Molecular cloning and functional analysis of Drosophila TAF110 reveal properties expected of coactivators
Article Abstract:
The gene that encodes the TATA-binding associated factor (TAF) protein was isolated for the first time and functionally characterized. Several Glu- and Ser/Thr-rich regions in TAF110 resemble the protein-protein interacting domains of the regulatory transcription factor Sp1, which is involved in transfer activation and multimerization. In addition, specific interaction was observed between TAF110 and the Glu-rich activating domains of Sp1 in Drosophila and yeast cells. These results indicate that TAF110 acts as a coactivator, providing the site for protein-protein contact between Sp1 and the genetic transcription factor TFIID complex.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1993
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In vitro analysis of Huntingtin-mediated transcriptional repression reveals multiple transcription factor targets
Article Abstract:
The development of a biochemically defined in vitro transcription assay that is responsive to mutant htt is reported. Both gene-specific activator protein Sp1 and selective components of the core transcription apparatus, including TFIIS and TFIIF, are direct targets inhibited by mutant htt in a polyglutamine dependent manner and the results suggest that a mutant htt-directed repression mechanism involving multiple specific components of the basal transcription apparatus.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 2005
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Transcriptional repression of PGC-1[alpha] by mutant huntingtin leads to mitochondrial dysfunction and neurodegeneration
Article Abstract:
A study was conducted to demonstrate that mutant huntingtin interferes with energy metabolism by transcriptional repression of PGC-1[alpha] that is peroxisome proliferator-activated receptor gamma coactivator-1 [alpha]. The results obtained indicate that inhibition of PGC-1[alpha] function by mutant huntingtin limits the ability of striatal neurons to adequately respond to metabolic demands in huntington's disease (HD).
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 2006
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