Search Criteria: Research Area is "Neurobiology Research: Alzheimer's Disease (Tau (Mapt) mutants)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 007251 | B6.129-Mapttm1Hnd/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by RT-PCR analysis of total brain RNA, Western blot analysis of total brain homogenates or immunostraining of coronal brain sections. Hippocampal neurons from homozygous embryos, in primary culture, have delayed axonal extension and shorter total dendritic length when compared to wildtype controls. Mitochondria in the primary culture cells cluster at the distal end of axons. The frequency and velocity of mitochondrial anterograde movements is increased. This mutant mouse strain may be useful in studies of neuronal development, axonogenesis, and organelle movement. | ||
| 005491 | B6.Cg-Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J | Repository- Live |
| Mice that are homozygous for the targeted allele and hemizygous for the transgene are viable and fertile. Although no endogenous mouse MAPT is detected, all six isoforms (including both 3R and 4R forms) of human MAPT are expressed. Hyperphosphorylated MAPT is detected in cell bodies and dendrites by three months of age. Paired helical filaments of aggregated insoluble MAPT can be isolated from brain tissue as early as two months of age. These mutant mice may be useful in studies examining the relationship between human MAPT and Alzheimer's disease pathogenesis In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 008169 | B6;C3-Tg(Prnp-MAPT*P301S)PS19Vle/J | Repository- Live |
| These transgenic mice express the P301S mutant human microtubule-associated protein tau, MAPT, under the direction of the mouse prion protein, Prnp, promoter. The expression of the mutant human MAPT is five-fold higher than the expression of the endogenous mouse MAPT protein. Hyperphosphorylated, insoluble mutant human MAPT protein in the brain accumulates with age causing decreased microtubule binding. At three months of age, transgenic mice exhibit clasping and limb retraction when lifted by the tail, which progresses to limb weakness. By 10 months of age the mice exhibit a hunched back and paralysis, followed by inability to feed. Transgenic mice have a median lifespan of approximately nine months with approximately 80% dying by 12 months. Histological analysis reveals neuron degeneration in hippocampus and ventricular dilatation (brain atrophy) by eight months of age, although significant neuron degeneration in the hippocampus occurs at approximately nine months of a
..... For more information please see the full descriiption on the strain data sheet | ||
| 004779 | STOCK Mapttm1(EGFP)Klt/J | Repository- Live |
| Mice that are homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. A knock-in of the EGFP coding sequence into the first exon disrupts expression of the Mapt gene and produces a cytoplasmic EGFP fused to the first 31 amino acids. No gene product (isoform proteins) is detected in whole brain lysates by Western blot analysis. EGFP signal is detected beginning at 9.0 days post coitum in the trigeminal ganglion and by 10.75 days post coitum fluorescent signal is detected throughout the developing central nervous system. EGFP expression persists to adult and closely patterns the expression of neuron specific beta-tubulin III, as detected by the TuJ1 antibody. The expression of cytoplasmic EGFP in the central nervous system of this mutant allows for non-invasive visualization of elongating nerve axons. | ||
| 003741 | B6D2-Tg(Prnp-MAPT)43Vle/J | Repository-Cryopreserved |
| These transgenic mice express the human fetal tau MAPT isoform under the direction of the mouse prion protein promoter. Hyperphosphorylated, insoluble MAPT protein is widely expressed in neurons of the CNS at levels approximately ten-fold higher than the endogenous mouse counterpart. Mice homozygous for the transgenic insert die at about three months of age. In the hemizygous mice intraneural inclusions that stain positive with T14, a monoclonal antibody specific for MAPT, are observed in brain and spinal cord tissue at 1 month of age. The number of inclusions increases until 6-9 months of age. Transmission electron microscopy studies of these inclusions reveals tightly packed aggregates of randomly arranged 10-20 nm straight filaments. Mice suffer progressive, age-dependant neuronal damage, motor weakness and gliosis. These mice recapitulate key features of tauopathies and provide a model for studying the underlying mechanism of related diseases such as FTDP-17, Alzheimer's and
..... For more information please see the full descriiption on the strain data sheet | ||
| 004808 | STOCK Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted allele and hemizygous for the transgene are viable and fertile. Although no endogenous mouse MAPT is detected, all six isoforms (including both 3R and 4R forms) of human MAPT are expressed. Hyperphosphorylated MAPT is detected in cell bodies and dendrites by three months of age. Paired helical filaments of aggregated insoluble MAPT can be isolated from brain tissue as early as two months of age. These mutant mice may be useful in studies examining the relationship between human MAPT and Alzheimer's disease pathogenesis. | ||
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