期刊
CURRENT PHARMACEUTICAL DESIGN
卷 15, 期 20, 页码 2288-2299出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/138161209788682442
关键词
ADAM10; disintegrin; metalloproteinase; inhibition; cancer; inflammation; erbB; Notch; signaling; CD44; FasL; E-cadherin; CD23; Chemokine; TNF alpha
资金
- NCI NIH HHS [R41 CA139856] Funding Source: Medline
- NIDDK NIH HHS [R01 DK063363, R01 DK059778] Funding Source: Medline
Both cancer and chronic inflammatory diseases are often marked by homeostatic signal transduction pathways run amok. Cleavage of membrane-bound substrates by extracellular metalloproteinases is frequently the rate limiting step in activating many of these pathways, resulting either in liberation of active ligands (shedding) or initiating further processing into bioactive cytoplasmic domains (regulated intramembrane proteolysis or RIP). ADAM10 is a member of the ADAM (A Disintegrin And Metalloproteinase) family of transmembrane metalloproteinases implicated in the RIPing and shedding of dozens of substrates that drive cancer progression and inflammatory disease, including Notch, E-cadherin, EGF, ErbB2 and inflammatory cytokines. ADAM10's emerging role as a significant contributor to these pathologies has led to intense interest in it as a potential drug target for disease treatment. Here we discuss some of the established functions of ADAM10 and the implications of its inhibition in disease progression.
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