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• W2157496543 endingPage "4641" @default.
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• W2157496543 abstract "The hypoxia-inducible factor-1α (HIF-1α) is a transcription factor that mediates adaptive cellular responses to decreased oxygen availability (hypoxia). At normoxia, HIF-1α is targeted by the von Hippel-Lindau tumor suppressor protein (pVHL) for degradation by the ubiquitin-proteasome pathway. In the present study we have observed distinct cell-type-specific differences in the ability of various tested pVHL-interacting subfragments to stabilize HIF-1α and unmask its function at normoxia. These properties correlated with differences in subcellular compartmentalization and degradation of HIF-1α. We observed that the absence or presence of nuclear localization or export signals differently affected the ability of a minimal HIF-1α peptide spanning residues 559 to 573 of mouse HIF-1α to stabilize endogenous HIFα and induce HIF-driven reporter gene activity in two different cell types (primary mouse endothelial and HepG2 hepatoma cells). Degradation of HIF-1α occurred mainly in the cytoplasm of HepG2 cells, whereas it occurs with equal efficiency in nuclear and cytoplasmic compartments of primary endothelial cells. Consistent with these observations, green fluorescent protein-HIF-1α is differently distributed during hypoxia and reoxygenation in hepatoma and endothelial cells. Consequently, we propose that differential compartmentalization of degradation of HIF-1α and the subcellular distribution of HIF-1α may account for cell-type-specific differences in stabilizing HIF-1α protein levels under hypoxic conditions." @default.
• W2157496543 created "2016-06-24" @default.
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• W2157496543 date "2006-06-01" @default.
• W2157496543 modified "2023-10-16" @default.
• W2157496543 title "Cell-Type-Specific Regulation of Degradation of Hypoxia-Inducible Factor 1α: Role of Subcellular Compartmentalization" @default.
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• W2157496543 doi "https://doi.org/10.1128/mcb.02236-05" @default.
• W2157496543 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1489139" @default.
• W2157496543 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16738327" @default.
• W2157496543 hasPublicationYear "2006" @default.
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