Ann N Y Acad Sci. 2001 Dec;947:341-3.

Bcr in vascular smooth muscle cells involvement of Ras and Raf-1 activation by Bcr.

Abe JI, Che W, Yoshizumi M, Huang Q, Glassman M, Ohta S, Wu Y, Arlinghaus R, Berk BC.

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Center for Cardiovascular Research, University of Rochester, New York 14642, USA. jun-ichi_abe@urmc.rochester.edu

Abstract

Bcr gene was originally identified by its presence in the chimeric Bcr/Abl oncogene. In vascular smooth muscle cells, platelet-derived growth factor-BB (PDGF) stimulated Bcr kinase activity. The mutant PDGF receptor for PI3-K, but not for PLC-gamma binding sites, showed significantly reduced Bcr kinase activity. Bcr wild-type enhanced, whereas Bcr kinase negative form inhibited PDGF-stimulated ERK1/2 activity. A dominant negative Ras did not inhibit Bcr kinase activation, and overexpression of Bcr increased Ras/Raf-1 activity and DNA synthesis. These results demonstrated the importance of Bcr in PDGF-mediated events such as activation of Ras, Raf-1, and ERK1/2 and stimulation of DNA synthesis.

PMID:: 11795286; [PubMed - indexed for MEDLINE]

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