ArticleEMBO reports2020
SMC5/6 acts jointly with Fanconi anemia factors to support DNA repair and genome stability.
Article in EMBO reports, 2020. 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
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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
24 citing papers in PubMed.
- The Multifunctional SMC5/6 Complex in Genome Stability, Antiviral Restriction, and Human Disease.Current issues in molecular biology · 2026Review
- SLF2 and SMC5 dysfunction drives HSC aging and predisposes to MDS, defining a new inherited bone marrow failure syndrome.Leukemia · 2026Article
- DDX11 interacts with PARP1 to facilitate PARylation, thereby promoting gallbladder cancer progression and conferring gemcitabine resistance.Acta biochimica et biophysica Sinica · 2025Article
- Comprehensive review on Fanconi anemia: insights into DNA interstrand cross-links, repair pathways, and associated tumors.Orphanet journal of rare diseases · 2025Review
- Article
- Multifaceted roles of SUMO in DNA metabolism.Nucleus (Austin, Tex.) · 2024Review
- Crucial role of the NSE1 RING domain in Smc5/6 stability and FANCM-independent fork progression.Cellular and molecular life sciences : CMLS · 2024Article
- The Causes and Consequences of DNA Damage and Chromosomal Instability Induced by Human Papillomavirus.Cancers · 2024Review
- RNF4 sustains Myc-driven tumorigenesis by facilitating DNA replication.The Journal of clinical investigation · 2024Article
- The SMC5/6 complex: folding chromosomes back into shape when genomes take a break.Nucleic acids research · 2024Review
- 1,6-Hexanediol Is Inducing Homologous Recombination by Releasing BLM from Assemblysomes inInternational journal of molecular sciences · 2024Article
- SMC5/6 Promotes Replication Fork Stability via Negative Regulation of the COP9 Signalosome.International journal of molecular sciences · 2024Article
- Article
- Article
- Genome control by SMC complexes.Nature reviews. Molecular cell biology · 2023Review
- The multi-functional Smc5/6 complex in genome protection and disease.Nature structural & molecular biology · 2023Review
- Pathogenic variants in SLF2 and SMC5 cause segmented chromosomes and mosaic variegated hyperploidy.Nature communications · 2022Article
- Causes and consequences of micronuclei.Current opinion in cell biology · 2021Review
- DDX11 loss causes replication stress and pharmacologically exploitable DNA repair defects.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Smc5/6 functions with Sgs1-Top3-Rmi1 to complete chromosome replication at natural pause sites.Nature communications · 2021Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
SMC5/6 function in genome integrity remains elusive. Here, we show that SMC5 dysfunction in avian DT40 B cells causes mitotic delay and hypersensitivity toward DNA intra- and inter-strand crosslinkers (ICLs), with smc5 mutants being epistatic to FANCC and FANCM mutations affecting the Fanconi anemia (FA) pathway. Mutations in the checkpoint clamp loader RAD17 and the DNA helicase DDX11, acting in an FA-like pathway, do not aggravate the damage sensitivity caused by SMC5 dysfunction in DT40 cells. SMC5/6 knockdown in HeLa cells causes MMC sensitivity, increases nuclear bridges, micronuclei, and mitotic catastrophes in a manner similar and non-additive to FANCD2 knockdown. In both DT40 and HeLa systems, SMC5/6 deficiency does not affect FANCD2 ubiquitylation and, unlike FANCD2 depletion, RAD51 focus formation. SMC5/6 components further physically interact with FANCD2-I in human cells. Altogether, our data suggest that SMC5/6 functions jointly with the FA pathway to support genome integrity and DNA repair and may be implicated in FA or FA-related human disorders.
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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.