Hydroxylation-Dependent Interaction of Substrates to the Von Hippel-Lindau Tumor Suppressor Protein (VHL)

Methods Mol Biol. 2016:1458:87-94. doi: 10.1007/978-1-4939-3801-8_7.

Abstract

Oxygen-dependent hydroxylation of critical proline residues, catalyzed by prolyl hydroxylase (PHD1-3) enzymes, is a crucial posttranslational modification (PTM) within the canonical hypoxia-inducible factor (HIF)-centric cellular oxygen-sensing pathway. Alteration of substrates in this way often leads to proteasomal degradation mediated by the von Hippel-Lindau Tumor Suppressor protein (VHL) containing E3-ubiquitin ligase complex known as ECV (Elongins B/C, CUL2, VHL). Here, we outline in vitro protocols to demonstrate the ability of VHL to bind to a prolyl-hydroxylated substrate.

Keywords: HIF1α; In vitro binding assay; In vitro hydroxylation; PHD; Proline; VHL.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Humans
  • Hydroxylation
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • In Vitro Techniques
  • Oxygen / metabolism
  • Proline / metabolism
  • Rabbits
  • Substrate Specificity
  • Von Hippel-Lindau Tumor Suppressor Protein / genetics
  • Von Hippel-Lindau Tumor Suppressor Protein / metabolism*

Substances

  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Proline
  • Von Hippel-Lindau Tumor Suppressor Protein
  • Oxygen

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