ArticleDNA repair2008
Smc5-Smc6 complex suppresses gross chromosomal rearrangements mediated by break-induced replications.
Article in DNA repair, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 30 citations in OpenAlex.
- The Multifunctional SMC5/6 Complex in Genome Stability, Antiviral Restriction, and Human Disease.Current issues in molecular biology · 2026Review
- The Smc5/6 complex counteracts R-loop formation at highly transcribed genes in cooperation with RNase H2.eLife · 2024Article
- EssentialProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Insights into the Link between the Organization of DNA Replication and the Mutational Landscape.Genes · 2019Review
- SMC5/6: Multifunctional Player in Replication.Genes · 2018Review
- Review
- Acute Smc5/6 depletion reveals its primary role in rDNA replication by restraining recombination at fork pausing sites.PLoS genetics · 2018Article
- Pathways and Mechanisms that Prevent Genome Instability inGenetics · 2017Review
- Incision of damaged DNA in the presence of an impaired Smc5/6 complex imperils genome stability.Nucleic acids research · 2016Article
- PolySUMOylation by Siz2 and Mms21 triggers relocation of DNA breaks to nuclear pores through the Slx5/Slx8 STUbL.Genes & development · 2016Article
- A saccharomyces cerevisiae RNase H2 interaction network functions to suppress genome instability.Molecular and cellular biology · 2014Article
- Multiple Mechanisms Contribute To Telomere Maintenance.Journal of cancer biology & research · 2013Article
- Inhibition of the Smc5/6 complex during meiosis perturbs joint molecule formation and resolution without significantly changing crossover or non-crossover levels.PLoS genetics · 2013Article
- Distinct SUMO ligases cooperate with Esc2 and Slx5 to suppress duplication-mediated genome rearrangements.PLoS genetics · 2013Article
- Rad5-dependent DNA repair functions of the Saccharomyces cerevisiae FANCM protein homolog Mph1.The Journal of biological chemistry · 2012Article
- During replication stress, non-SMC element 5 (NSE5) is required for Smc5/6 protein complex functionality at stalled forks.The Journal of biological chemistry · 2012Article
- The Smc5-Smc6 complex regulates recombination at centromeric regions and affects kinetochore protein sumoylation during normal growth.PloS one · 2012Article
- Article
- The Smc5/6 complex is required for dissolution of DNA-mediated sister chromatid linkages.Nucleic acids research · 2010Article
- Faithful after break-up: suppression of chromosomal translocations.Cellular and molecular life sciences : CMLS · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Translocations in chromosomes alter genetic information. Although the frequent translocations observed in many tumors suggest the altered genetic information by translocation could promote tumorigenesis, the mechanisms for how translocations are suppressed and produced are poorly understood. The smc6-9 mutation increased the translocation class gross chromosomal rearrangement (GCR). Translocations produced in the smc6-9 strain are unique because they are non-reciprocal and dependent on break-induced replication (BIR) and independent of non-homologous end joining. The high incidence of translocations near repetitive sequences such as delta sequences, ARS, tRNA genes, and telomeres in the smc6-9 strain indicates that Smc5-Smc6 suppresses translocations by reducing DNA damage at repetitive sequences. Synergistic enhancements of translocations in strains defective in DNA damage checkpoints by the smc6-9 mutation without affecting de novo telomere addition class GCR suggest that Smc5-Smc6 defines a new pathway to suppress GCR formation.
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.