ArticleThe Journal of biological chemistry2012
RING finger nuclear factor RNF168 is important for defects in homologous recombination caused by loss of the breast cancer susceptibility factor BRCA1.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 49 citations in OpenAlex.
- Daxx-Dependent H3.3 Deposition Promotes Double-Strand Breaks Repair by Homologous Recombination.Cells · 2026Article
- Review
- Targeting the HECTD3-p62 axis increases the radiosensitivity of triple negative breast cancer cells.Cell death discovery · 2024Article
- The contribution of DNA repair pathways to genome editing and evolution in filamentous pathogens.FEMS microbiology reviews · 2022Review
- O-GlcNAc transferase is important for homology-directed repair.DNA repair · 2022Article
- New answers to the old RIDDLE: RNF168 and the DNA damage response pathway.The FEBS journal · 2022Review
- Disruption of Chromatin Dynamics by Hypotonic Stress Suppresses HR and Shifts DSB Processing to Error-Prone SSA.International journal of molecular sciences · 2021Article
- RNF168-mediated localization of BARD1 recruits the BRCA1-PALB2 complex to DNA damage.Nature communications · 2021Article
- Non-canonical function of DGCR8 in DNA double-strand break repair signaling and tumor radioresistance.Nature communications · 2021Article
- Single-Strand Annealing in Cancer.International journal of molecular sciences · 2021Review
- Homologous recombination deficiency: how genomic signatures are generated.Current opinion in genetics & development · 2021Review
- BRCA1 Mutations in Cancer: Coordinating Deficiencies in Homologous Recombination with Tumorigenesis.Cancer research · 2020Review
- RNF168-Mediated Ubiquitin Signaling Inhibits the Viability ofCancer research · 2020Article
- BLM has Contrary Effects on Repeat-Mediated Deletions, based on the Distance of DNA DSBs to a Repeat and Repeat Divergence.Cell reports · 2020Article
- Review
- The p97-Ataxin 3 complex regulates homeostasis of the DNA damage response E3 ubiquitin ligase RNF8.The EMBO journal · 2019Article
- BRCA1 Haploinsufficiency Is Masked by RNF168-Mediated Chromatin Ubiquitylation.Molecular cell · 2019Article
- RNF169 limits 53BP1 deposition at DSBs to stimulate single-strand annealing repair.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Repair of DNA double-strand breaks by mammalian alternative end-joining pathways.The Journal of biological chemistry · 2018Review
- USP48 restrains resection by site-specific cleavage of the BRCA1 ubiquitin mark from H2A.Nature communications · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundRNF168 promotes chromosomal break localization of 53BP1 and BRCA1; 53BP1 loss rescues homologous recombination (HR) in BRCA1-deficient cells.
resultsRNF168 depletion suppresses HR defects caused by BRCA1 silencing; RNF168 influences HR similarly to 53BP1.
conclusionRNF168 is important for HR defects caused by BRCA1 loss. SIGNIFICANCE: Although RNF168 promotes BRCA1 and 53BP1 localization to chromosomal breaks, RNF168 affects HR similarly to 53BP1. The RING finger nuclear factor RNF168 is required for recruitment of several DNA damage response factors to double strand breaks (DSBs), including 53BP1 and BRCA1. Because 53BP1 and BRCA1 function antagonistically during the DSB repair pathway homologous recombination (HR), the influence of RNF168 on HR has been unclear. We report that RNF168 depletion causes an elevated frequency of two distinct HR pathways (homology-directed repair and single strand annealing), suppresses defects in HR caused by BRCA1 silencing, but does not suppress HR defects caused by disruption of CtIP, RAD50, BRCA2, or RAD51. Furthermore, RNF168-depleted cells can form ionizing radiation-induced foci of the recombinase RAD51 without forming BRCA1 ionizing radiation-induced foci, indicating that this loss of BRCA1 recruitment to DSBs does not reflect a loss of function during HR. Additionally, we find that RNF168 and 53BP1 have a similar influence on HR. We suggest that RNF168 is important for HR defects caused by BRCA1 loss.
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.