ReviewCurrent genetics2019
Recruitment, loading, and activation of the Smc5-Smc6 SUMO ligase.
Review in Current genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
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.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- The SMC5/SMC6 complex is critical for resolving R-loop-induced transcription-replication conflicts.Nucleic acids research · 2026Article
- NSE5 subunit interacts with distant regions of the SMC arms in the Physcomitrium patens SMC5/6 complex.The Plant journal : for cell and molecular biology · 2024Article
- RAD18 directs DNA double-strand break repair by homologous recombination to post-replicative chromatin.Nucleic acids research · 2024Article
- The SMC5/6 complex: folding chromosomes back into shape when genomes take a break.Nucleic acids research · 2024Review
- The SAGA histone acetyltransferase module targets SMC5/6 to specific genes.Epigenetics & chromatin · 2023Article
- Article
- Machine learning-based automated fungal cell counting under a complicated background with ilastik and ImageJ.Engineering in life sciences · 2021Article
- Nse5/6 is a negative regulator of the ATPase activity of the Smc5/6 complex.Nucleic acids research · 2021Article
- Identification of novel biomarkers involved in pulmonary arterial hypertension based on multiple-microarray analysis.Bioscience reports · 2020Article
- Topological DNA-binding of structural maintenance of chromosomes-like RecN promotes DNA double-strand break repair inCommunications biology · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Duplication of the genome poses one of the most significant threats to genetic integrity, cellular fitness, and organismal health. Therefore, numerous mechanisms have evolved that maintain replication fork stability in the face of DNA damage and allow faithful genome duplication. The fission yeast BRCT-domain-containing protein Brc1, and its budding yeast orthologue Rtt107, has emerged as a "hub" factor that integrates multiple replication fork protection mechanisms. Notably, the cofactors and pathways through which Brc1, Rtt107, and their human orthologue (PTIP) act have appeared largely distinct. This either represents true evolutionary functional divergence, or perhaps an incomplete genetic and biochemical analysis of each protein. In this regard, we recently showed that like Rtt107, Brc1 supports key functions of the Smc5-Smc6 complex, including its recruitment into DNA repair foci, chromatin association, and SUMO ligase activity. Furthermore, fission yeast cells lacking the Nse5-Nse6 genome stability factor were found to exhibit defects in Smc5-Smc6 function, similar to but more severe than those in cells lacking Brc1. Here, we place these findings in context with the known functions of Brc1, Rtt107, and Smc5-Smc6, present data suggesting a role for acetylation in Smc5-Smc6 chromatin loading, and discuss wider implications for genome stability.
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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.