Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Gap Junction Protein Cx37 Interacts With Endothelial Nitric Oxide Synthase in Endothelial Cells

Gap Junction Protein Cx37 Interacts With Endothelial Nitric Oxide Synthase in Endothelial Cells Gap Junction Protein Cx37 Interacts With Endothelial Nitric Oxide Synthase in Endothelial Cells Anna Pfenniger, Jean-Paul Derouette, Vandana Verma, Xianming Lin, Bernard Foglia, Wanda Coombs, Isabelle Roth, Nathalie Satta, Sylvie Dunoyer-Geindre, Paul Sorgen, Steven Taffet, Brenda R. Kwak, Mario Delmar Objective—The gap junction protein connexin37 (Cx37) plays an important role in cell-cell communication in the vasculature. A C1019T Cx37 gene polymorphism, encoding a P319S substitution in the regulatory C terminus of Cx37 (Cx37CT), correlates with arterial stenosis and myocardial infarction in humans. This study was designed to identify potential binding partners for Cx37CT and to determine whether the polymorphism modified this interaction. Methods and Results—Using a high-throughput phage display, we retrieved 2 binding motifs for Cx37CT: WHK... [K,R]XP...and FHK... [K,R]XXP..., the first being more common for Cx37CT-319P and the second more common for Cx37CT-319S. One of the peptides (WHRTPRLPPPVP) showed 77.7% homology with residues 843 to 854 of endothelial nitric oxide synthase (eNOS). In vitro binding of this peptide or of the homologous eNOS sequence to both Cx37CT isoforms was confirmed by cross-linking and surface plasmon resonance. Electrophysiological analysis of Cx37 single channel activity in transfected N2a cells showed that eNOS-like and eNOS(843–854) increased the frequency of events with http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis, Thrombosis, and Vascular Biology Wolters Kluwer Health

Gap Junction Protein Cx37 Interacts With Endothelial Nitric Oxide Synthase in Endothelial Cells

Loading next page...
 
/lp/wolters-kluwer-health/gap-junction-protein-cx37-interacts-with-endothelial-nitric-oxide-iSID46vvYo
ISSN
1079-5642
eISSN
1524-4636
DOI
10.1161/ATVBAHA.109.200816
pmid
20081116
Publisher site
See Article on Publisher Site

Abstract

Gap Junction Protein Cx37 Interacts With Endothelial Nitric Oxide Synthase in Endothelial Cells Anna Pfenniger, Jean-Paul Derouette, Vandana Verma, Xianming Lin, Bernard Foglia, Wanda Coombs, Isabelle Roth, Nathalie Satta, Sylvie Dunoyer-Geindre, Paul Sorgen, Steven Taffet, Brenda R. Kwak, Mario Delmar Objective—The gap junction protein connexin37 (Cx37) plays an important role in cell-cell communication in the vasculature. A C1019T Cx37 gene polymorphism, encoding a P319S substitution in the regulatory C terminus of Cx37 (Cx37CT), correlates with arterial stenosis and myocardial infarction in humans. This study was designed to identify potential binding partners for Cx37CT and to determine whether the polymorphism modified this interaction. Methods and Results—Using a high-throughput phage display, we retrieved 2 binding motifs for Cx37CT: WHK... [K,R]XP...and FHK... [K,R]XXP..., the first being more common for Cx37CT-319P and the second more common for Cx37CT-319S. One of the peptides (WHRTPRLPPPVP) showed 77.7% homology with residues 843 to 854 of endothelial nitric oxide synthase (eNOS). In vitro binding of this peptide or of the homologous eNOS sequence to both Cx37CT isoforms was confirmed by cross-linking and surface plasmon resonance. Electrophysiological analysis of Cx37 single channel activity in transfected N2a cells showed that eNOS-like and eNOS(843–854) increased the frequency of events with

Journal

Arteriosclerosis, Thrombosis, and Vascular BiologyWolters Kluwer Health

Published: Apr 1, 2010

There are no references for this article.