Abstract
The von Hippel-Lindau tumor suppressor protein (pVHL) has been shown to bind directly to the alpha subunits of the heterodimeric transcription factor HIF (hypoxia inducible factor). pVHL directs the polyubiquitination and, hence, destruction of HIF in the presence of oxygen. Loss of pVHL function leads to deregulation of HIF target genes, which play critical roles in angiogenesis.
MeSH terms
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Animals
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Aryl Hydrocarbon Receptor Nuclear Translocator
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Cell Cycle
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Cell Cycle Proteins / metabolism
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Chaperonin Containing TCP-1
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Chaperonins / metabolism
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Cullin Proteins*
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / metabolism
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Elongin
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Extracellular Matrix / metabolism
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Genes, Tumor Suppressor*
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Hypoxia-Inducible Factor 1
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Hypoxia-Inducible Factor 1, alpha Subunit
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Isoenzymes / metabolism
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Ligases*
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Nuclear Proteins / genetics
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Nuclear Proteins / metabolism
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Protein Kinase C / metabolism
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Proteins / genetics*
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Proteins / metabolism
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Receptors, Aryl Hydrocarbon*
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Transcription Factors / genetics
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Transcription Factors / metabolism
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Transcription, Genetic
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Tumor Suppressor Proteins*
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Ubiquitin-Protein Ligases*
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Ubiquitins / metabolism
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Von Hippel-Lindau Tumor Suppressor Protein
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von Hippel-Lindau Disease / genetics*
Substances
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CUL2 protein, human
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Cell Cycle Proteins
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Cullin Proteins
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DNA-Binding Proteins
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Elongin
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Hypoxia-Inducible Factor 1
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Hypoxia-Inducible Factor 1, alpha Subunit
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Isoenzymes
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Nuclear Proteins
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Proteins
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Receptors, Aryl Hydrocarbon
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Transcription Factors
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Tumor Suppressor Proteins
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Ubiquitins
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Aryl Hydrocarbon Receptor Nuclear Translocator
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Ubiquitin-Protein Ligases
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Von Hippel-Lindau Tumor Suppressor Protein
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Protein Kinase C
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Chaperonin Containing TCP-1
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Chaperonins
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Ligases