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Blood, 1 July 2006, Vol. 108, No. 1, pp. 160-166. Prepublished online as a Blood First Edition Paper on March 14, 2006; DOI 10.1182/blood-2005-09-3706. This Article Full Text Full Text (PDF) Supplemental Figures and Videos All Versions of this Article: 2005-09-3706v1 108/1/160    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Leung, T. Articles by Robishaw, J. D. Search for Related Content PubMed PubMed Citation Articles by Leung, T. Articles by Robishaw, J. D. Related Collections Hemostasis, Thrombosis, and Vascular Biology Signal Transduction Free Research Articles Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Zebrafish G protein 2 is required for VEGF signaling during angiogenesis TinChung Leung, Hui Chen, Anna M. Stauffer, Kathryn E. Giger, Soniya Sinha, Eric J. Horstick, Jasper E. Humbert, Carl A. Hansen, and Janet D. Robishaw From the Weis Center for Research, Geisinger Health System, Danville, PA; and the Department of Biological and Allied Health Sciences, Bloomsburg University, Bloomsburg, PA. Vascular endothelial growth factor (VEGF) is a major mediator of pathologic angiogenesis, a process necessary for the formation of new blood vessels to support tumor growth. Historically, VEGF has been thought to signal via receptor tyrosine kinases, which are not typically considered to be G protein dependent. Here, we show that targeted knockdown of the G protein gng2 gene (G2) blocks the normal angiogenic process in developing zebrafish embryos. Moreover, loss of gng2 function inhibits the ability of VEGF to promote the angiogenic sprouting of blood vessels by attenuating VEGF induced phosphorylation of phospholipase C-gamma1 (PLC1) and serine/threonine kinase (AKT). Collectively, these results demonstrate a novel interaction between G2- and VEGF-dependent pathways to regulate the angiogenic process in a whole-animal model. Blocking VEGF function using a humanized anti-VEGF antibody has emerged as a promising treatment for colorectal, non-small lung cell, and breast cancers. However, this treatment may cause considerable side effects. Our findings provide a new opportunity for cotargeting G protein- and VEGF-dependent pathways to synergistically block pathologic angiogenesis, which may lead to a safer and more efficacious therapeutic regimen to fight cancer. (Blood. 2006;108:160-166) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: R. Bhattacharya, J. Kwon, X. Li, E. Wang, S. Patra, J. P. Bida, Z. Bajzer, L. Claesson-Welsh, and D. Mukhopadhyay Distinct role of PLC{beta}3 in VEGF-mediated directional migration and vascular sprouting J. Cell Sci., April 1, 2009; 122(7): 1025 - 1034. [Abstract] [Full Text] [PDF] Y. Alsayed, H. Ngo, J. Runnels, X. Leleu, U. K. Singha, C. M. Pitsillides, J. A. Spencer, T. Kimlinger, J. M. Ghobrial, X. Jia, et al. Mechanisms of regulation of CXCR4/SDF-1 (CXCL12)-dependent migration and homing in multiple myeloma Blood, April 1, 2007; 109(7): 2708 - 2717. [Abstract] [Full Text] [PDF]

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