Further evidence for a common mechanism for shedding of cell surface proteins

FEBS Lett. 1997 Jan 20;401(2-3):235-8. doi: 10.1016/s0014-5793(96)01480-9.

Abstract

Pro-TNF alpha, Steel factor, type II IL-1R and IL-2R alpha were expressed in COS-7 cells and the generation of their soluble forms was examined. The release of all four proteins was strongly stimulated by the phorbol ester PMA and completely blocked by a hydroxamate-based inhibitor of metalloproteases. COS-7 cell membranes were found to cleave various synthetic pro-TNF alpha peptides with the same specificity as a partially purified TNF alpha converting enzyme purified from human monocytic cells, suggesting that the same enzyme may be responsible for at least some of the COS-7 cell shedding activity.

MeSH terms

  • Animals
  • COS Cells
  • Cell Line
  • Dipeptides / pharmacology
  • Humans
  • Hydroxamic Acids / pharmacology
  • Membrane Proteins / metabolism*
  • Receptors, Interleukin / metabolism
  • Stem Cell Factor / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Dipeptides
  • Hydroxamic Acids
  • Membrane Proteins
  • N-((2-(hydroxyaminocarbonyl)methyl)-4-methylpentanoyl)-3-(2'-naphthyl)alanylalanine, 2-aminoethylamide
  • Receptors, Interleukin
  • Stem Cell Factor
  • Tumor Necrosis Factor-alpha