermetabolic

growth/size/body
• at birth and 11 weeks




Genotype
MGI:5897176
cn12
Allelic
Composition
Tg(CAG-Ppard*E411P)#Als/0
Tg(Nes-cre)1Kln/0
Genetic
Background
B6J.Cg-Tg(Nes-cre)1Kln Tg(CAG-Ppard*E411P)#Als
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-Ppard*E411P)#Als mutation (0 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• mice appear smaller by 4-6 months of age and weigh less than controls by 8 months of age

behavior/neurological
• mice exhibit reduced novel-environment exploration
• mice exhibit reduced novel-object recognition
• mice exhibit prominent motor abnormalities by 8 months of age
• in the cage-ledge test, mice cannot easily dismount from the cage ledge
• mice exhibit a prominent clasping phenotype
• mice exhibit worse latency-to-fall times on the accelerating rotarod
• reduction in combined mesh and grip-strength
• decrease in mean stride-length

cellular
• mitochondria in the striatum and cortex are smaller in size
• activities of mitochondrial complex IV and complex V are reduced in the striatum and overall ATP concentration is reduced in the striatum and cortex

nervous system
• brain size of adults is reduced
• reduction in the volume of the basal ganglia
• reduction in the volume of the cortex
• reactive gliosis in the brain
• brain shows reduction in neuron numbers
• reduction in tyrosine hydroxylase-positive dopaminergic neurons in the substantia nigra

skeleton

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Huntington's disease DOID:12858 OMIM:143100
J:233176




Genotype
MGI:3629065
cn13
Allelic
Composition
Abcb7tm1Mdf/Y
Tg(Nes-cre)1Kln/0
Genetic
Background
either: B6.Cg-Tg(Nes-cre)1Kln Abcb7tm1Mdf or (involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * SJL)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abcb7tm1Mdf mutation (1 available); any Abcb7 mutation (13 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• only 4.3% of pups rather than the expected 12.5% are found at P1
• none are found at weaning

nervous system
N
• no gross brain abnormalities are detected




Genotype
MGI:5817609
cn14
Allelic
Composition
Rai1tm2.1Luo/Rai1+
Tg(Nes-cre)1Kln/?
Genetic
Background
either: (involves: 129S1/Sv * C57BL/6 * SJL) or (involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rai1tm2.1Luo mutation (1 available); any Rai1 mutation (51 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• males exhibit a decreased latency to fall in wire hang test

growth/size/body
• female mice become overweight beginning at 7 weeks of age
• at 20 weeks female mice are 35% heavier than controls




Genotype
MGI:5817614
cn15
Allelic
Composition
Rai1tm2.2Luo/Rai1tm2.1Luo
Tg(Nes-cre)1Kln/?
Genetic
Background
either: (involves: 129S1/Sv * C57BL/6 * SJL) or (involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rai1tm2.1Luo mutation (1 available); any Rai1 mutation (51 available)
Rai1tm2.2Luo mutation (0 available); any Rai1 mutation (51 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• female mice become overweight beginning at 7 weeks of age




Genotype
MGI:5817471
cn16
Allelic
Composition
Rai1tm2.1Luo/Rai1tm2.1Luo
Tg(Nes-cre)1Kln/?
Genetic
Background
either: (involves: 129S1/Sv * C57BL/6 * SJL) or (involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rai1tm2.1Luo mutation (1 available); any Rai1 mutation (51 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• males perform similar to controls in assays for gait, velocity, vertical activity, anxiety, sociability and cognition
• males have normal hearing and pain responses
• decreased freezing behavior after repeated tone-shock pairings during training
• decreased freezing behavior in contextual recall in trace fear-conditioning task
• decreased freezing behavior in cued recall
• reduced tendency to explore new arm in Y maze
• hindlimb clasping
• in pole test males slip from pole or climb down in a slow and uncoordinated fashion
• decreased latency to fall in wire hang test

growth/size/body
• female mice become overweight beginning at 5 weeks of age
• at 20 weeks female mice are 101% heavier than controls
• mice are smaller than littermates prior to weaning

mortality/aging
• more than 80% of mice die before 25 weeks of age

skeleton
• kyphosis in 10% of mice that die before 10 weeks of age

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Smith-Magenis syndrome DOID:0060768 OMIM:182290
J:237687




Genotype
MGI:4398746
cn17
Allelic
Composition
Sox2tm2Skn/Sox2tm4.1Skn
Tg(Nes-cre)1Kln/0
Genetic
Background
either: (involves: 129S/Sv * C57BL/6 * SJL) or (involves: 129S/Sv * C57BL/6 * DBA/2 * SJL)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sox2tm2Skn mutation (1 available); any Sox2 mutation (34 available)
Sox2tm4.1Skn mutation (1 available); any Sox2 mutation (34 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most mice die by 4 weeks of age

nervous system
• brain cultures of P0 neurospheres in EGF exhibit reduced neural stem cells by the second and fourth passage compared to wild-type cultures that continue to proliferate
• neurospheres from P0 brain cultures in EGF die out by the fifth or sixth passage unlike wild-type cultures that continue to proliferate
• P0 brain cultures in EGF and bFGF adhere to the plate at early passages before becoming exhausted unlike similarly treated wild-type cultures that continue to proliferate
• defects in neural stem cell maintenance are accompanied by a strong decrease in neurosphere size
• P7 brain cultures are exhausted between the first and fourth passage unlike wild-type cultures that continue to proliferate
• brain cultures from E14.5 mice are more viable than later cultures but exhibit reduced proliferation compared with wild-type cultures
• however, treatment of P0 cultures with media from wild-type cultures restores proliferation
• from P0 hippocampal development is reduced compared to in wild-type mice
• moderately at P0
• prematurely interrupted at P0
• at P0, the number of GFAP/nestin+ cells in the dentate gyrus sub-granular layer is slightly decreased compared to in wild-type mice
• at P2, the number of GFAP/nestin+ cells in the dentate gyrus is strongly reduced compared to in wild-type mice
• the reduction in dentate gyrus cells is attributed to decreased proliferation and transient increase in apoptosis compared to in wild-type mice
• almost completely by P7
• the reduction in dentate gyrus cells is attributed to decreased proliferation and transient increase in apoptosis compared to in wild-type mice
• slightly at P0 and markedly at P7
• at P0, the posterior ventrolateral cortex is slightly reduced in size compared to in wild-type mice

cellular
• brain cultures of P0 neurospheres in EGF exhibit reduced neural stem cells by the second and fourth passage compared to wild-type cultures that continue to proliferate
• neurospheres from P0 brain cultures in EGF die out by the fifth or sixth passage unlike wild-type cultures that continue to proliferate
• P0 brain cultures in EGF and bFGF adhere to the plate at early passages before becoming exhausted unlike similarly treated wild-type cultures that continue to proliferate
• defects in neural stem cell maintenance are accompanied by a strong decrease in neurosphere size
• P7 brain cultures are exhausted between the first and fourth passage unlike wild-type cultures that continue to proliferate
• brain cultures from E14.5 mice are more viable than later cultures but exhibit reduced proliferation compared with wild-type cultures
• however, treatment of P0 cultures with media from wild-type cultures restores proliferation




Genotype
MGI:4840275
cn18
Allelic
Composition
Stat5atm2Mam/Stat5atm2Mam
Stat5btm1Mam/Stat5btm1Mam
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * 129S6/SvEvTac * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Stat5atm2Mam mutation (1 available); any Stat5a mutation (25 available)
Stat5btm1Mam mutation (0 available); any Stat5b mutation (19 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• increase 40% and 20% in male and female mice, respectively at 22 weeks of age
• gain more weight than control littermates starting from 8 weeks of age
• more profound after 16 weeks of age
• weigh on the average 65% (males) and 60% (females) more at 26 weeks of age

behavior/neurological
• increased food intake in male at 16 weeks of age
• increased food intake in both male and female at 26 weeks of age

homeostasis/metabolism
• reduced cold tolerance at 26 weeks of age
• 8-fold at 22 weeks of age
• 4.5-fold at 22 weeks of age
• reduced oxygen consumption normalized to lean mass in male mice at 26 weeks of age
• at 22 weeks of age
• at 22 weeks of age

adipose tissue
• increase 2.5- and 3.5-fold in male and female mice, respectively at 22 weeks of age
• increase in both subcutaneous and visceral fat mass
• larger mean cross-sectional areas of adipocytes in inguinal, parametrial and mesenteric fat pads
• at least 2 fold increase in weight of all 5 fat pads (inguinal, parametrial, retroperitoneal, mesenteric and perirenal)
• 150% and 200% in male and female mice, respectively of that measured in control mice at 22 weeks of age




Genotype
MGI:4840276
cn19
Allelic
Composition
Stat5btm1Mam/Stat5btm1Mam
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * 129S6/SvEvTac * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Stat5btm1Mam mutation (0 available); any Stat5b mutation (19 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• increase 40% and 20% in male and female mice, respectively at 22 weeks of age
• gain more weight than control littermates starting from 8 weeks of age
• more profound after 16 weeks of age
• weigh on the average 65% (males) and 60% (females) more at 26 weeks of age

behavior/neurological
• increased food intake in male at 16 weeks of age
• increased food intake in both male and female at 26 weeks of age

homeostasis/metabolism
• reduced cold tolerance at 26 weeks of age
• 8-fold at 22 weeks of age
• 4.5-fold at 22 weeks of age
• reduced oxygen consumption normalized to lean mass in male mice at 26 weeks of age
• at 22 weeks of age
• at 22 weeks of age

adipose tissue
• increase 2.5- and 3.5-fold in male and female mice, respectively at 22 weeks of age
• increase in both subcutaneous and visceral fat mass
• larger mean cross-sectional areas of adipocytes in inguinal, parametrial and mesenteric fat pads
• at least 2 fold increase in weight of all 5 fat pads (inguinal, parametrial, retroperitoneal, mesenteric and perirenal)
• 150% and 200% in male and female mice, respectively of that measured in control mice at 22 weeks of age




Genotype
MGI:4943294
cn20
Allelic
Composition
Cfl1tm1.1Wit/Cfl1+
Dstntm1.1Wit/Dstntm1.1Wit
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * BALB/cJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cfl1tm1.1Wit mutation (0 available); any Cfl1 mutation (19 available)
Dstntm1.1Wit mutation (0 available); any Dstn mutation (41 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype
• mice are viable and phenotypically normal




Genotype
MGI:3051638
cn21
Allelic
Composition
Socs3tm1Ayos/Socs3tm1Ayos
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Socs3tm1Ayos mutation (2 available); any Socs3 mutation (10 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
• on a high fat diet total fat weight and individual fat pad weights increase less in mutants compared to wild-type mice

behavior/neurological
• food intake is decreased on a high fat diet compared to wild-type mice on the same diet
• leptin treatment induces a greater decrease in food intake in mutants compared to wild-type mice

growth/size/body
• on a high fat diet total fat weight and individual fat pad weights increase less in mutants compared to wild-type mice
• on a high fat diet mutants gain less weight
• treatment with leptin induces greater weight loss in mutants

homeostasis/metabolism
• after 22 weeks on a high fat diet plasma free fatty acid levels are significantly lower in mutants
• after 22 weeks on a high fat diet triglyceride levels are significantly lower in mutants
• glucose clearance is significantly faster in mutants compared to wild-type mice
• on a high fat diet mutants do not develop insulin resistance




Genotype
MGI:5825029
cn22
Allelic
Composition
Slc6a8tm1.1Lbar/Y
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * C57BL/6J * C57BL/6N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc6a8tm1.1Lbar mutation (0 available); any Slc6a8 mutation (6 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• mice show impaired performance in the object recognition test, indicating impaired declarative memory, showing both a defect in short-term (1-hour) and long-term (24-hour) memory at P180
• mice show a defect in long-term (24-hour) memory at P180
• mice show a defect in short-term (1-hour) memory at P180
• mice show bout a 10% lower alternation rate in the Y maze, indicating impaired working memory

cellular
• the number of Ki67-positive cells in the dentate gyrus is decreased at P180, indicating reduced neurogenesis

homeostasis/metabolism
• creatine levels in the brain are decreased

nervous system
• the number of Ki67-positive cells in the dentate gyrus is decreased at P180, indicating reduced neurogenesis
• the number of Ki67-positive cells in the dentate gyrus is decreased at P180, indicating reduced neurogenesis




Genotype
MGI:4850044
cn23
Allelic
Composition
Abl1tm2.1Goff/Abl1tm2.1Goff
Abl2tm1Ajk/Abl2tm1Ajk
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abl1tm2.1Goff mutation (1 available); any Abl1 mutation (75 available)
Abl2tm1Ajk mutation (0 available); any Abl2 mutation (52 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• recovered at a frequency (20.5%) slightly less than the expected Mendelian ratio at two weeks of age

nervous system
• reduced number of proliferating granule cell precursors (GCPs) in the secondary fissure in the posterior cerebellum at P8
• loss of proliferating GCPs is concentrated in areas where the basement membrane (BM) is disrupted
• normal proliferation of GCPs in the cerebella-derived culture
• scores of granule cell precursors (GCPs) abnormally protrude into the subarachnoid space between the midbrain and cerebellum at E17
• laminin-labeled basement membrane (BM) is fragmented at E15 and E17
• loss of the pial BM in the cerebellum starting from around P8
• reduced anterior-posterior extent of the mutant adult cerebellum
• basic laminar structure of the anterior cerebellum, encompassing lobules I-V, is completely lost
• obvious defects in the organization of anterior lobules I-V in P7 and P1 cerebella
• adjacent lobules, such as lobules VIII and IX, are fused
• patches of granule cells are randomly scattered throughout the white matter
• abnormal Bergmann glial network correlates with breaches of the BM in the cerebellum at P8
• highly disorganized radial glial processes, with some of their endfeet protruding into the meninges in the mutant cerebellum at E15
• loosely aligned Purkinje cells, with some abnormally distributing at the cerebellar surface at P1
• GCPs ectopically embed within the cortex at P1
• ectopic granule cell differentiation near the broken BM at P8
• many granule cells ectopias at the cerebellar surface in the posterior regions of adult cerebella and along the fusion lines of adjacent lobules
• normal extent of migration of granule cells and granule cell-glia interactions at P10 before the loss of the BM
• decreased depth of the fissures
• both the cerebellar vermis and the two lateral hemispheres lack clear fissures on the surface
• disappearance of lobules IV and V in the anterior vermis
• smaller cerebellum in adult mice

behavior/neurological
• take approximately twice as long to cross the elevated balance beam
• dramatic increase in the number of foot slips

cellular
• reduced number of proliferating granule cell precursors (GCPs) in the secondary fissure in the posterior cerebellum at P8
• loss of proliferating GCPs is concentrated in areas where the basement membrane (BM) is disrupted
• normal proliferation of GCPs in the cerebella-derived culture




Genotype
MGI:4415816
cn24
Allelic
Composition
Tnfrsf11atm1.1Pngr/Tnfrsf11atm1.2Pngr
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * C57BL/6NTac * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Nes-cre)1Kln mutation (4 available)
Tnfrsf11atm1.1Pngr mutation (0 available); any Tnfrsf11a mutation (22 available)
Tnfrsf11atm1.2Pngr mutation (0 available); any Tnfrsf11a mutation (22 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• ovariectomized mice fail to exhibit a change in body temperature unlike similarly treated wild-type mice
• in female mice during the light phase
• mice injected with RANKL (Tnfsf11) or LPS fail to develop severe hyperthermia unlike similarly treated wild-type mice
• mice injected with RANKL (Tnfsf11) fail to exhibit an increase in prostagladin levels unlike similarly treated wild-type mice
• mice injected with RANKL (Tnfsf11) fail to develop severe hyperthermia and do not exhibit a change in diurnal activity unlike similarly treated wild-type mice
• mice injected with Il1b or TNF exhibit an impaired fever response and alterations in circadian activity compared with similarly treated wild-type mice
• mice injected with RANKL (Tnfsf11) fail to exhibit an increase in prostagladin levels unlike similarly treated wild-type mice

immune system
• mice injected with LPS fail to develop severe hyperthermia and do not exhibit a change in diurnal activity unlike similarly treated wild-type mice

behavior/neurological
• in female mice during the light phase




Genotype
MGI:5523421
cn25
Allelic
Composition
Gnl3tm2.1Rylt/Gnl3tm2.1Rylt
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gnl3tm2.1Rylt mutation (0 available); any Gnl3 mutation (50 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Severe brain defects in Gnl3tm2.1Rylt/Gnl3tm2.1Rylt Tg(Nes-cre)1Kln/0 embryos

mortality/aging

respiratory system

nervous system
• decrease in cellularity starting at E12.5
• increase in gamma-H2AFX protein in cells expressing this protein at E12.5
• major defects in the cerebellar primordium at E14.5 and E16.5
• major defects at E14.5 and E16.5
• smaller midbrain and hindbrain tegmentum at E14.5 and E16.5
• smaller at E14.5 and E16.5
• major defects in the cortex at E14.5 and E16.5
• major defects in the ganglionic eminence at E14.5 and E16.5
• decrease in neuronal stem cell numbers in the neuroepithelium at E12.5
• at E14.5 and E16.5

embryo
• decrease in cellularity starting at E12.5
• increase in gamma-H2AFX protein in cells expressing this protein at E12.5




Genotype
MGI:4437796
cn26
Allelic
Composition
Ahi1tm1Jgg/Ahi1tm2.1Jgg
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ahi1tm1Jgg mutation (1 available); any Ahi1 mutation (41 available)
Ahi1tm2.1Jgg mutation (1 available); any Ahi1 mutation (41 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• mice exhibit normal mortality through weaning

vision/eye
• at P19, dark-adapted electrical activity is absent unlike in wild-type mice

nervous system
N
• brain morphology is normal




Genotype
MGI:4353815
cn27
Allelic
Composition
Gt(ROSA)26Sortm1(SNCA*A53T)Djmo/Gt(ROSA)26Sor+
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(SNCA*A53T)Djmo mutation (1 available); any Gt(ROSA)26Sor mutation (378 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
normal phenotype




Genotype
MGI:3851591
cn28
Allelic
Composition
Tg(EEF1A1-SHC1*)1Ravi/0
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(EEF1A1-SHC1*)1Ravi mutation (1 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• at birth and during early postnatal development, there is a slight body weight difference
• the biggest differences occur at 21 days of age
• later in life males have bigger body weight differences than females

nervous system
• apoptosis among neural progenitors is increased during embryonic brain development
• apoptosis is noted in the frontal cortex at E12.5 and in the pons at E10.5 and E12.5
• brain weight is less than controls from 2 days of age to 1 year in age
• the biggest differences occur at 21 days of age
• the stratium area is smaller at 2 days of age than controls and becomes even smaller at 21 days of age
• the entire thickness of the primary somatosensory cortex is reduced to less than 85% of controls
• layers II through IV are more dramatically affected (reduced by less 60% of controls in layer IV) than layers V-VI (reduced by 92% of controls)
• the cerebral cortex is thinner at 2 days of age than controls and becomes even thinner at 21 days of age
• at 2 days of age, the cerebral cortex is 58% smaller than controls which is more affected than other parts of the brain
• olfactory bulb is 82% of controls at 2 days of age
• the SVZ area is smaller at 2 days of age than controls and becomes even smaller at 21 days of age
• apoptosis among neural progenitors is increased during embryonic brain development
• proliferation of neural progenitors is not changed so presumably there are less progenitor cells in the developing brain

cellular
• apoptosis among neural progenitors is increased during embryonic brain development
• apoptosis is noted in the frontal cortex at E12.5 and in the pons at E10.5 and E12.5




Genotype
MGI:3851590
cn29
Allelic
Composition
Shc1tm1Ravi/Shc1tm1Ravi
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Shc1tm1Ravi mutation (1 available); any Shc1 mutation (56 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• body weight is less than controls at 25 days of age

nervous system
• brain weight is less than controls at 25 days of age




Genotype
MGI:3836814
cn30
Allelic
Composition
Mycntm1Psk/Mycntm1Psk
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mycntm1Psk mutation (2 available); any Mycn mutation (16 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• decrease in head size can be detected at E12.5
• moderate growth retardation

nervous system
N
• neuronal precursor cell apoptosis is similar to controls
• progenitor cells display smaller nuclei
• premature differentiation is seen both in vivo and in vitro
• striking reduction in proliferation in the central nervous system in general at E13
• only a very small fraction of cells in the interior of the cerebellum primordium are proliferating at E13
• significant decrease in the number of proliferating cells in the ventricular zone of the telencephalon at E13
• the cerebellar neuroepithelium appears thinner, displays breaks, and has a deficiency in progenitor cells
• the cerebellar neuroepithelium appears thinner
• many regions of the VZ are noticeably reduced in thickness
• at E17.5 in the lateral VZ neuroprogenitor cells are more rounded and more densely packed
• at 8 - 16 weeks of age mice display profound microencephaly
• decrease in brain size can be detected at E12.5
• total brain mass relative to total body weight is reduced 2 fold compared to controls
• the developing cerebral cortex is particularly small
• cerebellum appears disorganized
• at P20 in the rostral region all 3 layers are severely affected
• profound reduction in the progenitor cell pool in both the external granule cell layer and in the neuroepithelium
• at E12.5 a significant reduction in neuroprogenitor cell numbers is seen in the cerebellar neuroepithelium and rhombic lip and the interior differentiating zone is reduced in size
• at E17.5 a subset of rhombic lip neuroprogenitor cells are more rounded and more densely packed
• severe defects in foliation
• profound reduction in the progenitor cell pool
• decrease is more pronounced in the rostral region
• the most rostral portion of the EGL is absent
• granule cell density is reduced 3- to 6-fold
• at P20 total granule cell numbers are reduced about 30-fold
• fails to expand resulting in decreased area and decreased cell number
• the developing cerebellum is particularly small
• at P20 the absolute weight and percent of total brain weight of the cerebellum is reduced by 4- to 6-fold compared to controls
• in the cerebellar neuroepithelium, rhombic lip, and external granule cell layer at E12.5 and E17.5

vision/eye

embryo
• the cerebellar neuroepithelium appears thinner, displays breaks, and has a deficiency in progenitor cells
• the cerebellar neuroepithelium appears thinner

cellular
• progenitor cells display smaller nuclei
• premature differentiation is seen both in vivo and in vitro
• striking reduction in proliferation in the central nervous system in general at E13
• only a very small fraction of cells in the interior of the cerebellum primordium are proliferating at E13
• significant decrease in the number of proliferating cells in the ventricular zone of the telencephalon at E13




Genotype
MGI:3831343
cn31
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 (74 available)
Ptch1tm1Mps mutation (2 available); any Ptch1 mutation (79 available)
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Tyj mutation (9 available); any Trp53 mutation (153 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: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 (74 available)
Ptch1tm1Mps mutation (2 available); any Ptch1 mutation (79 available)
Tg(Nes-cre)1Kln mutation (4 available)
Trp53tm1Tyj mutation (9 available); any Trp53 mutation (153 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:5576197
cn33
Allelic
Composition
Deaf1tm1.1Mico/Deaf1tm1.1Mico
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Deaf1tm1.1Mico mutation (1 available); any Deaf1 mutation (16 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• learn to find a visible platform in a Morris water maze with efficiency equivalent to controls
• find a submerged platform moved to the opposite quadrant faster than controls when retested 48 hours after first exposure, but only on first trial
• subsequent trials and trials 7 days later are like controls
• reduced freezing behavior in response to foot shock
• significantly reduced contextual fear memory 24 hours after first test (similar result with heterozygotes)




Genotype
MGI:5523950
cn34
Allelic
Composition
Hsd17b4tm2Baes/Hsd17b4tm2Baes
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hsd17b4tm2Baes mutation (0 available); any Hsd17b4 mutation (21 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice are euthanized beyond 12 months due to severe coordination defects
• however, most mice survive to at least 1 year of age

reproductive system
• fewer and smaller litters than control mice
• from female mice

nervous system
• minor at 6 months
• cerebella atrophy
• neuronal death after 6 months
• at 12 months of age
• loss of axonal integrity with swelling prior to demyelination
• myelin loss between 4 and 6 months in cerebellar branches, worsen at 10 to 12 months
• however, myelination in the central white matter is normal

behavior/neurological
• anxious phenotype beyond 12 weeks
• beyond 12 weeks
• beyond 12 weeks
• severe at 12 months
• on a rotarod from 4 weeks, worsening with age
• from 12 weeks of age, mice exhibit frequent falls
• unsteady gait beyond 12 weeks, worsening by 6 months
• mice exhibit poor fore limb hind limb coordination with ipsilateral paw placement
• with increased stance at 6 months

homeostasis/metabolism
• accumulation of long chain fatty acids in the cerebellum and cortex

growth/size/body
• at P7, P21 and beyond
• pre- and post-weaning

hematopoietic system
• minor at 6 months

immune system
• minor at 6 months




Genotype
MGI:5512711
cn35
Allelic
Composition
Braftm2Urr/Braftm2Urr
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm2Urr mutation (0 available); any Braf mutation (37 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Cerebellar abnormalities in Braftm2Urr/Braftm2Urr Tg(Nes-cre)1Kln/0 and Braftm2.1Urr/Braftm2.1Urr Tg(Nes-cre)1Kln/0 mice

mortality/aging
• mice begin to die around P17
• no mice survive beyond P28

nervous system
• in the dentate granule cell layer
• however, no increase in astrocytic differentiation is observed in the dentate gyrus
• expansion of the pool of proliferating hippocampal progenitor cells in the third postnatal week
• at P10 and P20
• reduced volume of the dentate granule cell layer
• reduced volume at P21 but not P12
• cytoarchitectonic alterations affecting all lobes at P21
• irregular positions in the flocculonodular lobe LX
• Purkinje cells appear elongated
• reduced and irregular arborization in the cerebellar molecular layer with more than 2 times lengthening of primary dendrite length
• in the flocculonodular lobe LX
• reduced and irregular arborization in the cerebellar molecular layer with more than 2 times lengthening of primary dendrite length
• reduced glomeruli size indicating that the synapses of the granule cells with mossy fiber and Golgi cells do not form correctly
• reduced length with less well demarcated and fuzzy border
• reduced length with less well demarcated and fuzzy border
• less well demarcated and fuzzy border
• ced length with less well demarcated and fuzzy border and disorganized glomeruli

behavior/neurological
• autoaggression (biting of their toes) in 13 of 15 mice
• impaired ability to walk and balance on a rod
• however, mice walk normally otherwise
• impaired ability to walk and balance on a rod
• however, mice walk normally otherwise

growth/size/body

cellular
• in the dentate granule cell layer
• however, no increase in astrocytic differentiation is observed in the dentate gyrus
• expansion of the pool of proliferating hippocampal progenitor cells in the third postnatal week




Genotype
MGI:5512710
cn36
Allelic
Composition
Braftm2.1Urr/Braftm2.1Urr
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm2.1Urr mutation (0 available); any Braf mutation (37 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Cerebellar abnormalities in Braftm2Urr/Braftm2Urr Tg(Nes-cre)1Kln/0 and Braftm2.1Urr/Braftm2.1Urr Tg(Nes-cre)1Kln/0 mice

mortality/aging
• mice begin to die around P17
• no mice survive beyond P28

nervous system
• in the dentate granule cell layer
• however, no increase in astrocytic differentiation is observed in the dentate gyrus
• expansion of the pool of proliferating hippocampal progenitor cells in the third postnatal week
• at P10 and P20
• reduced volume of the dentate granule cell layer
• reduced volume at P21 but not P12
• cytoarchitectonic alterations affecting all lobes at P21
• irregular positions in the flocculonodular lobe LX
• Purkinje cells appear elongated
• reduced and irregular arborization in the cerebellar molecular layer with more than 2 times lengthening of primary dendrite length
• in the flocculonodular lobe LX
• reduced and irregular arborization in the cerebellar molecular layer with more than 2 times lengthening of primary dendrite length
• reduced glomeruli size indicating that the synapses of the granule cells with mossy fiber and Golgi cells do not form correctly
• reduced length with less well demarcated and fuzzy border
• reduced length with less well demarcated and fuzzy border
• less well demarcated and fuzzy border
• ced length with less well demarcated and fuzzy border and disorganized glomeruli

behavior/neurological
• autoaggression (biting of their toes) in 13 of 15 mice
• impaired ability to walk and balance on a rod
• however, mice walk normally otherwise
• impaired ability to walk and balance on a rod
• however, mice walk normally otherwise

growth/size/body

cellular
• in the dentate granule cell layer
• however, no increase in astrocytic differentiation is observed in the dentate gyrus
• expansion of the pool of proliferating hippocampal progenitor cells in the third postnatal week




Genotype
MGI:5490900
cn37
Allelic
Composition
Asic1tm1.1Ccli/Asic1tm1.1Ccli
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Asic1tm1.1Ccli mutation (0 available); any Asic1 mutation (23 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• hippocampal long term potentiation is similar to controls
• absence of ASIC-like currents in nucleated patches isolated from interneurons in stratum oriens alveus

behavior/neurological
N
• spatial memory and learning are similar to controls




Genotype
MGI:5471311
cn38
Allelic
Composition
Sp2tm1.1Htg/Sp2+
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sp2tm1.1Htg mutation (0 available); any Sp2 mutation (144 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• reduced proliferation of neural stem and neural progenitor cells in the subependymal zone and rostral migratory stream
• enlarged due to increased neuroblasts
• reduced volume at P21
• reduced volume at P21
• reduced volume at P21

growth/size/body
• at P7 and P21

cellular
• reduced proliferation of neural stem and neural progenitor cells in the subependymal zone and rostral migratory stream




Genotype
MGI:5471309
cn39
Allelic
Composition
Sp2tm1.1Htg/Sp2tm1.1Htg
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sp2tm1.1Htg mutation (0 available); any Sp2 mutation (144 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• many mice die between 2 and 5 weeks after birth with few surviving into adulthood
• many mice die between 2 and 5 weeks after birth with few surviving into adulthood

nervous system
• severely disrupted neuronal and glial differentiation
• reduced proliferation of neural stem and neural progenitor cells in the subependymal zone and rostral migratory stream
• enlarged due to increased neuroblasts
• mild in some mice at P21
• reduced volume at P21
• reduced volume at P21
• reduced volume at P21

growth/size/body
• at P7 and P21

cellular
• increased M-phase of neural stem and neural progenitor cells in the subependymal zone and rostral migratory stream of postnatal mice
• shortened G2-M transition in neural stem and neural progenitor cells
• partial arrest in G2 and M phase in neural stem and neural progenitor cells
• reduced proportion of neural stem and neural progenitor cells in G1/G0
• however, S phase duration is normal
• severely disrupted neuronal and glial differentiation
• reduced proliferation of neural stem and neural progenitor cells in the subependymal zone and rostral migratory stream




Genotype
MGI:5449209
cn40
Allelic
Composition
Ccdc88atm4.1Mat/Ccdc88a+
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ccdc88atm4.1Mat mutation (0 available); any Ccdc88a mutation (45 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• not as severe as in homozygous mice




Genotype
MGI:5449208
cn41
Allelic
Composition
Ccdc88atm4.1Mat/Ccdc88atm4.1Mat
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ccdc88atm4.1Mat mutation (0 available); any Ccdc88a mutation (45 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• no mice are successfully weaned
• start to die after P12 with none surviving past P29

growth/size/body
• starting at P5

behavior/neurological
• inactive

nervous system
• increase in the width of the layer of DCX-positive neurons at P15




Genotype
MGI:5002665
cn42
Allelic
Composition
Pdcd10tm1Wami/Pdcd10tm1Wami
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pdcd10tm1Wami mutation (0 available); any Pdcd10 mutation (15 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• mice exhibit normal Mendelian ratio after birth
• mice do not survive past P3
• fewer than expected mice are born

nervous system
• abnormal cytoarchitecture




Genotype
MGI:4867645
cn43
Allelic
Composition
Fbxw7tm1.1Axbe/Fbxw7tm1.1Axbe
Notch1tm1Agt/Notch1+
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fbxw7tm1.1Axbe