Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2010 May;88(5):501-9.
doi: 10.1139/y10-030.

Involvement of insulin-like growth factor 1 receptor transactivation in endothelin-1-induced signaling in vascular smooth muscle cells

Affiliations
Review

Involvement of insulin-like growth factor 1 receptor transactivation in endothelin-1-induced signaling in vascular smooth muscle cells

Ali Bouallegue et al. Can J Physiol Pharmacol. 2010 May.

Abstract

Endothelin-1 (ET-1) is a potent vasoactive peptide that exerts hypertrophic, migratory, and mitogenic effects in vascular smooth muscle cells. ET-1-induced activation of several signaling events has been shown to mediate the cellular effects of ET-1. In the past several years, transactivation of growth factor receptor has gained much recognition in transducing the signaling responses of ET-1. Among various growth factor receptors studied, the involvement of epidermal growth factor receptor transactivation in triggering ET-1-induced responses has been studied in some detail. However, recent studies have implicated insulin-like growth factor 1 receptor transactivation in this process. There are also some suggestions for a role of the Src family of nonreceptor protein tyrosine kinases, such as c-Src, in transducing the signaling responses of vasoactive peptides. In this review, we will examine the contribution of both insulin-like growth factor 1 receptor and c-Src in mediating ET-1-induced signaling responses in vascular smooth muscle cells.

PubMed Disclaimer

Similar articles

Publication types

LinkOut - more resources