ArticleScience signaling2011
A genome-wide RNAi screen identifies core components of the G₂-M DNA damage checkpoint.
Article in Science signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 52 citations in OpenAlex.
- Persistent DNA damage signaling and DNA polymerase theta promote broken chromosome segregation.The Journal of cell biology · 2021Article
- Polyploid mitosis and depolyploidization promote chromosomal instability and tumor progression in a Notch-induced tumor model.Developmental cell · 2021Article
- Phosphoproteomics reveals novel modes of function and inter-relationships among PIKKs in response to genotoxic stress.The EMBO journal · 2021Article
- The Splicing Factor SF2 Is Critical for Hyperproliferation and Survival in a TORC1-Dependent Model of Early Tumorigenesis inInternational journal of molecular sciences · 2020Article
- Involvement of DNA Repair Genes and System of Radiation-Induced Activation of Transposons in Formation of Transgenerational Effects.Frontiers in genetics · 2020Article
- Altered Localization of Hybrid Incompatibility Proteins in Drosophila.Molecular biology and evolution · 2019Article
- COPS2 Antagonizes OCT4 to Accelerate the G2/M Transition of Mouse Embryonic Stem Cells.Stem cell reports · 2018Article
- GFZF, a GlutathioneMolecular and cellular biology · 2018Article
- DNA Replication Control DuringGenetics · 2017Review
- Genetically engineered mouse models for studying radiation biology.Translational cancer research · 2017Article
- Initiation of Drosophila chorion gene amplification requires Claspin and mus101, whereas Claspin, but not mus101, plays a major role during elongation.Developmental dynamics : an official publication of the American Association of Anatomists · 2017Article
- NEK8 regulates DNA damage-induced RAD51 foci formation and replication fork protection.Cell cycle (Georgetown, Tex.) · 2017Article
- Systematic epistatic mapping of cellular processes.Cell division · 2017Article
- Computational approaches for the identification of cancer genes and pathways.Wiley interdisciplinary reviews. Systems biology and medicine · 2017Review
- Article
- Roles for the Histone Modifying and Exchange Complex NuA4 in Cell Cycle Progression in Drosophila melanogaster.Genetics · 2016Article
- Direct Binding to Replication Protein A (RPA)-coated Single-stranded DNA Allows Recruitment of the ATR Activator TopBP1 to Sites of DNA Damage.The Journal of biological chemistry · 2016Article
- Proliferation of Double-Strand Break-Resistant Polyploid Cells Requires Drosophila FANCD2.Developmental cell · 2016Article
- A genetic interaction map of cell cycle regulators.Molecular biology of the cell · 2016Article
- The histone demethylase dKDM5/LID interacts with the SIN3 histone deacetylase complex and shares functional similarities with SIN3.Epigenetics & chromatin · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The DNA damage checkpoint, the first pathway known to be activated in response to DNA damage, is a mechanism by which the cell cycle is temporarily arrested to allow DNA repair. The checkpoint pathway transmits signals from the sites of DNA damage to the cell cycle machinery through the evolutionarily conserved ATM (ataxia telangiectasia mutated) and ATR (ATM- and Rad3-related) kinase cascades. We conducted a genome-wide RNAi (RNA interference) screen in Drosophila cells to identify previously unknown genes and pathways required for the G₂-M checkpoint induced by DNA double-strand breaks (DSBs). Our large-scale analysis provided a systems-level view of the G₂-M checkpoint and revealed the coordinated actions of particular classes of proteins, which include those involved in DNA repair, DNA replication, cell cycle control, chromatin regulation, and RNA processing. Further, from the screen and in vivo analysis, we identified previously unrecognized roles of two DNA damage response genes, mus101 and mus312. Our results suggest that the DNA replication preinitiation complex, which includes MUS101, and the MUS312-containing nuclease complexes, which are important for DSB repair, also function in the G₂-M checkpoint. Our results provide insight into the diverse mechanisms that link DNA damage and the checkpoint signaling pathway.
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.