ArticleOncotarget2016
Chromatin determinants of the inner-centromere rely on replication factors with functions that impart cohesion.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 37 citations in OpenAlex.
- TOP1 and TOP2 complementarily maintain DNA replication fork progression in vertebrates.The Journal of biological chemistry · 2026Article
- Cell cycle control of cohesion establishment.bioRxiv : the preprint server for biology · 2025Article
- RAD18- and BRCA1-dependent pathways promote cellular tolerance to the nucleoside analog ganciclovir.Genes to cells : devoted to molecular & cellular mechanisms · 2024Article
- The multifaceted roles of the Ctf4 replisome hub in the maintenance of genome integrity.DNA repair · 2024Review
- REV3 promotes cellular tolerance to 5-fluorodeoxyuridine by activating translesion DNA synthesis and intra-S checkpoint.PLoS genetics · 2024Article
- CRISPR screens in sister chromatid cohesion defective cells reveal PAXIP1-PAGR1 as regulator of chromatin association of cohesin.Nucleic acids research · 2023Article
- PCNA recruits cohesin loader Scc2 to ensure sister chromatid cohesion.Nature structural & molecular biology · 2023Article
- MMS22L-TONSL functions in sister chromatid cohesion in a pathway parallel to DSCC1-RFC.Life science alliance · 2023Article
- Synthetic lethal interactions of DEAD/H-box helicases as targets for cancer therapy.Frontiers in oncology · 2022Review
- The Interplay of Cohesin and the Replisome at Processive and Stressed DNA Replication Forks.Cells · 2021Review
- Vertebrate CTF18 and DDX11 essential function in cohesion is bypassed by preventing WAPL-mediated cohesin release.Genes & development · 2021Article
- Targeting chromosome trisomy for chromosome editing.Scientific reports · 2021Article
- DDX11 loss causes replication stress and pharmacologically exploitable DNA repair defects.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Article
- Timeless couples G-quadruplex detection with processing by DDX11 helicase during DNA replication.The EMBO journal · 2020Article
- Warsaw Breakage Syndrome associated DDX11 helicase resolves G-quadruplex structures to support sister chromatid cohesion.Nature communications · 2020Article
- A scalable CRISPR/Cas9-based fluorescent reporter assay to study DNA double-strand break repair choice.Nature communications · 2020Article
- The iron-sulfur helicase DDX11 promotes the generation of single-stranded DNA for CHK1 activation.Life science alliance · 2020Article
- SMC5/6 acts jointly with Fanconi anemia factors to support DNA repair and genome stability.EMBO reports · 2020Article
- Non-redundant roles in sister chromatid cohesion of the DNA helicase DDX11 and the SMC3 acetyl transferases ESCO1 and ESCO2.PloS one · 2020Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Replication fork-associated factors promote genome integrity and protect against cancer. Mutations in the DDX11 helicase and the ESCO2 acetyltransferase also cause related developmental disorders classified as cohesinopathies. Here we generated vertebrate model cell lines of these disorders and cohesinopathies-related genes. We found that vertebrate DDX11 and Tim-Tipin are individually needed to compensate for ESCO2 loss in chromosome segregation, with DDX11 also playing complementary roles with ESCO2 in centromeric cohesion. Our study reveals that overt centromeric cohesion loss does not necessarily precede chromosome missegregation, while both these problems correlate with, and possibly originate from, inner-centromere defects involving reduced phosphorylation of histone H3T3 (pH3T3) in the region. Interestingly, the mitotic pH3T3 mark was defective in all analyzed replication-related mutants with functions in cohesion. The results pinpoint mitotic pH3T3 as a postreplicative chromatin mark that is sensitive to replication stress and conducts with different kinetics to robust centromeric cohesion and correct chromosome segregation.
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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.