p53, transcriptional repression and drug sensitivity

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p53, transcriptional repression and drug sensitivity

Deregulation of the cell cycle (cell division) has long been known to contribute to the induction of cancer. Similarly, disruption of protein synthesis (cell growth) has also been shown to lead to several pathological conditions including cancer. 1 The tumor suppressor p53 is pivotal in inducing cell cycle arrest in response to DNA damage, and it has recently been recognized that p53 also plays...

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Loss of p53 function through PAX-mediated transcriptional repression.

Direct interactions between the genes that regulate development and those which regulate the cell cycle would provide a mechanism by which numerous biological events could be better understood. We have identified a direct role for PAX5 in the control of p53 transcription. In primary human diffuse astrocytomas, PAX5 expression inversely correlated with p53 expression. The human p53 gene harbours...

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Adenovirus E1B oncoprotein tethers a transcriptional repression domain to p53.

Many DNA tumor viruses express a protein that inhibits transcriptional activation by the tumor-suppressing transcription factor p53. We report that adenovirus E1B 55K represses p53-mediated activation by a mechanism not described previously. E1B 55K binds p53 without displacing it from its DNA-binding site. A fusion of E1B 55K to the GAL4 DNA-binding domain represses transcription from a variet...

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E2F7, a novel target, is up-regulated by p53 and mediates DNA damage-dependent transcriptional repression.

The p53 tumor suppressor protein is a transcription factor that exerts its effects on the cell cycle via regulation of gene expression. Although the mechanism of p53-dependent transcriptional activation has been well-studied, the molecular basis for p53-mediated repression has been elusive. The E2F family of transcription factors has been implicated in regulation of cell cycle-related genes, wi...

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ژورنال

عنوان ژورنال: Cell Cycle

سال: 2010

ISSN: 1538-4101,1551-4005

DOI: 10.4161/cc.9.22.13927