Ubiquitination of p27 is regulated by Cdk-dependent phosphorylation and trimeric complex formation
Article Abstract:
Cdk-dependent phosphorylation and trimeric complex formation regulate ubiquitination of p27, acting as signals of a Cdk inhibitor. It has been shown that p27 ubiquitination is cell-cycle regulated, assayed in an in vitro reconstituted system and in vivo. Cdk activity is necessary for the in vitro ubiquitination of p27. Ubiquitination of wild-type p27 can take place in G(sub.1)-enriched extracts only with addition of cyclin A/Cdk2 or cyclin E/Cdk2, which is not true of p27 (T187A). Threonine 187 phosphorylation of p27 is cell-cycle dependent as well. Efficient p27 ubiquitination must have formation of a trimeric complex with the cyclin and Cdk subunits.
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 1999
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pX, the HBV-encoded coactivator, suppresses the phenotypes of TBP and TAFII250 mutants
Article Abstract:
Hepatitis B virus (HBV) brings on an assortment of clinical problems including hepatocellular carcinoma (HCC). The relationship between pX and cellular coactivators has been studied and it was found that pX restores wild-type activity to inactive TBPsubAS mutants with poor TAFII250 and activator-binding activity. It appears that pX suppresses some of the phenotypes of TBP and TAFII250 mutations. That would indicate that pX may get around the need for a holo-TFIID complex for transcription activation to proceed.
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 1998
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Stage-specific apoptosis, developmental delay, and embryonic lethality in mice homozygous for a targeted distruption in the murine Bloom's syndrome gene
Article Abstract:
Bloom's syndrome, the cause of dwarfism, is caused by genome instability and causes death by 13.5 days when introduced to mouse embryos. The embryos have displayed similar symptoms to those seen in humans with this genetic disorder, and this can be accounted for by a high rate of increased apoptosis and the appearance of micronuclei in red blood cells, which are probably caused by damaged DNA.
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 1998
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