Human Gene Set: RANKIN_ANGIOGENIC_TARGETS_OF_VHL_HIF2A_UP

For the Mouse gene set with the same name, see RANKIN_ANGIOGENIC_TARGETS_OF_VHL_HIF2A_UP

Standard name RANKIN_ANGIOGENIC_TARGETS_OF_VHL_HIF2A_UP
Systematic name M1336
Brief description Angiogenic genes up-regulated in hepatocytes after knockout of VHL and HIF2A [GeneID=7428;2034].
Full description or abstract The von Hippel-Lindau tumor suppressor pVHL regulates the stability of hypoxia-inducible factors (HIF)-1 and -2, oxygen-sensitive basic helix-loop-helix transcription factors, which mediate the hypoxic induction of angiogenic growth factors such as vascular endothelial growth factor. Loss of pVHL function results in constitutive activation of HIF-1 and HIF-2 and is associated with the development of highly vascularized tumors in multiple organs. We have used a conditional gene-targeting approach to investigate the relative contributions of HIF-1 and HIF-2 to VHL-associated vascular tumorigenesis in a mouse model of liver hemangiomas. Here we demonstrate genetically that conditional inactivation of HIF-2alpha suppressed the development of VHL-associated liver hemangiomas and that angiogenic gene expression in hepatocytes is predominantly regulated by HIF-2 and not by HIF-1. These findings suggest that HIF-2 is the dominant HIF in the pathogenesis of VHL-associated vascular tumors and that pharmacologic targeting of HIF-2 may be an effective strategy for their treatment.
Collection C2: Curated
      CGP: Chemical and Genetic Perturbations
Source publication Pubmed 18490920   Authors: Rankin EB,Rha J,Unger TL,Wu CH,Shutt HP,Johnson RS,Simon MC,Keith B,Haase VH
Exact source Fig 2b: red in B & C vs A
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Source species Mus musculus
Contributed by Jessica Robertson (MSigDB Team)
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Version history 3.1: First introduced

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