ArticleProceedings of the National Academy of Sciences of the United States of America2009
The histone gene activator HINFP is a nonredundant cyclin E/CDK2 effector during early embryonic cell cycles.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 33 citations in OpenAlex.
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- Integration of TE Induces Cancer Specific Alternative Splicing Events.International journal of molecular sciences · 2022Review
- Transcriptome analysis of fasudil treatment in the APPswe/PSEN1dE9 transgenic (APP/PS1) mice model of Alzheimer's disease.Scientific reports · 2022Article
- Loss of a newly discovered microRNA in Chinese hamster ovary cells leads to upregulation of N-glycolylneuraminic acid sialylation on monoclonal antibodies.Biotechnology and bioengineering · 2022Article
- 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
- Epigenetic-Mediated Regulation of Gene Expression for Biological Control and Cancer: Cell and Tissue Structure, Function, and Phenotype.Results and problems in cell differentiation · 2022Review
- Hinfp is a guardian of the somatic genome by repressing transposable elements.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- ELL Facilitates RNA Polymerase II-Mediated Transcription of Human Epidermal Proliferation Genes.The Journal of investigative dermatology · 2021Article
- A Survey of Essential Genome Stability Genes Reveals That Replication Stress Mitigation Is Critical for Peri-Implantation Embryogenesis.Frontiers in cell and developmental biology · 2020Review
- Total Functional Score of Enhancer Elements Identifies Lineage-Specific Enhancers That Drive Differentiation of Pancreatic Cells.Bioinformatics and biology insights · 2020Article
- Higher order genomic organization and regulatory compartmentalization for cell cycle control at the G1/S-phase transition.Journal of cellular physiology · 2018Review
- Maternal expression and early induction of histone gene transcription factor Hinfp sustains development in pre-implantation embryos.Developmental biology · 2016Article
- Cell cycle gene expression networks discovered using systems biology: Significance in carcinogenesis.Journal of cellular physiology · 2015Article
- p53 checkpoint ablation exacerbates the phenotype of Hinfp dependent histone H4 deficiency.Cell cycle (Georgetown, Tex.) · 2015Article
- Fidelity of histone gene regulation is obligatory for genome replication and stability.Molecular and cellular biology · 2014Article
- A screen of zebrafish mutants identifies ethanol-sensitive genetic loci.Alcoholism, clinical and experimental research · 2014Article
- Article
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
Abstract
Competency for DNA replication is functionally coupled to the activation of histone gene expression at the onset of S phase to form chromatin. Human histone nuclear factor P (HiNF-P; gene symbol HINFP) bound to its cyclin E/cyclin-dependent kinase 2 (CDK2) responsive coactivator p220(NPAT) is a key regulator of multiple human histone H4 genes that encode a major subunit of the nucleosome. Induction of the histone H4 transcription factor (HINFP)/p220(NPAT) coactivation complex occurs in parallel with the CDK-dependent release of pRB from E2F at the restriction point. Here, we show that the downstream CDK-dependent cell cycle effector HINFP is genetically required and, in contrast to the CDK2/cyclin E complex, cannot be compensated. We constructed a mouse Hinfp-null mutation and found that heterozygous Hinfp mice survive, indicating that 1 allele suffices for embryogenesis. Homozygous loss-of-function causes embryonic lethality: No homozygous Hinfp-null mice are obtained at or beyond embryonic day (E) 6.5. In blastocyst cultures, Hinfp-null embryos exhibit a delay in hatching, abnormal growth, and loss of histone H4 gene expression. Our data indicate that the CDK2/cyclin E/p220(NPAT)/HINFP/histone gene signaling pathway at the G1/S phase transition is an essential, nonredundant cell cycle regulatory mechanism that is established early in embryogenesis.
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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.