ArticleExperimental & molecular medicine2010
ATM modulates transcription in response to histone deacetylase inhibition as part of its DNA damage response.
Article in Experimental & molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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
20 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Discovery of a Novel and Potent Dual-Targeting Inhibitor of ATM and HDAC2 Through Structure-Based Virtual Screening for the Treatment of Testicular Cancer.Drug design, development and therapy · 2024Article
- ATM Modulates Nuclear Mechanics by Regulating Lamin A Levels.Frontiers in cell and developmental biology · 2022Article
- MLK4 regulates DNA damage response and promotes triple-negative breast cancer chemoresistance.Cell death & disease · 2021Article
- Development and validation of the TGx-HDACi transcriptomic biomarker to detect histone deacetylase inhibitors in human TK6 cells.Archives of toxicology · 2021Article
- Loss of the spectraplakin gene Short stop induces a DNA damage response in Drosophila epithelia.Scientific reports · 2020Article
- A patient-derived iPSC model revealed oxidative stress increases facioscapulohumeral muscular dystrophy-causative DUX4.Human molecular genetics · 2018Article
- PARP inhibitor veliparib and HDAC inhibitor SAHA synergistically co-target the UHRF1/BRCA1 DNA damage repair complex in prostate cancer cells.Journal of experimental & clinical cancer research : CR · 2018Article
- Review
- Synergy between histone deacetylase inhibitors and DNA-damaging agents is mediated by histone deacetylase 2 in colorectal cancer.Oncotarget · 2016Article
- Regulation of the latent-lytic switch in Epstein-Barr virus.Seminars in cancer biology · 2014Review
- Nitric oxide induces ataxia telangiectasia mutated (ATM) protein-dependent γH2AX protein formation in pancreatic β cells.The Journal of biological chemistry · 2014Article
- Antitumoral effects of 9-cis retinoic acid in adrenocortical cancer.Cellular and molecular life sciences : CMLS · 2014Article
- Chromatin modifications associated with DNA double-strand breaks repair as potential targets for neurological diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2013Review
- The role of D-GADD45 in oxidative, thermal and genotoxic stress resistance.Cell cycle (Georgetown, Tex.) · 2012Article
- 10-acetylirciformonin B, a sponge furanoterpenoid, induces DNA damage and apoptosis in leukemia cells.Molecules (Basel, Switzerland) · 2012Article
- Distinct and overlapping gene regulatory networks in BMP- and HDAC-controlled cell fate determination in the embryonic forebrain.BMC genomics · 2012Article
- Article
- Dietary phytochemicals, HDAC inhibition, and DNA damage/repair defects in cancer cells.Clinical epigenetics · 2011Article
- The MRN complex in double-strand break repair and telomere maintenance.FEBS letters · 2010Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromatin structure has a crucial role in a diversity of physiological processes, including development, differentiation and stress responses, via regulation of transcription, DNA replication and DNA damage repair. Histone deacetylase (HDAC) inhibitors regulate chromatin structure and activate the DNA damage checkpoint pathway involving Ataxia-telangiectasia mutated (ATM). Herein, we investigated the impact of histone acetylation/deacetylation modification on the ATM-mediated transcriptional modulation to provide a better understanding of the transcriptional function of ATM. The prototype HDAC inhibitor trichostain A (TSA) reprograms expression of the myeloid cell leukemia-1 (MCL1) and Gadd45 genes via the ATM-mediated signal pathway. Transcription of MCL1 and Gadd45alpha is enhanced following TSA treatment in ATM(+) cells, but not in isogenic ATM(-) or kinase-dead ATM expressing cells, in the ATM-activated E2F1 or BRCA1- dependent manner, respectively. These findings suggest that ATM and its kinase activity are essential for the TSA-induced regulation of gene expression. In summary, ATM controls the transcriptional upregulation of MCL1 and Gadd45 through the activation of the ATM-mediated signal pathway in response to HDAC inhibition. These findings are important in helping to design combinatory treatment schedules for anticancer radio- or chemo-therapy with HDAC inhibitors.
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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.