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

view/43304?key=816259dd2d3d68f9ddd9


ONCOLOGY A new role for the protein MyD88 in tumor development

MyD88 is an adaptor protein in inflammatory signaling that has previously been implicated in inflammation-mediated tumor development. Renno Toufic and colleagues, at the University of Lyon, France, have now identified an additional role for MyD88 in cellular transformation, an event central to tumor formation, mediated by Ras, a common cancer-causing protein. They found that MyD88-deficient mice were resistant to Ras-dependent tumor formation, and that isolated MyD88-deficient cells were resistant to Ras-meditated transformation. Notably, this defect was not reliant on changes in inflammatory signaling. Further evidence linked MyD88 to human carcinogenesis, as it was highly expressed in a number of human tumor tissues, and reduction in MyD88 expression reduced proliferation rates in human tumor cell lines. This work suggests that in addition to its involvement in inflammatory pathways, MyD88 plays a cell-autonomous role in transformation.

TITLE:

Dual function of MyD88 in RAS signaling and inflammation, leading to mouse and human cell transformation

AUTHOR CONTACT:
Toufic Renno,
CNRS, Lyon, France.
Phone: 33.469.166.629; Fax: 33.469.166.660;
E-mail: renno@lyon.fnclcc.fr.

View this article at: http://www.jci.org/articles/view/42771?key=ee4b3bce94d50b626f16


NEPHROLOGY The role of complement in Dense Deposit Disease

The complement system is a key component of the innate immune system. However, chronic activation can result in deposition of complement activation products in the kidney, resulting in tissue injury. Dense Deposit Disease (DDD) is a severe kidney disease that has been associated with deficiency in factor H
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Contact: Karen Honey
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Journal of Clinical Investigation
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