ReviewCell cycle (Georgetown, Tex.)2015
Histone deacetylases 1 and 2 regulate DNA replication and DNA repair: potential targets for genome stability-mechanism-based therapeutics for a subset of cancers.
Review in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- Article
- Targeting cytokine and chemokine signaling pathways for enhancing chemo-sensitivity in colorectal cancer.Cell communication and signaling : CCS · 2025Review
- Tumor-associated macrophages contribute to cisplatin resistance via regulating Pol η-mediated translesion DNA synthesis in ovarian cancer.Cellular and molecular life sciences : CMLS · 2025Article
- Engineered exosomes: a promising design platform for overcoming cancer therapy resistance.Frontiers in cell and developmental biology · 2025Review
- Ribosomal frameshifting at normal codon repeats recodes functional chimeric proteins in human.Nucleic acids research · 2024Article
- In the quest for histone deacetylase inhibitors: current trends in the application of multilayered computational methods.Amino acids · 2023Review
- Exosome-transported circHDAC1_004 Promotes Proliferation, Migration, and Angiogenesis of Hepatocellular Carcinoma by the miR-361-3p/NACC1 Axis.Journal of clinical and translational hepatology · 2023Article
- Multifaceted Influence of Histone Deacetylases on DNA Damage Repair: Implications for Hepatocellular Carcinoma.Journal of clinical and translational hepatology · 2023Review
- Rational Combinations of PARP Inhibitors with HRD-Inducing Molecularly Targeted Agents.Cancer treatment and research · 2023Review
- Single-Cell Analysis of Histone Acetylation Dynamics at Replication Forks Using PLA and SIRF.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Differential molecular mechanistic behavior of HDACs in cancer progression.Medical oncology (Northwood, London, England) · 2022Review
- SNP rs4971059 predisposes to breast carcinogenesis and chemoresistance via TRIM46-mediated HDAC1 degradation.The EMBO journal · 2021Article
- Restoration of HDAC1 Enzymatic Activity after Stroke Protects Neurons from Ischemia/Reperfusion Damage and Attenuates Behavioral Deficits in Rats.International journal of molecular sciences · 2021Article
- EGFR phosphorylates HDAC1 to regulate its expression and anti-apoptotic function.Cell death & disease · 2021Article
- Article
- Genome-Protecting Compounds as Potential Geroprotectors.International journal of molecular sciences · 2020Review
- Assessment of epigenetic mechanisms and DNA double-strand break repair using laser micro-irradiation technique developed for hematological cells.EBioMedicine · 2019Article
- Vorinostat, a pan-HDAC inhibitor, abrogates productive HPV-18 DNA amplification.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Lactic acid alleviates stress: good for female genital tract homeostasis, bad for protection against malignancy.Cell stress & chaperones · 2018Review
- A NuRD Complex from Xenopus laevis Eggs Is Essential for DNA Replication during Early Embryogenesis.Cell reports · 2018Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Histone deacetylases 1 and 2 (HDAC1,2) belong to the class I HDAC family, which are targeted by the FDA-approved small molecule HDAC inhibitors currently used in cancer therapy. HDAC1,2 are recruited to DNA break sites during DNA repair and to chromatin around forks during DNA replication. Cancer cells use DNA repair and DNA replication as survival mechanisms and to evade chemotherapy-induced cytotoxicity. Hence, it is vital to understand how HDAC1,2 function during the genome maintenance processes (DNA replication and DNA repair) in order to gain insights into the mode-of-action of HDAC inhibitors in cancer therapeutics. The first-in-class HDAC1,2-selective inhibitors and Hdac1,2 conditional knockout systems greatly facilitated dissecting the precise mechanisms by which HDAC1,2 control genome stability in normal and cancer cells. In this perspective, I summarize the findings on the mechanistic functions of class I HDACs, specifically, HDAC1,2 in genome maintenance, unanswered questions for future investigations and views on how this knowledge could be harnessed for better-targeted cancer therapeutics for a subset of cancers.
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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.