Herzog J, et al. (2016) Cyclin-dependent kinase 5 stabilizes hypoxia-inducible factor-1α: a novel approach for inhibiting angiogenesis in hepatocellular carcinoma. Oncotarget 7, 27108-21 27027353

This page summarizes selected information from the record referenced above and curated into PhosphoSitePlus®, a comprehensive online resource for the study of protein post-translational modifications (NAR, 2015, 43:D512-20). To learn more about the scope of PhosphoSitePlus®, click here.

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S687-p - HIF1A (human) ▲

Modsite: TEksHPRsPNVLsVA SwissProt Entrez-Gene Orthologous residues HIF1A (human): S687‑p, HIF1A (mouse): S698‑p, HIF1A (rat): S687‑p Characterization Methods used to characterize site in vivo:  immunoprecipitation, mass spectrometry, mutation of modification site, phospho-antibody, western blotting Disease tissue studied:  liver cancer, hepatocellular carcinoma Relevant cell lines - cell types - tissues:  Huh7 (hepatic), HUVEC (endothelial) Cellular systems studied:  cell lines Species studied:  human Enzymes shown to modify site in vitro:  Type Enzyme KINASE CDK5 (human) Upstream Regulation Potential in vivo enzymes for site:  Type Enzyme Evidence Notes KINASE CDK5 (human) co-immunoprecipitation, phosphopeptide analysis Treatments, proteins and their effect on site modification:  Treatments Referenced Treatments Manipulated Protein Referenced Protein Effect Notes deferoxamine increase seliciclib decrease Downstream Regulation Effect of modification (function):  protein stabilization