ArticleMolecular and cellular biology2002
Activation of the mouse histone deacetylase 1 gene by cooperative histone phosphorylation and acetylation.
Article in Molecular and cellular biology, 2002. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
45 citing papers in PubMed, 81 citations in OpenAlex.
- STAT3/LKB1 controls metastatic prostate cancer by regulating mTORC1/CREB pathway.Molecular cancer · 2023Article
- Analysis of HDACi-Coupled Nanoparticles: Opportunities and Challenges.Methods in molecular biology (Clifton, N.J.) · 2023Article
- The HUSH complex controls brain architecture and protocadherin fidelity.Science advances · 2022Article
- Overexpression of peptidase inhibitor 16 attenuates angiotensin II-induced cardiac fibrosis via regulating HDAC1 of cardiac fibroblasts.Journal of cellular and molecular medicine · 2020Article
- STAT3-dependent analysis reveals PDK4 as independent predictor of recurrence in prostate cancer.Molecular systems biology · 2020Article
- Promoter conservation in HDACs points to functional implications.BMC genomics · 2019Article
- The C-Terminal Transactivation Domain of STAT1 Has a Gene-Specific Role in Transactivation and Cofactor Recruitment.Frontiers in immunology · 2018Article
- Tissue specific regulation of the chick Sox10E1 enhancer by different Sox family members.Developmental biology · 2017Article
- Transcriptome-wide effects of inverted SINEs on gene expression and their impact on RNA polymerase II activity.Genome biology · 2016Article
- A-type lamins bind both hetero- and euchromatin, the latter being regulated by lamina-associated polypeptide 2 alpha.Genome research · 2016Article
- Response to interferons and antibacterial innate immunity in the absence of tyrosine-phosphorylated STAT1.EMBO reports · 2016Article
- Essential Nonredundant Function of the Catalytic Activity of Histone Deacetylase 2 in Mouse Development.Molecular and cellular biology · 2016Article
- Desmin enters the nucleus of cardiac stem cells and modulates Nkx2.5 expression by participating in transcription factor complexes that interact with the nkx2.5 gene.Biology open · 2016Article
- Proliferation of progeria cells is enhanced by lamina-associated polypeptide 2α (LAP2α) through expression of extracellular matrix proteins.Genes & development · 2015Article
- H3S28 phosphorylation is a hallmark of the transcriptional response to cellular stress.Genome research · 2014Article
- A single allele of Hdac2 but not Hdac1 is sufficient for normal mouse brain development in the absence of its paralog.Development (Cambridge, England) · 2014Article
- Histone deacetylase classes I and II regulate Kaposi's sarcoma-associated herpesvirus reactivation.Journal of virology · 2014Article
- Article
- Divergent roles of HDAC1 and HDAC2 in the regulation of epidermal development and tumorigenesis.The EMBO journal · 2013Article
- Histone H3 phosphorylation - a versatile chromatin modification for different occasions.Biochimie · 2012Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylase 1 (HDAC1) is a major regulator of chromatin structure and gene expression. Tight control of HDAC1 expression is essential for normal cell cycle progression of mammalian cells. HDAC1 mRNA levels are regulated by growth factors and by changes in intracellular deacetylase activity levels. Stimulation of the mitogen-activated protein kinase cascade by anisomycin or growth factors, together with inhibition of deacetylases by trichostatin A (TSA), leads to stable histone H3 phosphoacetylation and strongly induced HDAC1 expression. In contrast, activation of the nucleosomal response by anisomycin alone results only in transient phosphoacetylation of histone H3 without affecting HDAC1 mRNA levels. The transcriptional induction of the HDAC1 gene by anisomycin and TSA is efficiently blocked by H89, an inhibitor of the nucleosomal response. Detailed studies of the kinetics of histone acetylation and phosphorylation show that the two modifications are synergistic and essential for induced HDAC1 transcription. Activation of the HDAC1 gene by anisomycin together with TSA or by growth factors is accompanied by phosphoacetylation of HDAC1 promoter-associated histone H3. Our results present evidence for a precise regulatory mechanism which allows induction of the HDAC1 gene in response to proliferation signals and modulation of HDAC1 expression dependent on intracellular deacetylase levels.
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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.