Title Phenotype Contact
STOCK Tg(Igf2/LacZ,H19)YZ17Aco/AcoH Investigating how expression of Igf2 and H19 are regulated is of relevance to understanding Beckwith Weidemann syndrome. The physiological impact of over expressing H19 is not fully characterised. Deletion of the intergenic region with Cre recombinase results in partial (mesoderm specific) reactivation of Igf2 LacZ expression following maternal transmission. Contact
STOCK Tg(Igf2/LacZ,H19)YZ20Aco/AcoH Investigating how expression of Igf2 and H19 are regulated is of relevance to understanding Beckwith Weidemann syndrome. The physiological impact of over?expressing H19 is not fully characterised. Contact
STOCK Tg(Igf2/LacZ,H19)YZ46Aco/H Investigating how expression of Igf2 and H19 are regulated is of relevance to understanding Beckwith Weidemann syndrome. The physiological impact of over expressing H19 is not fully characterised. Contact
STOCK Tg(Igf2/LacZ,H19)YZ8Aco/AcoH Investigating how expression of Igf2 and H19 are regulated is of relevance to understanding Beckwith Weidemann syndrome. The physiological impact of over expressing H19 is not fully characterised. The imprinted H19 gene is only expressed when transmitted through the maternal germline. After paternal transmission the gene is repressed. The Igf2 LacZ gene shows appropriate reciprocal imprinted behaviour (paternal allele specific expression, maternal repression). Contact
STOCK Tg(PRNP*)K6M6Pcg/Pcg Overexpression of transgenic kudu PrPC in brain and other tissues, in order to confer increased susceptibility to TSE diseases, including BSE, compared to wild-type mice. Contact
STOCK Tg(Prnp-SMN)92Ahmb/H These mice are aphenotypic Contact
STOCK Tg(SMN2)89Ahmb Smg6Tg(SMN1*delta5)1Pks Smn1<tm1Msd>/H Rescues post natal lethality of SMN2 low strain. Contact
STOCK Tg(SMN2)89Ahmb Smn1<tm1Msd> Tg(SMN1*E134K)1Tlbt/H Mice that are homozygous transgenic for SMN2 and SMN134K and heterozygous or Wt for the Smn knockout allele have no phenotype. Mice that are homozygous transgenic for SMN2 and SMN134K and homozygous deleted for the Smn knockout allele die at approximately P0. Contact
STOCK Tg(Vpreb1-IL2RB)F133Ilm/H No known effects Contact
STOCK Tmc1<dn>/WtsiH Deafness. Contact
STOCK Tmem255b<tm1a(EUCOMM)Hmgu>/H To see phenotype data (when available) visit www.mousephenotype.org Contact
STOCK Tpm1<tm1a(EUCOMM)Wtsi>/WtsiH To see phenotype data (when available) visit www.mousephenotype.org Contact
STOCK Trpm1<tm1a(KOMP)Wtsi>/H To see phenotype data (when available) visit www.mousephenotype.org Contact
STOCK Utrn<tm1Ked> Dmd<mdx> Tg(Ckm-Dmd*)11956Chmb/H Contact
STOCK Whrn<wi>/H Deaf, head tossing and circling. Whirler. Contact
STOCK Xpo4<Gt(PT1-ATG)3EVal>/H Phenotypically normal. Contact
STOCK Yod1<tm1aNarl>/H To see phenotype data (when available) visit www.mousephenotype.org Heterozygotes: males lose hair at 4 weeks of age, stated tat "recovery accompanies age". Contact
STOCK-Tecta<tm4.1Gpr> In Tecta<tm4.1Gpr>/<tm4.1Gpr> homozygotes the tectorial membrane is completely detached from the spiral limbus and is associated instead with the Reissner membrane. Tecta is readily detectable by immunofluorescence in the detached tectorial membrane. Heterozygotes: inner ear phenotype shows malformation of the tectorial membrane, ABR thresholds elevated by ~30 dB and an enhanced susceptibility to audiogenic seizure at low sound pressure levels. See PubMed 24363064 Legan et al Human Mol Genet 2013: Three deaf mice. Contact
STOCK-Tg(MMTV-VEGFB*)1Sjh/SjhH The offspring of hemizygous mothers, but not hemizygous fathers, die shortly after birth. The female transgenic mice have fewer blood vessels, less blood in the mammary tissue, and impaired alveolar coverage of the fat pad, and do not produce sufficient milk for nourishment of their pups. Contact
TAS6 Belly spot, white feet, head spot Contact

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