ArticleNature communications2016
A genome-wide screening uncovers the role of CCAR2 as an antagonist of DNA end resection.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 64 citations in OpenAlex.
- miRNA-mediated cell-to-cell communications boost DNA repair during the radioadaptive response.Nucleic acids research · 2026Article
- Circadian regulation of homologous recombination by cryptochrome1-mediated dampening of DNA end resection.Nature communications · 2025Article
- Review
- The Common Hallmarks and Interconnected Pathways of Aging, Circadian Rhythms, and Cancer: Implications for Therapeutic Strategies.Research (Washington, D.C.) · 2025Review
- Loss of tet methyl cytosine dioxygenase 3 (TET3) enhances cardiac fibrosis via modulating the DNA damage repair response.Clinical epigenetics · 2024Article
- Multifaceted roles of CCAR family proteins in the DNA damage response and cancer.Experimental & molecular medicine · 2024Review
- Centriolar subdistal appendages promote double-strand break repair through homologous recombination.EMBO reports · 2023Article
- Revolutionizing DNA repair research and cancer therapy with CRISPR-Cas screens.Nature reviews. Molecular cell biology · 2023Review
- CCAR2 functions downstream of the Shieldin complex to promote double-strand break end-joining.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- CtIP-dependent nascent RNA expression flanking DNA breaks guides the choice of DNA repair pathway.Nature communications · 2022Article
- Functional Screening of Parkinson's Disease Susceptibility Genes to Identify Novel Modulators of α-Synuclein Neurotoxicity inFrontiers in aging neuroscience · 2022Article
- PLK1-mediated phosphorylation of PPIL2 regulates HRFrontiers in cell and developmental biology · 2022Article
- ADAR-mediated RNA editing of DNA:RNA hybrids is required for DNA double strand break repair.Nature communications · 2021Article
- Damage-Net: A program for DNA repair meta-analysis identifies a network of novel repair genes that facilitate cancer evolution.DNA repair · 2021Article
- Deacetylase Plus Bromodomain Inhibition Downregulates ERCC2 and Suppresses the Growth of Metastatic Colon Cancer Cells.Cancers · 2021Article
- MRGBP, a member of the NuA4 complex, inhibits DNA double-strand break repair.FEBS open bio · 2021Article
- Phosphoproteomics reveals novel modes of function and inter-relationships among PIKKs in response to genotoxic stress.The EMBO journal · 2021Article
- To Join or Not to Join: Decision Points Along the Pathway to Double-Strand Break Repair vs. Chromosome End Protection.Frontiers in cell and developmental biology · 2021Review
- CCAR1 and CCAR2 as gene chameleons with antagonistic duality: Preclinical, human translational, and mechanistic basis.Cancer science · 2020Review
- SPT6-driven error-free DNA repair safeguards genomic stability of glioblastoma cancer stem-like cells.Nature communications · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There are two major and alternative pathways to repair DNA double-strand breaks: non-homologous end-joining and homologous recombination. Here we identify and characterize novel factors involved in choosing between these pathways; in this study we took advantage of the SeeSaw Reporter, in which the repair of double-strand breaks by homology-independent or -dependent mechanisms is distinguished by the accumulation of green or red fluorescence, respectively. Using a genome-wide human esiRNA (endoribonuclease-prepared siRNA) library, we isolate genes that control the recombination/end-joining ratio. Here we report that two distinct sets of genes are involved in the control of the balance between NHEJ and HR: those that are required to facilitate recombination and those that favour NHEJ. This last category includes CCAR2/DBC1, which we show inhibits recombination by limiting the initiation and the extent of DNA end resection, thereby acting as an antagonist of CtIP.
Indexed as
Identifiers
What OpenQuestion holds
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.