Apc1638T: a mouse model delineating critical domains of the adenomatous polyposis coli protein involved in tumorigenesis and development

Article Abstract:

Apc1638T is a mouse model that delineates critical domains of the adenomatous polyposis coli (APC) protein involved in development and tumorigenesis. The APC gene is thought to be the actual gatekeeper of colonic epithelial proliferation. In more than half of colorectal tumors it is mutated and mutations take place at early stages of tumor development in man and mice. The mutant proteins do not have most of the seven 20-amino-acid repeats. All SAMP motifs that are associated with down-regulation of intracellular beta-catenin levels. It appears from generation of a mouse model with a targeted mutation at codon 1638 of the mouse Apc gene that the association of the SAMP motif with EB1, DLG and microtubulin is less critical for the maintenance of homeostasis by APC than had been thought. Proper beta-catenin regulation by APC likely is needed for normal embryonic development and tumor suppression.

Netherlands, Colorectal cancer, Mice, mutant strains, Mutant mice, Biological models, Carcinogenesis, Polyposis, Familial, Familial polyposis

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Somatic inactivation of Pkd2 results in polycystic kidney disease

Article Abstract:

The role of the Pkd2 protein in the pathogenesis of autosomal dominant polycystic kidney disease was investigated. A mutant exon 1 was introduced together with the wild-type exon 1 at the mouse Pkd2 locus. Results show that somatic inactivation of Pkd2 induces the onset of polycystic kidney disease. Renal cysts develop from renal tubular cells that do not have the capacity to produce Pkd2 protein. It was also found that Pkd2 occurs via a cellular recessive mechanism.

Development and progression, Polycystic kidney disease

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p27(super.Kip1) induction and inhibition of proliferation by the intracellular Ah receptor in developing thymus and hepatoma cells

Article Abstract:

The Ah receptor (AhR) mediates dioxin toxicity in skin, immune system, testis and liver, and inhibition/induction of proliferation by intracellular AhR has been studied in developing hepatoma and thymus cells. AhR is a basic helix-loop-helix (bHLH)/Paer/AhR/Arnt/Sim (PAS) transcription factor and induces the p27(super.Kip1) cyclin/cdk inhibitor by altering Kip1 transcription in a direct way with no need for ongoing cell proliferation or protein synthesis.

Germany, Statistical Data Included, Genetic regulation, Genetic transcription, Transcription (Genetics), Chromosome mapping, Protein kinases, Cell receptors, Messenger RNA, DNA binding proteins, Dioxin, Dioxins, Thymus, Thymus gland, Fetal tissues, Hepatoma, Hepatocellular carcinoma

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