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JCI online early table of contents: Dec. 19, 2011
Date:12/19/2011

a-cell survival. Importantly, in a mouse model of type 1 diabetes, production of an active heparan sulfatedegrading protein (heparanase) was associated with beta-cell destruction, while treatment with an inhibitor of heparanase protected the mice from disease. Simeonovic and colleagues therefore suggest that maintaining expression of heparan sulfate on beta-cells could provide a new approach to preventing the development of type 1 diabetes.

TITLE: Heparan sulfate and heparanase play key roles in mouse beta-cell survival and autoimmune diabetes

AUTHOR CONTACT:
Charmaine J. Simeonovic
The John Curtin School of Medical Research, The Australian National University, Canberra, Australia.
Phone: 61-2-6125-4709; Fax: 61-2-6125-2595; E-mail: Charmaine.Simeonovic@anu.edu.au.

View this article at: http://www.jci.org/articles/view/46177?key=f37890b794c1c03854d8

GENETICS: Linking genetic variation to changes in protein function

Many common human diseases, including type 2 diabetes, are thought to arise as a result of both genetic and environmental factors. It is hoped that defining the genetic component of such diseases could provide not only insight into cause but also candidate therapeutic approaches. In this context, variants of the GCKR gene have been suggested to be clinically important, with some linked to type 2 diabetes. However, how these variants affect protein function and influence disease has not been determined. Now, a team of researchers led by Francis Collins, at the National Human Genome Research Institute, Bethesda, has characterized the function of a large number of variants of the GCKR gene. The data generated indicate that the majority of the GCKR variants tested do affect protein function and are likely to provide an important genetic component of several clinica
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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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