## Abstract Cell cycle progression into S phase requires the induction of histone gene expression to package newly synthesized DNA as chromatin. Cyclin E stimulation of CDK2 at the Restriction point late in G1 controls both histone gene expression by the p220^NPAT^/HiNF‐P pathway and initiation of
HiNF-P is a bifunctional regulator of cell cycle controlled histone H4 gene transcription
✍ Scribed by Partha Mitra; Ronglin Xie; J. Wade Harper; Janet L. Stein; Gary S. Stein; Andre J. van Wijnen
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- English
- Weight
- 289 KB
- Volume
- 101
- Category
- Article
- ISSN
- 0730-2312
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Cell cycle progression beyond the G~1~/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. J. Cell. Biochem. 101: 181–191, 2007. © 2006 Wiley‐Liss, Inc.
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