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Protein Pept Lett. 2004 Oct;11(5):443-50.

Metalloproteinase-mediated shedding of heparin-binding EGF-like growth factor and its pathophysiological roles.

Author information

  • 1Division of Biochemistry and Molecular Genetics, Department of Molecular and Cellular Biology, Ehime University School of Medicine Shigenobu, Onsen-gun, Ehime, 791-0295, Japan. shigeki@m.ehime-u.ac.jp

Abstract

Heparin-binding EGF-like growth factor (HB-EGF) exists as a membrane-anchored form (proHB-EGF) and as its soluble cleaved product (sHB-EGF). The conversion (ectodomain shedding) of proHB-EGF to sHB-EGF is tightly regulated by specific metalloproteinases. Ectodomain shedding plays a central role in GPCR-mediated EGFR transactivation. Antagonizing metalloproteinases can inhibit EGFR transactivation and might be of therapeutic value, for example in cardiac hypertrophy, skin remodeling and tumor growth.

PMID:
15544565
[PubMed - indexed for MEDLINE]
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