Hypoxia-inducible factor 1α protein expression is controlled by oxygen-regulated ubiquitination that is disrupted by deletions and missense mutations

dc.creatorSutter, Carrie Hayes
dc.creatorLaughner, Erik
dc.creatorSemenza, Gregg L.
dc.date2000-04-11
dc.date.accessioned2026-08-02T19:47:19Z
dc.descriptionHypoxia-inducible factor 1 (HIF-1) is a transcription factor that mediates cellular and systemic homeostatic responses to reduced O(2) availability in mammals, including angiogenesis, erythropoiesis, and glycolysis. HIF-1 activity is controlled by the O(2)-regulated expression of the HIF-1α subunit. Under nonhypoxic conditions, HIF-1α protein is subject to ubiquitination and proteasomal degradation. Here we report that missense mutations and/or deletions involving several different regions of HIF-1α result in constitutive expression and transcriptional activity in nonhypoxic cells. We demonstrate that hypoxia results in decreased ubiquitination of HIF-1α and that missense mutations increase HIF-1α expression under nonhypoxic conditions by blocking ubiquitination.
dc.identifierhttps://pmc.ncbi.nlm.nih.gov/articles/PMC18304/
dc.identifierhttps://pubmed.ncbi.nlm.nih.gov/10758161/
dc.identifierhttps://doi.org/10.1073/pnas.080072497
dc.identifier.urihttps://repo.dare.co.zw/handle/123456789/78043
dc.languageen
dc.publisherNational Academy of Sciences
dc.rightsCopyright © The National Academy of Sciences
dc.sourceProc Natl Acad Sci U S A
dc.subjectBiological Sciences
dc.titleHypoxia-inducible factor 1α protein expression is controlled by oxygen-regulated ubiquitination that is disrupted by deletions and missense mutations
dc.typeText

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