ArticleNature2016
Cascading MutS and MutL sliding clamps control DNA diffusion to activate mismatch repair.
Article in Nature, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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.
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Who cites it
73 citing papers in PubMed, 118 citations in OpenAlex.
- Redundant mispair excision mechanisms in eukaryotic DNA mismatch repair.Nucleus (Austin, Tex.) · 2026Review
- Concentration-dependent stimulatory and inhibitory effects of β-cyclocitral, longifolene, and β-ionone on Microcystis aeruginosa.World journal of microbiology & biotechnology · 2026Article
- Article
- Single-trajectory Bayesian modeling reveals multi-state diffusion of the MSH sliding clamp.NPJ systems biology and applications · 2026Article
- The GHKL ATPase Family as a Paradigm for MutL Homolog Function in DNA Mismatch Repair.International journal of molecular sciences · 2025Review
- Mlh1-Pms1 couples ATP-driven DNA compaction with nick-dependent endonuclease activation.Nucleic acids research · 2025Article
- ATP-dependent one-dimensional movement maintains immune homeostasis by suppressing spontaneous MDA5 filament assembly.Cell research · 2025Article
- Therapeutic targeting of mismatch repair-deficient cancers.Nature reviews. Clinical oncology · 2025Review
- A high-throughput single-molecule platform to study DNA supercoiling effect on protein-DNA interactions.Nucleic acids research · 2025Article
- Glioblastoma multiforme: an updated overview of temozolomide resistance mechanisms and strategies to overcome resistance.Discover oncology · 2025Review
- Identification and characterization of a human MORC2 DNA binding region that is required for gene silencing.Nucleic acids research · 2025Article
- Mlh1-Pms1 ATPase activity is regulated distinctly by self-generated nicks and strand discrimination signals in mismatch repair.Nucleic acids research · 2025Article
- The mismatch repair factor Mlh1-Pms1 uses ATP to compact and remodel DNA.bioRxiv : the preprint server for biology · 2025Article
- Combining single-molecule and structural studies reveals protein and DNA conformations and assemblies that govern DNA mismatch repair.Current opinion in structural biology · 2024Review
- Action-At-A-Distance in DNA Mismatch Repair: Mechanistic Insights and Models for How DNA and Repair Proteins Facilitate Long-Range Communication.Biomolecules · 2024Review
- Structural characterisation of the complete cycle of sliding clamp loading in Escherichia coli.Nature communications · 2024Article
- Escherichia coli DNA replication: the old model organism still holds many surprises.FEMS microbiology reviews · 2024Review
- Identification and characterization of a human MORC2 DNA binding region that is required for gene silencing.bioRxiv : the preprint server for biology · 2024Article
- Insights into DNA cleavage by MutL homologs from analysis of conserved motifs in eukaryotic Mlh1.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Article
- A conserved motif in the disordered linker of human MLH1 is vital for DNA mismatch repair and its function is diminished by a cancer family mutation.Nucleic acids research · 2023Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Mismatched nucleotides arise from polymerase misincorporation errors, recombination between heteroallelic parents and chemical or physical DNA damage. Highly conserved MutS (MSH) and MutL (MLH/PMS) homologues initiate mismatch repair and, in higher eukaryotes, act as DNA damage sensors that can trigger apoptosis. Defects in human mismatch repair genes cause Lynch syndrome or hereditary non-polyposis colorectal cancer and 10-40% of related sporadic tumours. However, the collaborative mechanics of MSH and MLH/PMS proteins have not been resolved in any organism. We visualized Escherichia coli (Ec) ensemble mismatch repair and confirmed that EcMutS mismatch recognition results in the formation of stable ATP-bound sliding clamps that randomly diffuse along the DNA with intermittent backbone contact. The EcMutS sliding clamps act as a platform to recruit EcMutL onto the mismatched DNA, forming an EcMutS-EcMutL search complex that then closely follows the DNA backbone. ATP binding by EcMutL establishes a second long-lived DNA clamp that oscillates between the principal EcMutS-EcMutL search complex and unrestricted EcMutS and EcMutL sliding clamps. The EcMutH endonuclease that targets mismatch repair excision only binds clamped EcMutL, increasing its DNA association kinetics by more than 1,000-fold. The assembly of an EcMutS-EcMutL-EcMutH search complex illustrates how sequential stable sliding clamps can modulate one-dimensional diffusion mechanics along the DNA to direct mismatch repair.
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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.