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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAwqrscrWb6ObLXGOAop0TeY3nfPwMXthxrW8eBfC8s5A#_5 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RAwqrscrWb6ObLXGOAop0TeY3nfPwMXthxrW8eBfC8s5A#_4 http://www.w3.org/ns/prov#value Notably, naturally occurring mutations cluster in hotspots and predominantly affect the elongin C and HIF-a interface regions of pVHL (Table 3 and Figure 2) [6]. The VHL-mediated proteolytic degradation of HIF suppresses a transcription programme that is normally engaged by HIF as part of the adaptive response of the cell to hypoxia, such as the activation of vascular endothelial growth factor (VEGF), which is a potent angiogenic factor that is involved in the formation and differentiation of blood vessels. Aberrant HIF control, therefore, partially helps to explain the highly vascular phenotype of VHL-null tumours. 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