Membrane-proximal domain of a disintegrin and metalloprotease-17 represents the putative molecular switch of its shedding activity operated by protein-disulfide isomerase

J Am Chem Soc. 2013 Apr 17;135(15):5776-81. doi: 10.1021/ja400340u. Epub 2013 Apr 5.

Abstract

A disintegrin and metalloprotease-17 (ADAM17) is a major sheddase responsible for the regulation of a wide range of biological processes, like cellular differentiation, regeneration, or cancer progression. Hitherto, the mechanism regulating the enzymatic activity of ADAM17 is poorly understood. Recently, protein-disulfide isomerase (PDI) was shown to interact with ADAM17 and to down-regulate its enzymatic activity. Here we demonstrate by NMR spectroscopy and tandem-mass spectrometry that PDI directly interacts with the membrane-proximal domain (MPD), a domain of ADAM17 involved in its dimerization and substrate recognition. PDI catalyzes an isomerization of disulfide bridges within the thioredoxin motif C600XXC603 of the MPD and results in a drastic structural change between an active open state and an inactive closed conformation. This conformational change of the MPD putatively acts as a molecular switch, facilitating a global reorientation of the extracellular domains in ADAM17 and regulating its shedding activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • ADAM Proteins / chemistry*
  • ADAM Proteins / metabolism*
  • ADAM17 Protein
  • Cell Membrane / metabolism*
  • Cysteine / chemistry
  • Humans
  • Isomerism
  • Models, Molecular
  • Protein Disulfide-Isomerases / metabolism*
  • Protein Structure, Tertiary

Substances

  • ADAM Proteins
  • ADAM17 Protein
  • ADAM17 protein, human
  • Protein Disulfide-Isomerases
  • Cysteine