Alternative splicing in angiogenesis: The vascular endothelial growth factor paradigm

Ladomery, M., Harper, S. J. and Bates, D. O. (2007) Alternative splicing in angiogenesis: The vascular endothelial growth factor paradigm. Cancer Letters, 249 (2). pp. 133-142. ISSN 0304-3835

Full text not available from this repository

Publisher's URL: http://dx.doi.org/10.1016/j.canlet.2006.08.015

Abstract

Alternative splicing, first discovered in the 1970s, has emerged as one of the key generators of proteomic diversity. Not surprisingly, alternative splicing is increasingly linked to the etiology of cancer. This is illustrated by vascular endothelial growth factor (VEGF), the dominant angiogenic factor. Recently, an antiangiogenic family of VEGF isoforms was discovered, and termed VEGFxxxb. VEGFxxxb isoforms arise from an alternative 3′ splice site in exon 8, and differ by a mere six amino acids at the C-terminus. These alternative six amino acids radically change the functional properties of VEGF. VEGFxxxb isoform expression is regulated in human tissues and development, and disregulated in many pathological states including cancer. Understanding what regulates VEGFxxxb alternative splicing, and therefore the balance of pro- and antiangiogenic isoforms is of great importance and will be explored in detail over the next few years.

Item Type:Article
Uncontrolled Keywords:alternative splicing, VEGF, angiogenesis, tumors, VEGF165b
Faculty/Department:Faculty of Health and Applied Sciences > Department of Biological, Biomedical and Analytical Sciences
ID Code:10893
Deposited By: A. Lawson
Deposited On:10 Aug 2010 13:34
Last Modified:12 Aug 2013 08:02

Request a change to this item

Copyright 2013 © UWE better together