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|Title:||Regulation of gene expression by the hypoxia-inducible factors|
|Citation:||Molecular Interventions, 2002; 2(4):229-243|
|Publisher:||American Society for Pharmacology and Experimental Therapeutics (ASPET)|
|Organisation:||Centre for the Molecular Genetics of Development|
|Anthony O. Fedele, Murray L. Whitelaw, and Daniel J. Peet|
|Abstract:||Many molecular and physiological responses to hypoxia in mammals are controlled by the transcription factors Hypoxia-Inducible Factor-1α (HIF-1α) and HIF-2α. Their ability to promote the transcription of hypoxia-inducible genes is mediated by protein stability and regulation of a C-terminal transactivation domain. Oxygen-dependent hydroxylation of conserved proline and asparagine residues in HIF-α are required for targeting HIF-α to proteasomes for destruction, and for inhibiting its capacity for CBP/p300-dependent transactivation, respectively. In hypoxia, the O2 required for prolyl and asparaginyl hydroxylation is limiting, and HIF-α is thus stabilized and competent for transcription. Because these proteins participate in angiogenesis, glycolysis, programmed cell death, cancer, and ischemia, HIF-α and its mediators are attractive therapeutic targets.|
|Keywords:||Animals; Humans; Oxygen; Procollagen-Proline Dioxygenase; Asparagine; Proline; Transcription, Genetic; Gene Expression Regulation; Aryl Hydrocarbon Receptor Nuclear Translocator; Basic Helix-Loop-Helix Transcription Factors; Von Hippel-Lindau Tumor Suppressor Protein; Hypoxia-Inducible Factor 1, alpha Subunit|
|Description:||© 2002 American Society of Pharmacology and Experimental Therapeutics|
|Appears in Collections:||Molecular and Biomedical Science publications|
Centre for the Molecular Genetics of Development publications
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