Document Detail


CREB-binding protein sequestration by expanded polyglutamine.
MedLine Citation:
PMID:  10958659     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Spinal and bulbar muscular atrophy (SBMA) is one of eight inherited neurodegenerative diseases known to be caused by CAG repeat expansion. The expansion results in an expanded polyglutamine tract, which likely confers a novel, toxic function to the affected protein. Cell culture and transgenic mouse studies have implicated the nucleus as a site for pathogenesis, suggesting that a critical nuclear factor or process is disrupted by the polyglutamine expansion. In this report we present evidence that CREB-binding protein (CBP), a transcriptional co-activator that orchestrates nuclear response to a variety of cell signaling cascades, is incorporated into nuclear inclusions formed by polyglutamine-containing proteins in cultured cells, transgenic mice and tissue from patients with SBMA. We also show CBP incorporation into nuclear inclusions formed in a cell culture model of another polyglutamine disease, spinocerebellar ataxia type 3. We present evidence that soluble levels of CBP are reduced in cells expressing expanded polyglutamine despite increased levels of CBP mRNA. Finally, we demonstrate that over-expression of CBP rescues cells from polyglutamine-mediated toxicity in neuronal cell culture. These data support a CBP-sequestration model of polyglutamine expansion disease.
Authors:
A McCampbell; J P Taylor; A A Taye; J Robitschek; M Li; J Walcott; D Merry; Y Chai; H Paulson; G Sobue; K H Fischbeck
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Human molecular genetics     Volume:  9     ISSN:  0964-6906     ISO Abbreviation:  Hum. Mol. Genet.     Publication Date:  2000 Sep 
Date Detail:
Created Date:  2000-09-29     Completed Date:  2000-11-21     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9208958     Medline TA:  Hum Mol Genet     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  2197-202     Citation Subset:  IM    
Affiliation:
Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 10 Center Drive, Building 10, Room 3B11, Bethesda, MD 20892-1250, USA. mccampba@ninds.nih.gov
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MeSH Terms
Descriptor/Qualifier:
Animals
CREB-Binding Protein
Cell Death / drug effects
Cell Line
Cell Nucleus / metabolism
Cells, Cultured
DNA-Binding Proteins
Fungal Proteins / metabolism
Green Fluorescent Proteins
Hela Cells
Humans
Luciferases / metabolism
Luminescent Proteins / metabolism
Machado-Joseph Disease / genetics,  metabolism
Male
Mice
Mice, Transgenic
Muscular Atrophy, Spinal / genetics,  metabolism
Nerve Tissue Proteins / metabolism
Nuclear Proteins / metabolism*
Peptides / metabolism*,  pharmacology
RNA, Messenger / metabolism
Repressor Proteins
Saccharomyces cerevisiae Proteins*
Scrotum / metabolism
Tetrazolium Salts / pharmacology
Thiazoles / pharmacology
Time Factors
Trans-Activators / metabolism*
Transcription Factors / metabolism
Transcription, Genetic
Trinucleotide Repeat Expansion*
Chemical
Reg. No./Substance:
0/CREBBP protein, human; 0/Crebbp protein, mouse; 0/DNA-Binding Proteins; 0/Fungal Proteins; 0/GAL4 protein, S cerevisiae; 0/Luminescent Proteins; 0/Mjd protein, mouse; 0/Nerve Tissue Proteins; 0/Nuclear Proteins; 0/Peptides; 0/RNA, Messenger; 0/Repressor Proteins; 0/Saccharomyces cerevisiae Proteins; 0/Tetrazolium Salts; 0/Thiazoles; 0/Trans-Activators; 0/Transcription Factors; 147336-22-9/Green Fluorescent Proteins; 26700-71-0/polyglutamine; 298-93-1/thiazolyl blue; EC 1.13.12.-/Luciferases; EC 2.3.1.48/CREB-Binding Protein; EC 3.4.22.-/ATXN3 protein, human

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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