ArticleMolecular and cellular biology2018
MOF Suppresses Replication Stress and Contributes to Resolution of Stalled Replication Forks.
Article in Molecular and cellular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 39 citations in OpenAlex.
- KAT8-mediated epigenetic modifications: Physiological functions, heterogeneity in disease, and advances in targeted development.iScience · 2026Review
- When circular RNAs meet the genome: CiR-loops as chromatin regulators and disease drivers.Nucleic acids research · 2026Review
- HP1β recruits RING1A to ubiquitinate histone H2A for BRCA1-mediated resection of double-stand breaks.iScience · 2026Article
- C8orf33 dictates DNA double-strand break repair choice by modulating KAT8-mediated H4K16 acetylation.Cell death & disease · 2025Article
- Mammalian H4K16ac regulates the spatiotemporal order of genome replication rather than gene expression.Nucleic acids research · 2025Article
- Lysine Acetyltransferase 8: A Target for Natural Compounds in Cancer Therapy.International journal of molecular sciences · 2025Review
- Unraveling the metabolic‒epigenetic nexus: a new frontier in cardiovascular disease treatment.Cell death & disease · 2025Review
- KAT8 facilitates the proliferation of cancer cells through enhancing E7 function in HPV-associated cervical cancer.Acta biochimica et biophysica Sinica · 2025Article
- Long noncoding RNAs involved in therapeutic response: implications for cervical cancer drug resistance.Frontiers in oncology · 2025Review
- Unscheduled excessive R-loops in immune response.Functional & integrative genomics · 2024Article
- Ubiquitin specific peptidase 37 and PCNA interaction promotes osteosarcoma pathogenesis by modulating replication fork progression.Journal of translational medicine · 2023Article
- Role of primary aging hallmarks in Alzheimer´s disease.Theranostics · 2023Review
- Sources, resolution and physiological relevance of R-loops and RNA-DNA hybrids.Nature reviews. Molecular cell biology · 2022Review
- Heat-induced SIRT1-mediated H4K16ac deacetylation impairs resection and SMARCAD1 recruitment to double strand breaks.iScience · 2022Article
- Caspase-2 regulates S-phase cell cycle events to protect from DNA damage accumulation independent of apoptosis.Oncogene · 2022Article
- Role of the Histone Acetyl Transferase MOF and the Histone Deacetylase Sirtuins in Regulation of H4K16ac During DNA Damage Repair and Metabolic Programming: Implications in Cancer and Aging.Sub-cellular biochemistry · 2022Article
- EXO5-DNA structure and BLM interactions direct DNA resection critical for ATR-dependent replication restart.Molecular cell · 2021Article
- Autism-Associated Vigilin Depletion Impairs DNA Damage Repair.Molecular and cellular biology · 2021Article
- Role of HP1β during spermatogenesis and DNA replication.Chromosoma · 2020Article
- Epigenetic activation of the small GTPase TCL contributes to colorectal cancer cell migration and invasion.Oncogenesis · 2020Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The human MOF (hMOF) protein belongs to the MYST family of histone acetyltransferases and plays a critical role in transcription and the DNA damage response. MOF is essential for cell proliferation; however, its role during replication and replicative stress is unknown. Here we demonstrate that cells depleted of MOF and under replicative stress induced by cisplatin, hydroxyurea, or camptothecin have reduced survival, a higher frequency of S-phase-specific chromosome damage, and increased R-loop formation. MOF depletion decreased replication fork speed and, when combined with replicative stress, also increased stalled replication forks as well as new origin firing. MOF interacted with PCNA, a key coordinator of replication and repair machinery at replication forks, and affected its ubiquitination and recruitment to the DNA damage site. Depletion of MOF, therefore, compromised the DNA damage repair response as evidenced by decreased Mre11, RPA70, Rad51, and PCNA focus formation, reduced DNA end resection, and decreased CHK1 phosphorylation in cells after exposure to hydroxyurea or cisplatin. These results support the argument that MOF plays an important role in suppressing replication stress induced by genotoxic agents at several stages during the DNA damage response.
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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.