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JCI online early table of contents: Nov. 15, 2010
Date:11/15/2010

pher Touloukian, at Indiana University School of Medicine, Indianapolis, has developed an approach that led to long-lived antitumor immune responses by CD4+ T cells in a mouse model of melanoma skin cancer. They hope that it might be possible to one day translate this approach for clinical benefit.

TITLE: Transplantation of mouse HSCs genetically modified to express a CD4-restricted TCR results in long-term immunity that destroys tumors and initiates spontaneous autoimmunity

AUTHOR CONTACT:
Christopher E. Touloukian
Indiana University School of Medicine, Indianapolis, Indiana, USA.
Phone: 317.278.9945; Fax: 317.274.7592; E-mail: ctoulouk@iupui.edu.

View this article at: http://www.jci.org/articles/view/43274?key=7bf052002ef6fdaf85a4


METABOLIC DISEASE: Uncovering new way to stop fat accumulation in mice

The most common cause of liver dysfunction in the United States is a condition known as nonalcoholic fatty liver disease (NAFLD). A form of NAFLD known as hepatic steatosis is associated with obesity and type 2 diabetes. It arises as a result of increased generation and accumulation of lipids (fats) in the liver. Renaud Dentin and colleagues, at Institut Cochin, France, have now provided new insight into the mechanisms underlying hepatic steatosis in mice. Specifically, they find a role for the proteins p300 and SIK2 in regulating lipid production in the liver. Taken together, all the data lead the authors to suggest that SIK2 activators and specific p300 inhibitors might provide new approaches to treating hepatic steatosis in individuals with obesity and type 2 diabetes.

TITLE: Salt-inducible kinase 2 links transcriptional coactivator p300 phosphorylation to the prevention of ChREBP-dependent hepatic steatosis in mice

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

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