ArticleThe Journal of cell biology2011
Replication stress induces 53BP1-containing OPT domains in G1 cells.
Article in The Journal of cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 219 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
219 citing papers in PubMed, 329 citations in OpenAlex.
- Polymerase iota coordinates adaptation to replication stress in BRCA2-deficient mammary epithelial cells.iScience · 2026Article
- Replication stress in cancer: origins, consequences and therapeutic opportunities.Nature reviews. Cancer · 2026Review
- LIPT1 loss confers replication stress and PARP inhibitor sensitivity through PrimPol-mediated ssDNA gaps.Science advances · 2026Article
- BMI1 represses G-quadruplex DNA formation to maintain genomic stability during replication.The Journal of biological chemistry · 2026Article
- EP300 deficiency leads to chronic replication stress mediated by defective replication fork protection.Nature communications · 2025Article
- Liquid-Liquid Phase Separation: Mechanisms, Roles, and Implications in Cellular Function and Disease.FASEB bioAdvances · 2025Review
- Defects in the DNA Damage Response of Patient-derived Endometriosis Stromal Cells.bioRxiv : the preprint server for biology · 2025Article
- Endogenous p21 levels protect genomic stability by suppressing both excess and restrained nascent DNA syntheses.Science advances · 2025Article
- RAD51 is chromatin enriched and targetable in BRCA1-deficient cells.Molecular cell · 2025Article
- Human TLS DNA polymerase: saviors or threats under replication stress?Molecular and cellular biochemistry · 2025Review
- G-quadruplex stabilization induces DNA breaks in pericentromeric repetitive DNA sequences in B lymphocytes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Fluorescence recovery in the super-resolution regime reveals subcompartments of 53BP1 foci.Cell reports methods · 2025Article
- RNF20-mediated H2B monoubiquitination protects stalled forks from degradation and promotes fork restart.EMBO reports · 2025Article
- Versatile enhancement of the killing potential of anti-cancer agents achieved by peptide mimetics of the PCNA interface towards specialized DNA polymerases.Cell death & disease · 2025Article
- ANP32E drives vulnerability to ATR inhibitors by inducing R-loops-dependent transcription replication conflicts in triple negative breast cancer.Nature communications · 2025Article
- Targeting BRCA1-deficient PARP inhibitor-resistant cells with nickases reveals nick resection as a cancer vulnerability.Nature cancer · 2025Article
- RIF1 integrates DNA repair and transcriptional requirements during the establishment of humoral immune responses.Nature communications · 2025Article
- Catalytic Droplets: Enzyme Containing Microcompartments.Sub-cellular biochemistry · 2025Review
- Transgenerational Tracking of Chromosomes from Micronuclei.Methods in molecular biology (Clifton, N.J.) · 2025Review
- 53BP1-the 'Pandora's box' of genome integrity.DNA repair · 2024Review
159 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Chromosomal deletions and rearrangements in tumors are often associated with common fragile sites, which are specific genomic loci prone to gaps and breaks in metaphase chromosomes. Common fragile sites appear to arise through incomplete DNA replication because they are induced after partial replication inhibition by agents such as aphidicolin. Here, we show that in G1 cells, large nuclear bodies arise that contain p53 binding protein 1 (53BP1), phosphorylated H2AX (γH2AX), and mediator of DNA damage checkpoint 1 (MDC1), as well as components of previously characterized OPT (Oct-1, PTF, transcription) domains. Notably, we find that incubating cells with low aphidicolin doses increases the incidence and number of 53BP1-OPT domains in G1 cells, and by chromatin immunoprecipitation and massively parallel sequencing analysis of γH2AX, we demonstrate that OPT domains are enriched at common fragile sites. These findings invoke a model wherein incomplete DNA synthesis during S phase leads to a DNA damage response and formation of 53BP1-OPT domains in the subsequent G1.
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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.