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JCI online early table of contents: July 1, 2010
Date:7/1/2010

y patients with advanced squamous cell carcinoma to identify those that might benefit from antiTGF-beta therapies.

TITLE: Epigenetic downregulation of human disabled homolog 2 switches TGF-beta from a tumor suppressor to a tumor promoter

AUTHOR CONTACT:
Gareth J. Inman
Biomedical Research Institute, University of Dundee, Dundee, United Kingdom.
Phone: +44.1382.496696; Fax: +44.1382.669993; E-mail: g.j.inman@dundee.ac.uk.

View this article at: http://www.jci.org/articles/view/36125?key=9ba8f92e6a5c850ecf45


CARDIOVASCULAR DISEASE: Zebrafish help us understand human blood vessel disease in the brain

Cerebral cavernous malformation is a common human disease of the small blood vessels in the brain that often results in stroke, seizure, and brain hemorrhage. It is caused by genetic mutations that result in loss of function of any one of three proteins (CCM1, CCM2, and CCM3). These proteins cooperate during blood vessel development in mice and zebrafish, but the downstream molecules involved in this process have not been determined. A team of researchers, led by Mark Kahn, at the University of Pennsylvania, Philadelphia, has now determined that proteins known as STKs act downstream of CCM3 in zebrafish development and a new zebrafish model of cerebral cavernous malformation caused by mutations in CCM3. These data suggest that the functional role of CCM3 in zebrafish parallels its role in humans and that future studies in zebrafish will provide a way to better understand the role of this protein in human cerebral cavernous malformation as well as possible way to test the efficacy of new drugs designed to treat the disease.

TITLE: CCM3 signaling through sterile 20like kinases plays an essential role during zebrafish cardiovascular development and cerebral cavernous malf
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Contact: Karen Honey
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Journal of Clinical Investigation
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