HiNF-P is a bifunctional regulator of cell cycle controlled histone H4 gene transcription
Graduate School of Biomedical Sciences; Department of Cell Biology and Cancer Center
Medical Subject Headings
Animals; COS Cells; *Cell Cycle; Cell Cycle Proteins; Cell Line; Cell Line, Transformed; Cell Line, Tumor; Cell Transformation, Viral; Cercopithecus aethiops; Cyclin-Dependent Kinase Inhibitor p57; Genes, Reporter; Hela Cells; Histones; Humans; Luciferases; Nuclear Proteins; Promoter Regions (Genetics); Repressor Proteins; *Transcription, Genetic; Transfection
Life Sciences | Medicine and Health Sciences
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 (p220(NPAT)) in response to cyclin dependent kinase 2 (CDK2)/cyclin E signaling. We show here that the potent co-activating properties of HiNF-P/p220(NPAT) 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 p220(NPAT) 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 p57(KIP2) 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.
Rights and Permissions
Citation: J Cell Biochem. 2007 May 1;101(1):181-91. Link to article on publisher's site
DOI of Published Version
Journal of cellular biochemistry
Mitra, Partha; Xie, Ronglin; Harper, J. Wade; Stein, Janet L.; Stein, Gary S.; and Van Wijnen, Andre J., "HiNF-P is a bifunctional regulator of cell cycle controlled histone H4 gene transcription" (2006). GSBS Student Publications. 873.