Related Experiment Video
Updated: Aug 20, 2026

Using a GFP-tagged TMEM184A Construct for Confirmation of Heparin Receptor Identity
Published on: February 17, 2017
Metalloproteinase-mediated shedding of heparin-binding EGF-like growth factor and its pathophysiological roles
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.
Related Concept Videos
Role of Matrix Metalloproteases in Degradation of ECM
A...
Mitogens and the Cell Cycle
Regulation of Angiogenesis and Blood Supply
Healing I: Introduction
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR activation may...
Anticoagulant Drugs: Low-Molecular-Weight Heparins

