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J Biomed Sci Eng. 2014 Dec 01;7(14):1105-1121. doi: 10.4236/jbise.2014.714109.

The P2Y.

Journal of biomedical science and engineering

Zhongji Liao, Chen Cao, Jianjie Wang, Virginia H Huxley, Olga Baker, Gary A Weisman, Laurie Erb

Affiliations

  1. Department of Medicine, University of California, San Diego, USA.
  2. Department of Biochemistry, Life Sciences Center, University of Missouri, Columbia, USA.
  3. Department of Biomedical Sciences, Missouri State University, Springfield, USA.
  4. Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, USA.
  5. School of Dentistry, University of Utah, Salt Lake City, USA.

PMID: 25657827 PMCID: PMC4314728 DOI: 10.4236/jbise.2014.714109

Abstract

Vascular endothelial cadherin (VE-cadherin) mediates homophylic adhesion between endothelial cells and is an important regulator of angiogenesis, blood vessel permeability and leukocyte trafficking. Rac1, a member of the Rho family of GTPases, controls VE-cadherin adhesion by acting downstream of several growth factors, including angiopoietin-1 and vascular endothelial growth factor (VEGF). Here we show that UTP-induced activation of the G

Keywords: Adherens Junctions; Endothelium; P2Y Receptors; Rac; VE-Cadherin

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