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

J Müllberg1, C T Rauch, M F Wolfson

  • 1Immunex Corporation, Seattle, WA 98101, USA. mullbergj@immunex.com

FEBS Letters
|January 20, 1997
PubMed

Insights

Researchers studied the shedding of soluble proteins like pro-tumor necrosis factor alpha (TNF alpha). Phorbol ester PMA stimulated release, while a metalloprotease inhibitor blocked it, suggesting enzyme involvement in protein shedding.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Enzymology

Background:

  • Soluble forms of certain proteins are generated through shedding.
  • Tumor necrosis factor alpha (TNF alpha) and other growth factors have soluble counterparts.

Purpose of the Study:

  • To investigate the mechanisms of soluble protein generation from COS-7 cells.
  • To identify factors influencing the shedding of pro-tumor necrosis factor alpha (pro-TNF alpha), Steel factor, IL-1R type II, and IL-2R alpha.

Main Methods:

  • Expression of pro-TNF alpha, Steel factor, IL-1R type II, and IL-2R alpha in COS-7 cells.
  • Treatment with phorbol ester PMA to stimulate protein release.
  • Inhibition studies using a hydroxamate-based metalloprotease inhibitor.
  • Analysis of COS-7 cell membrane proteolytic activity on synthetic pro-TNF alpha peptides.

Main Results:

  • The release of all four studied proteins was significantly enhanced by PMA.
  • A hydroxamate-based metalloprotease inhibitor completely blocked the shedding of these proteins.
  • COS-7 cell membranes exhibited proteolytic cleavage of pro-TNF alpha peptides with specificity similar to a known TNF alpha converting enzyme.

Conclusions:

  • The shedding of pro-TNF alpha, Steel factor, IL-1R type II, and IL-2R alpha from COS-7 cells is mediated by metalloproteases.
  • The enzyme responsible for shedding in COS-7 cells may be similar or identical to the TNF alpha converting enzyme found in human cells.

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