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Hypoxia represents one of the most physiologically relevant stresses, having significant roles in both normal development and malignant progression. Exposure to severe hypoxia leads to the accumulation of p53 which can in turn lead to rapid apoptosis. In contrast to the response to DNA-damaging agents, hypoxia-induced p53 has little or no transcriptional transactivation capabilities and instead seems to function primarily as a transrepressor in order to induce apoptosis.

Original publication

DOI

10.1016/j.bbrc.2005.03.154

Type

Journal article

Journal

Biochem Biophys Res Commun

Publication Date

10/06/2005

Volume

331

Pages

718 - 725

Keywords

Animals, Apoptosis, Cell Hypoxia, Cell Line, Tumor, DNA Damage, DNA-Binding Proteins, Gene Expression Regulation, Humans, Hypoxia, Hypoxia-Inducible Factor 1, Hypoxia-Inducible Factor 1, alpha Subunit, Mice, Neoplasms, Nuclear Proteins, Phosphorylation, Repressor Proteins, Transcription Factors, Transcriptional Activation, Tumor Suppressor Protein p53