| Title | Phenotype | Contact | |
|---|---|---|---|
| B6.129S-Ctse<129S/SvHsd>/H | 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 | 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 | Homozygous mutant mice suffer hearing loss and have detatched tectorial membranes lacking all non-collagenous matrix. | Contact | |
| B6.129S-Tecta<tm2Gpr>/H | 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 | 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 | There is a behavioural phenotype, response to novel environments as measured through activity in various tasks. | Contact | |
| B6.129S2-Ctse<tm1Bchn>/H | 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 | Mouse model of Juvenile onset Batten disease (Neuronal Ceroid Luipofuscinosis) | Contact | |
| B6.129S6-Scn3a<tm1Jwo>/H | No obvious defects. | Contact | |
| B6.C-Ndrg1<str>/H | 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 | The stock has an abnormal coat colour pigmentation (ashen) due to the recessive mutation Rab27a<ash>. | Contact | |
| B6.C3H;B6-Crh<m1H> | Heterozygous Crh<m1H> are obese, exhibit muscle wasting, thin skin, hair loss, elevated plasma and urinary corticosterone, hyperglycaemia, hyperinsulinaemia, hypercholesterolemia, hypertryglyceridemia and hyperleptinaemia. They also have low bone mineral density, hypercalcemia, hypercalciuria and decreased concentrations of plasma PTH and osteocalcin. Heterozygotes can be visibly distinguished from wild types at about 5-6 weeks of age by their short, skinny tails and scruffy coat. They also have thin skin and their hair starts to thin as they age. | Contact | |
| B6.CAnNCrl(C3)-Dync1i2<m1H>/EmcfH | Currently being tested, trend towards slight locomotor deficit, nothing significant so far. | Contact | |
| B6.CAnNCrl(C3H)-Dync1li1<m1Emcf>/H | Mouse not completely assessed but so far homozygotes have behavioural and neurological changes. | Contact | |
| B6.Cg-Cited2<L247P>/H | Although the amino acid change occurs in a highly conserved residue, the mutant is homozygous viable and fertile, with no detectable phenotype. In trans to the Knock-out allele, it is viable and phenotypically normal. | Contact | |
| B6.Cg-Ddx5<tm1.1Arte> Gt(ROSA)26Sor<tm9(cre/ESR1)Arte>/H | Mouse strain has no detectable phenotype in the absence of activated Cre. Tamoxifen treatment induces p68 knockout in multiple tissues; this results in hypoplastic bone marrow and alterations in tissue organisation in the large intestine of a high proportion of mice. However, we have only been able to perform short term experiments. These mice would be ideal for the generation of tissue-specific p68 knockout models. | Contact | |
| B6.Cg-Mrc2<tm1Cmi>Tg(CAG-EGFP)1Osb/CmiH | Homozygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. All of the tissues, with the exception of erythrocytes and hair, appear green under excitation light. | Contact | |
| B6.Cg-Syce1<tm1Hgu>/H | Mice homozygous for this mutation in this background can not progress to diplotene stages of meiosis and show a failure of synapsis. Heterozygous mice show close to normal fertility. | Contact | |
| B6.Cg-Syce2<Gt(FHCRC-GT-S8-7E1)Sor>/H | Mice homozygous for this mutation in this background can not progress to diplotene stages of meiosis and show a failure of synapsis. Heterozygous mice show close to normal fertility. | Contact | |
| B6.Cg-Tg(ACTFLPe)9205Dym/H | No overt phenotype. | Contact |
