HiNF-P is a bifunctional regulator of cell cycle controlled histone H4 gene transcription

Cell cycle progression beyond the G1/S phase transition requires the activation of a transcription complex containing histone nuclear factor P (HiNF‐P) and nuclear protein mapped to ataxia telangiectasia (p220NPAT) in response to cyclin dependent kinase 2 (CDK2)/cyclin E signaling. We show here that...

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Bibliographic Details
Published in:Journal of cellular biochemistry 2007-05, Vol.101 (1), p.181-191
Main Authors: Mitra, Partha, Xie, Ronglin, Harper, J. Wade, Stein, Janet L., Stein, Gary S., van Wijnen, Andre J.
Format: Article
Language:English
Subjects:
Animals
CDK inhibitor
Cell Cycle
Cell Cycle Proteins - genetics
Cell Cycle Proteins - metabolism
Cell Line
Cell Line, Transformed
Cell Line, Tumor
Cell Transformation, Viral
Cercopithecus aethiops
COS Cells
Cyclin-Dependent Kinase Inhibitor p57 - genetics
Cyclin-Dependent Kinase Inhibitor p57 - metabolism
Genes, Reporter
HeLa Cells
HiNF-P
histone
Histones - genetics
Humans
KIP2
Luciferases - metabolism
NPAT
Nuclear Proteins - genetics
Nuclear Proteins - metabolism
p57
Promoter Regions, Genetic
Repressor Proteins - genetics
Repressor Proteins - metabolism
transcription factor
Transcription, Genetic
Transfection
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Summary:Cell cycle progression beyond the G1/S phase transition requires the activation of a transcription complex containing histone nuclear factor P (HiNF‐P) and nuclear protein mapped to ataxia telangiectasia (p220NPAT) in response to cyclin dependent kinase 2 (CDK2)/cyclin E signaling. We show here that the potent co‐activating properties of HiNF‐P/p220NPAT on the histone H4 gene promoter, which are evident in the majority of human cell types, are sporadically neutralized in distinct somatic cell lines. In cells where HiNF‐P and p220NPAT do not activate the H4 gene promoter, HiNF‐P instead represses transcription. Our data suggest that the cell type specific expression of the cyclin‐dependent kinase inhibitory (CKI) protein p57KIP2 inhibits the HiNF‐P dependent activation of the histone H4 promoter. We propose that, analogous to E2F proteins and other cell cycle regulatory proteins, HiNF‐P is a bifunctional transcriptional regulator that can activate or repress cell cycle controlled genes depending on the cellular context. J. Cell. Biochem. 101: 181–191, 2007. © 2006 Wiley‐Liss, Inc.
ISSN:0730-2312
1097-4644
DOI:10.1002/jcb.21157