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

Jun Ichi Abe; Wenyi Che; Masanori Yoshizumi; Qunhua Huang; Michael Glassman; Shinsuke Ohta; Yun Wu; Ralph Arlinghaus; Bradford C. Berk

doi:10.1111/j.1749-6632.2001.tb03959.x

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

Jun Ichi Abe, Wenyi Che, Masanori Yoshizumi, Qunhua Huang, Michael Glassman, Shinsuke Ohta, Yun Wu, Ralph Arlinghaus, Bradford C. Berk

Pathology

Research output: Contribution to journal › Article › peer-review

5 Scopus citations

Abstract

Bcr gene was originally identified by its presence in the chimeric Bcr/Ab1 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-γ 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.

Original language	English (US)
Pages (from-to)	341-343
Number of pages	3
Journal	Annals of the New York Academy of Sciences
Volume	947
DOIs	https://doi.org/10.1111/j.1749-6632.2001.tb03959.x
State	Published - 2001

Keywords

Bcr
ERK1/2
Platelet-derived growth factor: PDGF
Raf-1
Ras
Vascular smooth muscle cells

ASJC Scopus subject areas

General Neuroscience
General Biochemistry, Genetics and Molecular Biology
History and Philosophy of Science

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10.1111/j.1749-6632.2001.tb03959.x

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title = "Bcr in vascular smooth muscle cells involvement of Ras and Raf-1 activation by Bcr",

abstract = "Bcr gene was originally identified by its presence in the chimeric Bcr/Ab1 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-γ 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.",

keywords = "Bcr, ERK1/2, Platelet-derived growth factor: PDGF, Raf-1, Ras, Vascular smooth muscle cells",

author = "Abe, {Jun Ichi} and Wenyi Che and Masanori Yoshizumi and Qunhua Huang and Michael Glassman and Shinsuke Ohta and Yun Wu and Ralph Arlinghaus and Berk, {Bradford C.}",

year = "2001",

doi = "10.1111/j.1749-6632.2001.tb03959.x",

language = "English (US)",

volume = "947",

pages = "341--343",

journal = "Annals of the New York Academy of Sciences",

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publisher = "Wiley-Blackwell",

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TY - JOUR

T1 - Bcr in vascular smooth muscle cells involvement of Ras and Raf-1 activation by Bcr

AU - Abe, Jun Ichi

AU - Che, Wenyi

AU - Yoshizumi, Masanori

AU - Huang, Qunhua

AU - Glassman, Michael

AU - Ohta, Shinsuke

AU - Wu, Yun

AU - Arlinghaus, Ralph

AU - Berk, Bradford C.

PY - 2001

Y1 - 2001

N2 - Bcr gene was originally identified by its presence in the chimeric Bcr/Ab1 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-γ 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.

AB - Bcr gene was originally identified by its presence in the chimeric Bcr/Ab1 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-γ 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.

KW - Bcr

KW - ERK1/2

KW - Platelet-derived growth factor: PDGF

KW - Raf-1

KW - Ras

KW - Vascular smooth muscle cells

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DO - 10.1111/j.1749-6632.2001.tb03959.x

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AN - SCOPUS:0035687118

SN - 0077-8923

VL - 947

SP - 341

EP - 343

JO - Annals of the New York Academy of Sciences

JF - Annals of the New York Academy of Sciences

ER -

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

Abstract

Keywords

ASJC Scopus subject areas

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