Search Criteria: Research Area is "Neurobiology Research: Fragile X Mental Retardation Syndrome"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 013760 | C57BL/6-Tg(Camk2a-AIDPak)21Stl/J | Repository- Live |
| dnPAK transgenic mice have a mouse calcium/calmodulin-dependent protein kinase II alpha (Camk2a) promoter directing postnatal forebrain expression of the mouse dominant negative (dn) autoinhibitory domain (AID) of p21 protein (Cdc42/Rac)-activated kinase (Pak) gene (dnPAK). The AID is conserved in all three Pak genes (Pak1, Pak2, Pak3). Homozygous dnPAK mice are viable, fertile, and normal in size. Pak genes are expressed in multiple brain regions, including the cortex and hippocampus, and are critical regulators of actin remodeling. The activation of PAK catalytic activity requires the release of the catalytic domain from the AID and autophosphorylation of a gene specific threonine residue. dnPAK binds to the catalytic domain of PAK and blocks autophosphorylation, inhibiting activation of catalytic activity. dnPAK overexpression causes a decrease in the number of and increase is the size of cortical neuron dendri ..... For more information please see the full phenotype on the strain data sheet | ||
| 004624 | FVB.129P2-Pde6b+ Tyrc-ch Fmr1tm1Cgr/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable and fertile. Quantitative morphological analysis of dendritic spines of visual cortex pyramidal cells reveals mutant mice have more long dendritic spines, fewer short dendritic spines and more spines with an immature morphology than wildtype littermates. These mice were backcrossed for 11 generations onto the FVB background, are homozygous for the 129P2/OlaHsd wildtype Pde6b allele and do not suffer from blindness due to retinal degeneration. This mutant mouse strain may be useful in studies related to Fragile X Syndrome. | ||
| 010504 | B6.129-Fmr1tm1Rbd/J | Cryopreserved - Ready for recovery |
| These mice recapitulate the phenotype of null allele mice in terms of increased macroorchidism with age, protein synthesis-dependent metabotropic glutamate receptor (mGluR)-dependent long-term depression (LTD) at CA1 hippocampal neurons, and performance in multiple behavioral assays. There is a significant incidence of audiogenic seizures in adulthood. Their mRNA is of correct size and is expressed at correct levels, but protein levels are decreased to 15-30% that of wildtype, most pronounced at postnatal day 14 (P14) and normalizing somewhat in adulthood. This strain may be useful in studies of Fragile X Mental Retardation Syndrome. | ||
| 003025 | B6.129P2-Fmr1tm1Cgr/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Fmr1tm1Cg targeted mutation show macroorchidism (enlarged testes), learning deficits, and hyperactivity. Macroorchidism in caused by an increased rate of Sertoli cell proliferation during embryogenesis which may be independent of FSH signalling. Comparison of homozygotes to wildtype littermates in hidden- and visible-platform water maze learning showed deficits in spatial learning and motor performance. | ||
| 008909 | FVB.129-Fmr1tm1Rbd/J | Cryopreserved - Ready for recovery |
| These mice recapitulate the phenotype of null allele mice in terms of increased macroorchidism with age, protein synthesis-dependent metabotropic glutamate receptor (mGluR)-dependent long-term depression (LTD) at CA1 hippocampal neurons, and multiple behavioral assays. There is a significant incidence of audiogenic seizures in adulthood. Their mRNA is of correct size and is expressed at correct levels, but protein levels are decreased to 15-30% that of wildtype, most pronounced at postnatal day 14 (P14) and normalizing somewhat in adulthood. This strain may be useful in studies of Fragile X Mental Retardation Syndrome. | ||
| 003024 | FVB.129P2(B6)-Fmr1tm1Cgr/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Fmr1tm1Cg targeted mutation show macroorchidism (enlarged testes), learning deficits, and hyperactivity. Macroorchidism in caused by an increased rate of Sertoli cell proliferation during embryogenesis which may be independent of FSH signalling. Comparison of homozygotes to wildtype littermates in hidden- and visible-platform water maze learning showed deficits in spatial learning and motor performance. | ||
| 002700 | FVB;129P-Fmr1tm1Cgr/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Fmr1tm1Cg targeted mutation show macroorchidism (enlarged testes), learning deficits, and hyperactivity. Macroorchidism in caused by an increased rate of Sertoli cell proliferation during embryogenesis which may be independent of FSH signalling. Comparison of homozygotes to wildtype littermates in hidden- and visible-platform water maze learning showed deficits in spatial learning and motor performance. | ||
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