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Mol Cell Biol. 2001 Jun;21(11):3820-9.

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

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1
Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA.

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.

PMID:
11340173
PMCID:
PMC87041
DOI:
10.1128/MCB.21.11.3820-3829.2001
[Indexed for MEDLINE]
Free PMC Article
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