Title | Phenotype | Contact | |||||||||||||
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B6.129P2-Tacr1<tm1Sph>/H |
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Deletion of NK1 receptor gene. Viable, normal breeding pattern. No obvious phenotype. | Contact | ||||||||||||
B6.129P2-Tg(EEF1A1-Socs6)1Pwg/H |
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10% increased body weight & increased insulin sensitvity. | Contact | ||||||||||||
B6.129P2-Tln1<tm1Crit>/CritH |
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Contact | |||||||||||||
B6.129P2-Tln1<tm4.1Crit>/Crit |
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The homozygous floxed Tln1 mice are viable and fertile and have no phenotype. | Contact | ||||||||||||
B6.129P2-Trpc4<tm1Dgen>/H |
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No visible phenotype. | Contact | ||||||||||||
B6.129P2-Trpc6<tm1Dgen>/H |
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No visible phenotype | Contact | ||||||||||||
B6.129P2-Wt1<tm1Hst>/H |
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No detectable WT* protein isoforms by western blot. No overt phenotype. | Contact | ||||||||||||
B6.129P2-Zfp647<Gt(ES492)Hgs>/H |
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Homozygotes are embryonic lethal at before 6.5 dpc. | Contact | ||||||||||||
B6.129S-Ctse<129S/SvHsd>/H |
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Mice breed normally. No obvious phenotype has been described as yet but cathepsin E has been implicated in regulation of antigen processing, and other aspects of innate immunity. | Contact | ||||||||||||
B6.129S-Otoa<tm1Gpr>/H |
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In null mutant (OtoaEGFP/EGFP) mice the TM is detached at the spiral limbus but remains attached to the outer hair cells, Hensen's stripe is missing and the marginal band appears abnormal. Null mutants show hearing loss but excitation of the outer hair cells and cochlear amplification are almost normal. | Contact | ||||||||||||
B6.129S-Tecta<tm1Gpr>/H |
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Homozygous mutant mice suffer hearing loss and have detatched tectorial membranes lacking all non-collagenous matrix. | Contact | ||||||||||||
B6.129S-Tecta<tm2Gpr>/H |
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Heterozygous mice suffer hearing loss and have tectorial membranes with a thin limbal attachment zone, missing marginal band and Hensen's stripe and large holes in the main body of the matrix. The subtectorial space above the inner hair cells is also enlarged. Heterozygous mice show elevated neural thresholds, broadened neural tuning and a decrease in sensitivity at the tip of the neural tuning curve. | Contact | ||||||||||||
B6.129S-Tectb<tm1Gpr>/H |
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Homozygous mutant mice suffer low frequency hearing loss and have normally attached tectorial membranes that lack striated sheet matrix. Hensen's stripe is missing and the marginal band is absent in the apical coil of the cochlea. Sharpness of high frequency tuning is enhanced. | Contact | ||||||||||||
B6.129S1-Gnas<tm2Kel>/H |
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There is a behavioural phenotype, response to novel environments as measured through activity in various tasks. | Contact | ||||||||||||
B6.129S2-Ctse<tm1Bchn>/H |
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Mice breed normally. No obvious phenotype has been described as yet but cathepsin E has been implicated in regulation of antigen processing, and other aspects of innate immunity. | Contact | ||||||||||||
B6.129S6-Cln3<tm1Nbm>/H |
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Mouse model of Juvenile onset Batten disease (Neuronal Ceroid Luipofuscinosis) | Contact | ||||||||||||
B6.129S6-Rhbdf2<tm1.1Mfm>/H |
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Contact | |||||||||||||
B6.129S6-Scn3a<tm1Jwo>/H |
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No obvious defects. | Contact | ||||||||||||
B6.C-Ndrg1<str>/H |
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Mice at first develop normally but around the age of 5-6 weeks develop a peripheral demyelinating neuropathy resulting in weakness of the hind limbs. This manifests as clasping hind legs when suspended by tail, marked tremor, inability to maintain normal posture. Signs progress rapidly at first, stabilise after 20 weeks. | Contact | ||||||||||||
B6.C3-Rab27a<ash> 129-Rab27b<tm1.2Seab>/SeabH |
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The stock has an abnormal coat colour pigmentation (ashen) due to the recessive mutation Rab27a<ash>. | Contact |