Send to:

Choose Destination
See comment in PubMed Commons below
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.


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.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Bentham Science Publishers Ltd.
    Loading ...
    Write to the Help Desk