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UCLA scientists find molecular switch to prevent Huntington's disease in mice
Date:12/24/2009

lation, the other to prevent it.

The researchers found that preventing phosphorylation caused the mice to develop symptoms suggestive of Huntington's disease in humans. Mimicking phosphorylation, however, did not cause the disorder.

These results in mice have striking parallels to experiments performed by collaborator Ron Wetzel, of the University of Pittsburgh, who found that mimicking phosphorylation of a toxic fragment of mutant huntingtin reduces the protein's tendency to form clumps.

A separate UC Irvine study by Steffan and Thompson also suggests that phosphorylation of mutant huntingtin may help cells dispose of the toxic form of mutant huntingtin. Combined, these studies suggest new directions of research to understand the roles of huntingtin misfolding, clumping and clearance in the disease mechanism.

"Our study identified a critical molecular switch which lies next to the polyQ mutation in the huntingtin protein," Yang said. "We were surprised to find that subtle modification of only two amino acids in this very large protein can prevent the onset of disease. This finding suggests an exciting new avenue to develop therapeutics for Huntington's disease."


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Contact: Elaine Schmidt Haber
ehaber@mednet.ucla.edu
310-794-2272
University of California - Los Angeles
Source:Eurekalert

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