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P53 & Huntington's disease - a relationship?
June 26-27, 2000 - New York, New York
Prepared by Lisa J. Bain
Abstract
Following a report suggesting functional role for the tumor suppressor factor, p53, in Huntington's disease (HD), scientists who study p53 and its role in transcriptional regulation and tumor suppression joined with those that focus on HD to consider the p53-Huntington's connection. Research in Leslie Thompson's lab found that p53 interacts in vitro with the exon 1 protein (httexp1) and copurifies with p53 in cells grown in tissue culture. They also showed that expanded httexp1 interacts with the coactivator CREB binding protein (CBP) and the corepressor mSin3a; and that the expression of expanded httexp1 repressed transcription of genes regulated by p53. Discussion of the paper included suggestions for additional controls as well as other techniques to assess the effect of htt on transcriptional repression. There was also more general discussion about the effect of htt on apoptosis and nuclear inclusion formation, and whether a conformational change in the protein might play a role in neurodegeneration. Participants agreed that crossing one or more of the HD mice with a p53 null mouse would help clarify the role of p53 in HD and that further study is needed into the structure and function of both the mutant and the wild-type protein. Therapeutic implications of this research were also discussed.
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