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JCI early table of contents for Nov. 26, 2012
Date:11/26/2012

mulated angiogenesis. VEGF mediates angiogenesis by binding to a cell surface protein that instigates cellular changes that are required for blood vessel formation. Epsins are known to remove proteins from the cell surface, preventing their activation. Normally, the number of VEGF binding proteins (VEGFR) on the cell surface is tightly controlled, but Chen and colleagues found that mice lacking epsin1/2 had a greater number of VEGFR on the cell surface that led to extra VEGF signaling, abnormal tumor vasculature, and slower tumor growth. In a companion commentary, Nancy Klauber-DeMore of the University of North Carolina at Chapel Hill discusses how these findings could contribute to the development of epsin-based therapeutic targeting of tumor angiogenesis.

TITLE:
Endothelial epsin deficiency decreases tumor growth by enhancing VEGF signaling

AUTHOR CONTACT:
Hong Chen
Oklahoma Medical Research Foundation, Oklahoma City, OK, USA
Phone: 405-271-2750; E-mail: hong-chen@omrf.org

View this article at: http://www.jci.org/articles/view/64537?key=8b9e9a01382464f1fc75

ACCOMPANYING COMMENTARY

TITLE:
Are epsins a therapeutic target for tumor angiogenesis?

AUTHOR CONTACT:
Nancy Demore
University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
Phone: 919-216-9754; E-mail: nancy_demore@med.unc.edu

View this article at: http://www.jci.org/articles/view/66171?key=7e2e14d5e5eda41ede24


Mouse model explains how calcium channel mutation causes hypokalemic periodic paralysis

Hypokalemic periodic paralysis (HypoPP) is a skeletal muscle disorder that is characterized by episodes of severe mus
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Contact: Jillian Hurst
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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