Loss of HCF-1-chromatin association precedes temperature-induced growth arrest of tsBN67 cells.

Details

Serval ID
serval:BIB_514D1E31F48B
Type
Article: article from journal or magazin.
Collection
Publications
Title
Loss of HCF-1-chromatin association precedes temperature-induced growth arrest of tsBN67 cells.
Journal
Molecular and cellular biology
Author(s)
Wysocka J., Reilly P.T., Herr W.
ISSN
0270-7306
Publication state
Published
Issued date
06/2001
Peer-reviewed
Oui
Volume
21
Number
11
Pages
3820-3829
Language
english
Abstract
Human HCF-1 is a large, highly conserved, and abundant nuclear protein that plays an important but unknown role in cell proliferation. It also plays a role in activation of herpes simplex virus immediate-early gene transcription by the viral regulatory protein VP16. A single proline-to-serine substitution in the HCF-1 VP16 interaction domain causes a temperature-induced arrest of cell proliferation in hamster tsBN67 cells and prevents transcriptional activation by VP16. We show here that HCF-1 is naturally bound to chromatin in uninfected cells through its VP16 interaction domain. HCF-1 is chromatin bound in tsBN67 cells at permissive temperature but dissociates from chromatin before tsBN67 cells stop proliferating at the nonpermissive temperature, suggesting that loss of HCF-1 chromatin association is the primary cause of the temperature-induced tsBN67 cell proliferation arrest. We propose that the role of HCF-1 in cell proliferation is to regulate gene transcription by associating with a multiplicity of DNA-bound transcription factors through its VP16 interaction domain.
Keywords
Animals, Cell Division, Cell Line, Chromatin, Cricetinae, Hela Cells, Host Cell Factor C1, Humans, Nuclear Proteins, Proteins, Temperature, Transcription Factors
Pubmed
Web of science
Open Access
Yes
Create date
24/01/2008 16:36
Last modification date
20/08/2019 15:07
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