NDLI: The Huntington's disease protein interacts with p53 and CREB-binding protein and represses transcription.

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The Huntington's disease protein interacts with p53 and CREB-binding protein and represses transcription.

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The Huntington's disease protein interacts with p53 and CREB-binding protein and represses transcription.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Thompson, L. M. Spasic-boskovic, O. Housman, D. E. Zhu, Y. Z. Steffan, J. S. Gohler, H. Wanker, E. E. Greenwald, M. Bates, G. P. Kazantsev, A.
Description	Author Affiliation: Steffan JS ( Department of Biological Chemistry, D240 Medical Sciences I, University of California, Irvine, CA 92697-1700, USA.);
Abstract	Huntington's Disease (HD) is caused by an expansion of a polyglutamine tract within the huntingtin (htt) protein. Pathogenesis in HD appears to include the cytoplasmic cleavage of htt and release of an amino-terminal fragment capable of nuclear localization. We have investigated potential consequences to nuclear function of a pathogenic amino-terminal region of htt (httex1p) including aggregation, protein-protein interactions, and transcription. httex1p was found to coaggregate with p53 in inclusions generated in cell culture and to interact with p53 in vitro and in cell culture. Expanded httex1p represses transcription of the p53-regulated promoters, p21(WAF1/CIP1) and MDR-1. httex1p was also found to interact in vitro with CREB-binding protein (CBP) and mSin3a, and CBP to localize to neuronal intranuclear inclusions in a transgenic mouse model of HD. These results raise the possibility that expanded repeat htt causes aberrant transcriptional regulation through its interaction with cellular transcription factors which may result in neuronal dysfunction and cell death in HD.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	12
Volume Number	97
Language	English
Publisher	National Academy of Sciences
Publisher Date	2000-07-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cyclic AMP Response Element-Binding Protein Physiology Huntington Disease Genetics Nerve Tissue Proteins Nuclear Proteins Repressor Proteins Tumor Suppressor Protein P53 Animals Cells, Cultured Mice Mice, Inbred C57BL Mice, Inbred CBA Mice, Transgenic Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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