ArticleMolecular and cellular biology2003
Identification of HiNF-P, a key activator of cell cycle-controlled histone H4 genes at the onset of S phase.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 75 citations in OpenAlex.
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- Epigenetic-Mediated Regulation of Gene Expression for Biological Control and Cancer: Fidelity of Mechanisms Governing the Cell Cycle.Results and problems in cell differentiation · 2022Article
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- High-throughput single-cell chromatin accessibility CRISPR screens enable unbiased identification of regulatory networks in cancer.Nature communications · 2021Article
- HAT1 Coordinates Histone Production and Acetylation via H4 Promoter Binding.Molecular cell · 2019Article
- Higher order genomic organization and regulatory compartmentalization for cell cycle control at the G1/S-phase transition.Journal of cellular physiology · 2018Review
- Coordinating cell cycle-regulated histone gene expression through assembly and function of the Histone Locus Body.RNA biology · 2017Review
- Genome-wide screen of cell-cycle regulators in normal and tumor cells identifies a differential response to nucleosome depletion.Cell cycle (Georgetown, Tex.) · 2017Article
- Maternal expression and early induction of histone gene transcription factor Hinfp sustains development in pre-implantation embryos.Developmental biology · 2016Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
At the G(1)/S phase cell cycle transition, multiple histone genes are expressed to ensure that newly synthesized DNA is immediately packaged as chromatin. Here we have purified and functionally characterized the critical transcription factor HiNF-P, which is required for E2F-independent activation of the histone H4 multigene family. Using chromatin immunoprecipitation analysis and ligation-mediated PCR-assisted genomic sequencing, we show that HiNF-P interacts with conserved H4 cell cycle regulatory sequences in vivo. Antisense inhibition of HiNF-P reduces endogenous histone H4 gene expression. Furthermore, we find that HiNF-P utilizes NPAT/p220, a substrate of the cyclin E/cyclin-dependent kinase 2 (CDK2) kinase complex, as a key coactivator to enhance histone H4 gene transcription. The biological role of HiNF-P is reflected by impeded cell cycle progression into S phase upon antisense-mediated reduction of HiNF-P levels. Our results establish that HiNF-P is the ultimate link in a linear signaling pathway that is initiated with the growth factor-dependent induction of cyclin E/CDK2 kinase activity at the restriction point and culminates in the activation of histone H4 genes through HiNF-P at the G(1)/S phase transition.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.