Summary |
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Mutation origin |
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Mutation description |
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Phenotypes |
View phenotypes and curated references for all genotypes (concatenated display).
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Expression |
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Find Mice (IMSR) |
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Notes |
Tyrc-14CoS. This induced mutation was found at Oak Ridge National Laboratory. Homozygotes die neonatally (J:5063), and have deficiencies in activity of at least five liver enzymes, glucose-6-phosphatase, tyrosine aminotransferase, serine dehydratase, glutamine synthetase, and UDP-glucuronyltransferase, as well as low levels of liver microsomal cytochrome P-450 and the plasma proteins, albumin, a-fetoprotein, and transferrin (J:5715, J:5588, J:5730). Control of the level of two enzymes occurs at the transcriptional level; control of the level of the three plasma proteins occurs posttranscriptionally (J:7838, J:7840). There is a marked decrease in the number of receptors for insulin and glucocorticoids (J:6996) and for epidermal growth factor and glucagon (J:12047). Two specific liver polypeptides recognizable in two-dimensional gels are lacking (J:7420). The rough endoplasmic reticulum of the liver, and to a lesser extent of the kidneys, is dilated and vesiculated (J:5386). Complementation studies with other alleles have shown that this is probably the shortest of the six deletions (J:5435). It is known not to include the Mod2 locus (J:5437).
Compound heterozygotes carrying Tyrc-ch show dilution of the chinchilla pigmentation compared to homozygous chinchilla mice (Tyrc-ch/Tyrc-ch, J:5435). |
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References |
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 12/10/2024 MGI 6.24 |
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