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TAF7 is a heat-inducible unstable protein and is required for sustained expression of heat shock protein genes.
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- Additional Information
- Source:
Publisher: Published by Blackwell Pub. on behalf of the Federation of European Biochemical Societies Country of Publication: England NLM ID: 101229646 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1742-4658 (Electronic) Linking ISSN: 1742464X NLM ISO Abbreviation: FEBS J Subsets: MEDLINE
- Publication Information:
Original Publication: Oxford, UK : Published by Blackwell Pub. on behalf of the Federation of European Biochemical Societies, c2005-
- Subject Terms:
- Abstract:
TATA-binding protein-associated factor 7 (TAF7), a dissociable component of the general transcription factor IID (TFIID), plays a role as a check-point regulator at the step of RNA polymerase II (Pol II) transcription initiation. Here, we focused on the role of TAF7 in heat-shocked cells, where its expression is induced by heat shock factor HSF1. TAF7 is a phosphoprotein, and the phosphorylation status is related to its interaction with TFIID and to its stability controlled by the ubiquitin-proteasome pathway. TAF7 is necessary for the prolonged expression of heat shock protein genes and for efficient recovery of heat-shocked cells. During sustained transcription, TAF7, presumably its TFIID-independent form, binds the promoter and enhances the levels of Pol II at the gene body but not the promoter. These results showed the novel function of TAF7 that is necessary for the transition from initiation to elongation in multiple-round transcription.
(© 2018 Federation of European Biochemical Societies.)
- Contributed Indexing:
Keywords: HSP; HSF1; TAF7; transcription; ubiquitin
- Accession Number:
0 (HSF1 protein, human)
0 (Heat Shock Transcription Factors)
0 (Heat-Shock Proteins)
0 (TAF7 protein, human)
0 (TATA-Binding Protein Associated Factors)
0 (Transcription Factor TFIID)
0 (Ubiquitin)
- Publication Date:
Date Created: 20180721 Date Completed: 20190610 Latest Revision: 20190613
- Publication Date:
20231215
- Accession Number:
10.1111/febs.14604
- Accession Number:
30028080
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