Smith, GA, Fearnley, GW, Tomlinson, DC et al. (2 more authors) (2015) The cellular response to vascular endothelial growth factors requires co-ordinated signal transduction, trafficking and proteolysis. Bioscience Reports, 35 (5). e00253. ISSN 0144-8463
Abstract
VEGFs (vascular endothelial growth factors) are a family of conserved disulphide-linked soluble secretory glycoproteins found in higher eukaryotes. VEGFs mediate a wide range of responses in different tissues including metabolic homeostasis, cell proliferation, migration and tubulogenesis. Such responses are initiated by VEGF binding to soluble and membrane-bound VEGFRs (VEGF receptor tyrosine kinases) and co-receptors. VEGF and receptor splice isoform diversity further enhances complexity of membrane protein assembly and function in signal transduction pathways that control multiple cellular responses. Different signal transduction pathways are simultaneously activated by VEGFR-VEGF complexes with membrane trafficking along the endosome-lysosome network further modulating signal output from multiple enzymatic events associated with such pathways. Balancing VEGFR-VEGF signal transduction with trafficking and proteolysis is essential in controlling the intensity and duration of different intracellular signalling events. Dysfunction in VEGF-regulated signal transduction is important in chronic disease states including cancer, atherosclerosis and blindness. This family of growth factors and receptors is an important model system for understanding human disease pathology and developing new therapeutics for treating such ailments.
Metadata
Item Type: | Article |
---|---|
Authors/Creators: |
|
Copyright, Publisher and Additional Information: | © 2015, Authors. This is an open access article published by Portland Press. Limited and distributed under the Creative Commons Attribution Licence 3.0. |
Keywords: | Disease; Drugs; Isoforms; Membrane trafficking; Receptor tyrosine kinase; Signal transduction; Vascular endothelial growth factor (VEGF) |
Dates: |
|
Institution: | The University of Leeds |
Academic Units: | The University of Leeds > Faculty of Biological Sciences (Leeds) > School of Molecular and Cellular Biology (Leeds) |
Funding Information: | Funder Grant number Heart Research UK RG2612/12/15 British Heart Foundation FS/12/20/29462 |
Depositing User: | Symplectic Publications |
Date Deposited: | 25 Aug 2015 10:18 |
Last Modified: | 06 Dec 2018 17:48 |
Published Version: | http://dx.doi.org/10.1042/BSR20150171 |
Status: | Published |
Publisher: | Portland Press |
Identification Number: | 10.1042/BSR20150171 |
Open Archives Initiative ID (OAI ID): | oai:eprints.whiterose.ac.uk:89251 |