ArticleNucleic acids research2014
Genome-wide reorganization of histone H2AX toward particular fragile sites on cell activation.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 29 citations in OpenAlex.
- Direct recruitment of TONSOKU by the N-terminal tails of histone variants H2A.X and H2A.W coordinates DNA repair.Science advances · 2025Article
- Roles of Histone H2A Variants in Cancer Development, Prognosis, and Treatment.International journal of molecular sciences · 2024Review
- Architecture, Chromatin and Gene Organization ofEpigenomes · 2022Article
- Breaking the paradigm: early insights from mammalian DNA breakomes.The FEBS journal · 2022Review
- LINC00665 sponges miR-641 to promote the progression of breast cancer by targeting the SNF2-related CREBBP activator protein (SRCAP).Bioengineered · 2022Article
- Article
- Low Replicative Stress Triggers Cell-Type Specific Inheritable Advanced Replication Timing.International journal of molecular sciences · 2021Article
- MicroRNA-138 inhibits tumor growth and enhances chemosensitivity in human cervical cancer by targeting H2AX.Experimental and therapeutic medicine · 2020Article
- Transcription activity contributes to the firing of non-constitutive origins in African trypanosomes helping to maintain robustness in S-phase duration.Scientific reports · 2019Article
- Efficient disruption of bcr-abl gene by CRISPR RNA-guided FokI nucleases depresses the oncogenesis of chronic myeloid leukemia cells.Journal of experimental & clinical cancer research : CR · 2019Article
- Review
- The Histone Chaperone FACT Coordinates H2A.X-Dependent Signaling and Repair of DNA Damage.Molecular cell · 2018Article
- Large-scale heterochromatin remodeling linked to overreplication-associated DNA damage.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- ChARM: Discovery of combinatorial chromatin modification patterns in hepatitis B virus X-transformed mouse liver cancer using association rule mining.BMC bioinformatics · 2016Article
- Genome-wide Profiling Reveals Remarkable Parallels Between Insertion Site Selection Properties of the MLV Retrovirus and the piggyBac Transposon in Primary Human CD4(+) T Cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- Stress-induced chromatin changes in plants: of memories, metabolites and crop improvement.Cellular and molecular life sciences : CMLS · 2015Review
- Are common fragile sites merely structural domains or highly organized "functional" units susceptible to oncogenic stress?Cellular and molecular life sciences : CMLS · 2014Review
- γH2AX foci on apparently intact mitotic chromosomes: not signatures of misrejoining events but signals of unresolved DNA damage.Cell cycle (Georgetown, Tex.) · 2014Article
- The Role of γH2AX in Replication Stress-induced Carcinogenesis: Possible Links and Recent Developments.Cancer diagnosis & prognosisReview
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
γH2AX formation by phosphorylation of the histone variant H2AX is the key process in the repair of DNA lesions including those arising at fragile sites under replication stress. Here we demonstrate that H2AX is dynamically reorganized to preoccupy γH2AX hotspots on increased replication stress by activated cell proliferation and that H2AX is enriched in aphidicolin-induced replisome stalling sites in cycling cells. Interestingly, H2AX enrichment was particularly found in genomic regions that replicate in early S phase. High transcription activity, a hallmark of early replicating fragile sites, was a determinant of H2AX localization. Subtelomeric H2AX enrichment was also attributable to early replication and high gene density. In contrast, late replicating and infrequently transcribed regions, including common fragile sites and heterochromatin, lacked H2AX enrichment. In particular, heterochromatin was inaccessible to H2AX incorporation, maybe partly explaining the cause of mutation accumulation in cancer heterochromatin. Meanwhile, H2AX in actively dividing cells was intimately colocalized with INO80. INO80 silencing reduced H2AX levels, particularly at the INO80-enriched sites. Our findings suggest that active DNA replication is accompanied with the specific localization of H2AX and INO80 for efficient damage repair or replication-fork stabilization in actively transcribed regions.
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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.