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Signal transduction and oncogenesis by ErbB/HER receptors
Author(s): Marmor MD, Skaria KB, Yarden Y
Source: INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS    Volume: 58    Issue: 3    Pages: 903-913    Published: MAR 1 2004  
Times Cited: 128     References: 130     
Abstract: Growth factors enable cells to escape irradiation-induced death (apoptosis). One important family of growth factors share an epidermal growth factor motif, and all bind to ErbB transmembrane receptors. In response to growth factor ligands, ErbB receptor tyrosine kinases induce a variety of cellular responses, including proliferation, differentiation and motility. Signal transduction pathways are initiated upon ligand-induced receptor homo- or heterodimerization and activation of tyrosine kinase activity. The complement of induced signaling pathways, as well as their magnitude and duration, determines the biological outcome of signaling, and in turn, is regulated by the identity of the ligand and the receptor composition. Recent insights into the structural basis for receptor dimerization, as provided by crystallographic analysis, are described, as is the differential activation of signaling pathways and downregulatory mechanisms. Further, dysregulation of the ErbB network is implicated in a vareity of human cancers, and the nature of aberrant signaling through ErbB proteins, as well as current therapeutic approaches, are discussed, highlighting the role of the highly oncogenic ErbB-2 molecule. (C) 2004 Elsevier Inc.
Document Type: Proceedings Paper
Language: English
Reprint Address: Yarden, Y (reprint author), Weizmann Inst Sci, Dept Regulat Biol, IL-76100 Rehovot, Israel
Addresses:
1. Weizmann Inst Sci, Dept Regulat Biol, IL-76100 Rehovot, Israel
Publisher: ELSEVIER SCIENCE INC, 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
Subject Category: Oncology; Radiology, Nuclear Medicine & Medical Imaging
IDS Number: 773QP
ISSN: 0360-3016
DOI: 10.1016/j.ijrobp.2003.06.002
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