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JCI online early table of contents: Sept. 13, 2010
Date:9/13/2010

w York, New York.
Phone: 212.639.3573; E-mail: harrisok@mskcc.org.

View this article at: http://www.jci.org/articles/view/42442?key=7ef55d4a4ce9ffed3af0


EDITOR'S PICK Signaling hope for Polycystic Kidney Disease

Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a common genetic disease that results in chronic kidney failure. Although the genes responsible for ADPKD have been identified (PKD1, PKD2), relatively little is known about how mutations in these genes promote cyst growth molecularly. In this paper, scientists at Children's Hospital in Boston, lead by Jordon Kreidberg, investigated the signaling pathways that go awry in the disease using mouse kidney epithelial cells in which Pkd1 was genetically deleted. They found that the protein c-Met was hyperactive in Pkd1-deficient cells, resulting in increased mTOR signaling, a pathway that had previously been linked to cyst formation. The increase in c-Met activity was related to sequestration of the protein c-Cbl in a cellular compartment known as the golgi, which increased c-Met protein stability. In support of a critical role for c-Met activity in disease progression, pharmacological inhibition of c-Met decreased mTOR activity and blocked cyst formation in a mouse model of ADPKD, leading the authors to suggest that c-Met is a potential therapeutic target in patients with ADPKD.

TITLE:

Failure to ubiquitinate c-Met leads to hyperactivation of mTOR signaling in a mouse model of autosomal dominant polycystic kidney disease

AUTHOR CONTACT:

Jordan Kreidberg,
Children's Hospital, Boston, Massachusetts, USA.
Phone: 617.919.2959; Fax: 617.730.0129;
E-mail: Jordan.Kreidberg@childrens.harvard.edu.

View this article at:

Contact: Karen Honey
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
Source:Eurekalert

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