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

Partha Mitra, Ronglin Xie, J. Wade Harper, Janet L. Stein, Gary S. Stein, Andre J. Van Wijnen

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


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/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.

Original languageEnglish (US)
Pages (from-to)181-191
Number of pages11
JournalJournal of cellular biochemistry
Issue number1
StatePublished - May 1 2007


  • CDK inhibitor
  • Cell cycle
  • HiNF-P
  • Histone
  • KIP2
  • NPAT
  • Transcription factor
  • p57

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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