Affinage

EME1

Structure-specific endonuclease subunit EME1 · UniProt Q96AY2

Length
570 aa
Mass
63.3 kDa
Annotated
2026-06-09
47 papers in source corpus 30 papers cited in narrative 30 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

EME1 is the non-catalytic subunit of the heterodimeric Mus81-EME1 structure-selective endonuclease that resolves branched DNA intermediates arising during recombination and replication, thereby promoting meiotic crossover formation, replication fork processing, and interstrand crosslink repair (PMID:11719193, PMID:14609959). The complex preferentially cleaves replication fork structures, 3'-flaps, and nicked Holliday junctions over intact Holliday junctions, resolving nicked junctions through a nick-and-counternick mechanism in which incision occurs on the strand opposing the nick (PMID:12721304, PMID:14527419, PMID:12473680); the human enzyme can also achieve symmetrical bilateral cleavage of cruciform substrates through a cooperative, sequential mechanism (PMID:18310322). Crystal structures of Mus81-EME1 bound to DNA define both subunits as carrying a central nuclease domain and C-terminal helix-hairpin-helix motifs, with a flexible EME1 intradomain linker essential for DNA recognition and a Mus81 hydrophobic wedge and 5'-end binding pocket that bend and position the substrate for incision (PMID:18413719, PMID:24733841). EME1-dependent cleavage is genetically required for meiotic crossing over, where it acts specifically at crossover resolution while leaving gene conversion intact (PMID:14527420, PMID:14704204), and Eme1-deficient cells show hypersensitivity to crosslinking agents and spontaneous genomic instability (PMID:14609959). At the G2/M transition CDK-dependent phosphorylation drives assembly of MUS81-EME1 with SLX1-SLX4 into the SLX-MUS holoenzyme for coordinated Holliday junction resolution (PMID:24076221, PMID:36288699), and enzyme activity is further controlled by cell-cycle and checkpoint kinases including CDK/Polo-like kinase, ATR, Chk1, and CK2 acting on EME1 or its scaffold partner SLX4 (PMID:22730299, PMID:23584455, PMID:35452455, PMID:29850896). MUS81-EME1 cooperates with FANCA, which recruits it to and stimulates incision at interstrand crosslinks (PMID:24170812), localizes with ERCC1 and FANCD2 to common fragile sites to process under-replicated DNA in mitosis (PMID:23811686), and produces deleterious DNA breaks at replication forks when Chk1 is compromised (PMID:21858151, PMID:33298441). EME1 expression is transcriptionally regulated through STAT3 and SETD1A, and its levels influence sensitivity to topoisomerase and PARP inhibitors (PMID:18245483, PMID:39994444).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2001 High

    Established that EME1 is an obligate partner of Mus81 in a heterodimeric endonuclease and that this activity functions late in meiotic recombination, framing EME1 as a junction-resolving factor.

    Evidence Purified-complex endonuclease assay and genetic rescue of mus81 meiotic defect by the bacterial resolvase RusA, with co-IP identifying Eme1

    PMID:11719193

    Open questions at the time
    • Did not define which branched substrate is the physiological target in vivo
    • Catalytic versus structural roles of the two subunits not yet separated
  2. 2002 High

    Resolved the apparent substrate paradox by showing the enzyme cleaves replication fork and reversed-fork structures efficiently but synthetic Holliday junctions poorly, redirecting attention toward replication intermediates.

    Evidence In vitro endonuclease assays on defined substrates with cleavage-site mapping plus RusA suppressor genetics in fission and budding yeast

    PMID:12084712 PMID:12473680

    Open questions at the time
    • Did not reconcile in vitro fork preference with the genetic requirement for crossover resolution
    • Cleavage-site choice on physiological in vivo substrates not established
  3. 2003 High

    Demonstrated conservation and substrate specificity of the human and mouse enzymes and defined the nick-and-counternick mechanism for nicked Holliday junctions, linking biochemistry to meiotic crossover and crosslink-repair phenotypes.

    Evidence Purified human/mouse heterodimer endonuclease assays, kinetic analysis of nicked vs intact junctions, ES-cell knockout drug-sensitivity, and meiotic recombination genetics

    PMID:12721304 PMID:14527419 PMID:14527420 PMID:14609959 PMID:14704204

    Open questions at the time
    • How nicked junction intermediates are generated in vivo not established
    • Crossover-versus-gene-conversion separation mechanistically unexplained
  4. 2006 High

    Placed Mus81-EME1 in the interstrand-crosslink repair pathway by showing it generates ICL-induced double-strand breaks at S-phase forks and physically and genetically interacts with Rad54.

    Evidence Mus81-/- ES cells with PFGE DSB quantification, reciprocal co-IP, and Mus81/Rad54 double-mutant survival analysis

    PMID:17036055

    Open questions at the time
    • Whether Rad54 acts before or after EME1-dependent incision unclear
    • EME1's direct contribution distinct from Mus81 not isolated
  5. 2008 High

    Provided the structural basis for substrate recognition and bilateral cleavage, revealing how the EME1 linker and Mus81 active-site cleft position branched DNA for coordinated incision.

    Evidence Crystal structure of the Mus81-Eme1 complex with functional mutagenesis, plus kinetic analysis of cooperative cruciform cleavage

    PMID:18310322 PMID:18413719

    Open questions at the time
    • Structure lacked a bound DNA substrate at this stage
    • Regulation of the catalytic cycle in cells not addressed
  6. 2008 Medium

    Identified physical and transcriptional regulators of EME1, including Rad54 stimulation of activity, Np95 chromatin co-localization, and STAT3-driven transcriptional upregulation after topoisomerase inhibition.

    Evidence In vitro stimulation assays with species controls, co-IP, immunofluorescence co-localization, and ChIP/reporter analysis of the EME1 promoter

    PMID:18245483 PMID:18692478 PMID:19017809

    Open questions at the time
    • Functional consequence of Np95 co-localization not defined
    • Whether STAT3 regulation operates outside topoisomerase-inhibited cells unknown
  7. 2011 Medium

    Connected Mus81-EME1 to checkpoint control, showing that loss of Wee1 or Chk1 unleashes EME1-dependent fork cleavage that drives replication stress and DNA damage.

    Evidence Co-IP of Wee1-Mus81 and RNAi co-depletion epistasis with cell-cycle and DSB readouts in checkpoint-deficient cells

    PMID:21858151 PMID:21859861

    Open questions at the time
    • Direct phosphoregulation of EME1 by these kinases not demonstrated here
    • Single-lab epistasis without reconstitution
  8. 2013 High

    Defined cell-cycle and checkpoint phosphorylation as the master switch activating the enzyme and showed that CDK-triggered assembly into the SLX-MUS holoenzyme coordinates Holliday junction resolution at G2/M.

    Evidence Phospho-site mapping and mutant analysis (Cdc2/Rad3 on Eme1; CDK on the holoenzyme), in vitro reconstitution of SLX-MUS, HJ cleavage assays, and chromosome-segregation phenotyping

    PMID:22730299 PMID:23584455 PMID:24076219 PMID:24076221

    Open questions at the time
    • Precise phospho-sites on mammalian EME1 versus SLX4 not fully resolved
    • How phosphorylation restructures the active site biochemically unclear
  9. 2013 High

    Established the roles of MUS81-EME1 at interstrand crosslinks and common fragile sites, showing FANCA-dependent recruitment and stimulation of ICL incision and FANCD2/ERCC1 co-localization needed for mitotic processing of under-replicated DNA.

    Evidence Co-IP, cellular ICL recruitment, in vitro ICL-substrate incision assays, and mitotic-chromosome immunofluorescence with co-depletion phenotypes

    PMID:23811686 PMID:24170812

    Open questions at the time
    • Order of FANCA recruitment relative to other Fanconi factors not resolved
    • Distinct EME1 contribution to fragile-site processing not isolated from Mus81
  10. 2014 High

    Captured the enzyme bound to its substrate, defining the hydrophobic wedge and 5'-end binding pocket that bend DNA and explain preferential 3'-flap cleavage.

    Evidence X-ray crystallography of human Mus81-Eme1-DNA complexes with biochemical and biophysical validation

    PMID:24733841

    Open questions at the time
    • Structure of a productive Holliday-junction-bound state not obtained
    • How phosphoregulation alters the captured conformation unknown
  11. 2016 Medium

    Revealed pathological and viral regulation of EME1 abundance, with HIV-1 Vpr hijacking CRL4-DCAF1 to degrade MUS81-EME1, and demonstrated GEN1/EME1 redundancy in junction resolution in mice.

    Evidence Co-IP, Vpr mutant and ubiquitin-ligase perturbation analysis, and Gen1/Eme1 double-mutant mouse genetics

    PMID:27354282 PMID:27383418

    Open questions at the time
    • Functional rationale for viral targeting of EME1 unresolved
    • Degree of GEN1/EME1 redundancy in human cells untested
  12. 2022 High

    Refined the activation logic by showing direct ATR/Chk1 phosphorylation and SUMO-interacting motifs on Eme1, and by showing CDK1 phosphorylation of SLX4 folds an SAP domain that binds and relaxes MUS81-EME1 substrate specificity.

    Evidence In vitro kinase and endonuclease assays, phospho-site and SIM mutagenesis, structural analysis of phospho-SLX4MBR, and genetic viability assays

    PMID:29850896 PMID:35452455 PMID:36288699

    Open questions at the time
    • Integration of EME1-intrinsic versus SLX4-mediated regulation in a single model incomplete
    • Role of EME1 SUMO interactions in mammalian cells not tested
  13. 2025 Medium

    Linked EME1 expression to therapeutic vulnerability, showing SETD1A-driven EME1 transcription sets PARP-inhibitor sensitivity in HR-deficient cancers.

    Evidence siRNA/CRISPR depletion of SETD1A and EME1 with HR assays, Olaparib viability, and RNAseq

    PMID:39994444

    Open questions at the time
    • Mechanism by which EME1 loss restores HR not defined
    • Generality across tumor genotypes untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the multiple phosphorylation, SUMO, and scaffold inputs are integrated to switch EME1 between protective junction resolution and deleterious fork cleavage in vivo remains unresolved.
  • No unified model coupling EME1 regulation to substrate choice in cells
  • Distinct contributions of EME1 versus Mus81 to each pathway not fully separated

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140097 catalytic activity, acting on DNA 5 GO:0016787 hydrolase activity 3 GO:0003677 DNA binding 2
Localization
GO:0000228 nuclear chromosome 1 GO:0005634 nucleus 1
Pathway
R-HSA-1474165 Reproduction 3 R-HSA-1640170 Cell Cycle 3 R-HSA-69306 DNA Replication 3 R-HSA-73894 DNA Repair 3
Partners
ERCC1FANCAMUS81RAD54SLX1SLX4UHRF1WEE1
Complex memberships
Mus81-EME1SLX-MUS holoenzyme

Evidence

Reading pass · 30 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2001 Mus81 and Eme1 form a heterodimeric endonuclease complex that resolves Holliday junctions into linear duplex products. Both subunits are required during meiosis at a late step of meiotic recombination, and the meiotic defect of mus81 mutants is rescued by a bacterial Holliday junction resolvase. Biochemical endonuclease assay with purified complex, genetic epistasis (rescue by RusA resolvase), co-immunoprecipitation to identify Eme1 as associated partner Cell High 11719193
2002 Purified recombinant fission yeast Mus81-Eme1 readily cleaves replication fork structures but cleaves synthetic Holliday junctions relatively poorly in vitro; hypersensitivity of mus81, eme1, and rqh1 mutants to replication fork-stalling agents is suppressed by the Holliday junction resolvase RusA, and synthetic lethality of mus81− rqh1− is also suppressed by RusA. In vitro endonuclease assay with purified recombinant Mus81-Eme1; genetic epistasis/suppressor analysis with RusA The Journal of biological chemistry High 12084712
2002 Fission yeast Mus81-Eme1 and budding yeast Mus81-Mms4 preferentially cleave reversed replication fork structures (where leading/lagging strands are juxtaposed or a single-stranded tail is present) over normal replication forks or intact Holliday junctions; cleavage occurs predominantly 3–6 bp 5' of the junction point on the leading strand template. In vitro endonuclease assay with purified recombinant enzymes on defined DNA substrates with cleavage site mapping The Journal of biological chemistry High 12473680
2003 Human EME1 was identified as the homolog of S. pombe Eme1; purified human Mus81-Eme1 heterodimer is an endonuclease with high specificity for synthetic replication fork structures and 3'-flap substrates, cleaving Holliday junctions ~75-fold less efficiently than flap/fork structures. Protein purification and in vitro endonuclease assay on multiple defined DNA substrates The Journal of biological chemistry High 12721304
2003 Endogenous and recombinant fission yeast Mus81-Eme1 preferentially cleaves nicked Holliday junctions; cleavage occurs on the strand opposing the nick, resolving the structure by a 'nick and counternick' mechanism with quasi-simultaneous resolving cuts by the endogenous complex. In vitro endonuclease assay with endogenous and recombinant Mus81-Eme1 on nicked vs intact Holliday junctions; kinetic analysis Molecular cell High 14527419
2003 Purified fission yeast Mus81-Eme1 preferentially cleaves junctions mimicking intermediates formed during the transition from double-strand break to double Holliday junction (nicked HJ-like structures), cleaving in precisely the correct orientation to guarantee crossover formation; Mus81-Eme1 is required for meiotic crossover generation. In vitro endonuclease assay with purified enzyme; genetic analysis of meiotic crossover frequencies in mus81/eme1 mutants Molecular cell High 14527420
2003 Mouse Eme1 interacts with Mus81 to form a complex that preferentially cleaves 3'-flap structures and replication forks rather than Holliday junctions in vitro; Eme1-/- ES cells are hypersensitive to DNA cross-linking agents (mitomycin C, cisplatin) and exhibit spontaneous genomic instability. Co-immunoprecipitation, in vitro endonuclease assay, ES cell knockout with drug sensitivity assay and chromosome instability analysis The EMBO journal High 14609959
2003 Fission yeast mus81 mutants have normal or elevated gene conversion frequencies but 20- to 100-fold reduced crossing over, demonstrating that Mus81-Eme1 is specifically required for meiotic crossover resolution and that gene conversion and crossing over are genetically separable. Genetic analysis of meiotic recombination frequencies in mus81 mutants Genetics High 14704204
2006 Mus81, the catalytic subunit of the Mus81-Eme1 endonuclease, is involved in generating interstrand crosslink-induced DNA double-strand breaks from stalled replication forks during S-phase in mouse ES cells; Mus81 and Rad54 physically interact and function in the same ICL repair pathway. Mus81-/- mouse ES cells with DSB quantification by PFGE; co-immunoprecipitation of Mus81 and Rad54; double-mutant Mus81-/- Rad54-/- survival analysis The EMBO journal High 17036055
2008 Human Mus81-Eme1 catalyzes coordinate bilateral cleavage of Holliday junction structures sequentially within the lifetime of the enzyme-substrate complex, achieving symmetrical cleavage of cruciform substrates through a highly cooperative mechanism. Kinetic and enzymatic analysis with highly purified recombinant human Mus81-Eme1 using self-limiting cruciform substrates Proceedings of the National Academy of Sciences of the United States of America High 18310322
2008 Crystal structure of the Mus81-Eme1 complex was determined; both subunits contain a central nuclease domain and two C-terminal helix-hairpin-helix (HhH) motifs; a flexible 36-residue intradomain linker in Eme1's nuclease domain is essential for DNA recognition; basic residues in Mus81's active site cleft interact with the flexible arm of nicked Holliday junctions to position the opposing junction for catalysis. X-ray crystallography; functional mutagenesis of Eme1 linker and Mus81 active site residues Genes & development High 18413719
2008 Human Rad54 physically interacts with Mus81 (not Eme1) and stimulates Mus81-Eme1 endonuclease activity on Holliday junction-like intermediates in vitro; this stimulation is species-specific (S. cerevisiae Rad54 does not stimulate human Mus81-Eme1) and requires ATP-dependent formation of specific Rad54-DNA complexes. In vitro endonuclease stimulation assay; co-immunoprecipitation; species-specificity controls Proceedings of the National Academy of Sciences of the United States of America High 19017809
2008 EGFR-Src signaling activates STAT3, which binds the promoter of EME1 to transcriptionally upregulate EME1 expression in response to topoisomerase I inhibition, reducing DNA damage and enhancing cell survival. Chromatin immunoprecipitation (STAT3 binding to EME1 promoter); reporter assay; STAT3 activation analysis; EGFR/Src pathway inhibition Cancer research Medium 18245483
2008 Mammalian Eme1 interacts with Np95 (an E3 ubiquitin ligase involved in chromatin modification); Eme1 and Np95 co-localize on nuclear chromatin following camptothecin treatment and this co-localization depends on the Np95 RING finger domain. Co-immunoprecipitation; co-localization by immunofluorescence; RING finger mutant analysis Biochemical and biophysical research communications Medium 18692478
2011 Wee1 kinase physically interacts with Mus81 in vivo and regulates genomic stability during DNA replication through the Mus81-Eme1 endonuclease; the DNA damage response induced by Wee1 depletion critically depends on Mus81-Eme1, and co-depletion of Mus81 and Wee1 abrogates the S-phase delay caused by Wee1 loss. Co-immunoprecipitation (Wee1-Mus81 interaction); RNAi co-depletion epistasis; cell cycle analysis The Journal of cell biology Medium 21859861
2011 Mus81/Eme1 endonuclease complex generates DNA double-strand breaks at replication forks when Chk1 activity is compromised; Mus81/Eme1-dependent DNA damage (rather than increased fork stalling) is the cause of incomplete replication in Chk1-deficient cells, and Mus81/Eme1 depletion alleviates the S-phase progression defects of Chk1-deficient cells. RNAi depletion of Mus81/Eme1 in Chk1-inhibited cells; DSB quantification; S-phase progression analysis PloS one Medium 21858151
2012 Budding yeast Mus81-Mms4 nuclease activity is strictly regulated during the mitotic cell cycle by CDK (Cdc28)- and Polo-like kinase (Cdc5)-dependent phosphorylation of the non-catalytic subunit Mms4 (EME1 ortholog); phosphorylation occurs only after bulk DNA synthesis and before chromosome segregation and is absolutely required for Mus81-Mms4 function. Cell cycle phosphorylation analysis; phosphorylation-defective mms4 mutant; in vitro nuclease assay; genetic sensitivity assays Nucleic acids research High 22730299
2013 In human cells, SLX1-SLX4 and MUS81-EME1 associate at the G2/M transition in response to CDK-mediated phosphorylation to form a stable SLX-MUS holoenzyme that can be reconstituted in vitro; the SLX-MUS complex functions as a Holliday junction resolvase that coordinates the active sites of both endonucleases, achieving more efficient and orchestrated HJ resolution than SLX1-SLX4 alone. Co-immunoprecipitation; in vitro reconstitution of SLX-MUS holoenzyme; biochemical HJ cleavage assay; cell depletion with chromosome segregation phenotyping Molecular cell High 24076221
2013 In mouse cells, SLX1 and MUS81-EME1 act together to resolve Holliday junctions in a manner requiring tethering to the SLX4 scaffold; SLX1, like MUS81-EME1, is required for repair of DNA interstrand crosslinks. Mouse Slx1 and Slx4 gene disruption; HJ resolution assay; ICL repair assays; structure-function analysis Molecular cell High 24076219
2013 In fission yeast, Mus81-Eme1 Holliday junction resolvase is activated in response to DNA damage through both Cdc2(CDK1)- and Rad3(ATR)-dependent phosphorylation of Eme1; this activation prevents gross chromosomal rearrangements in cells lacking the BLM-related helicase Rqh1. Phosphorylation site mapping of Eme1; kinase-dead and phospho-mutant analysis; chromosome rearrangement assays; in vitro endonuclease activity measurements Nature structural & molecular biology High 23584455
2013 ERCC1 and MUS81-EME1 co-localize with FANCD2 on mitotic chromosomes at common fragile sites; depletion of either ERCC1 or MUS81-EME1 impairs processing of late replication intermediates/under-replicated DNA at CFSs during mitosis, leading to increased chromosome bridges during anaphase and DNA damage accumulation in the following G1 phase. Immunofluorescence co-localization on mitotic chromosomes; RNAi depletion; chromosome bridge quantification Nature cell biology High 23811686
2013 FANCA physically interacts with MUS81 and recruits it to interstrand crosslink (ICL) lesions; purified MUS81-EME1 incises DNA at the 5' side of a psoralen ICL in fork structures, and FANCA greatly enhances this MUS81-EME1-mediated ICL incision activity. Co-immunoprecipitation; laser-induced ICL formation in cells; in vitro endonuclease assay with ICL-containing substrates; truncated FANCA analysis Nucleic acids research High 24170812
2014 Crystal structures of human Mus81-Eme1 bound to 3'-flap DNA substrates reveal substrate-induced conformational changes; key structural features include a hydrophobic wedge in Mus81 that separates pre- and post-nick duplex DNA, and a '5' end binding pocket' that hosts the 5' nicked end of post-nick DNA; these features drive sharp DNA bending and incision strand placement at the active site, explaining the preferential cleavage of 3'-flap substrates with 5' nicked ends. X-ray crystallography of human Mus81-Eme1-DNA complexes; biochemical and biophysical validation The EMBO journal High 24733841
2016 HIV-1 Vpr down-regulates both MUS81 and EME1 by hijacking the host CRL4-DCAF1 E3 ubiquitin ligase complex; this down-regulation is independent of SLX4-SLX1 and does not require direct Vpr interaction with MUS81-EME1. Co-immunoprecipitation; Vpr mutant analysis; ubiquitin ligase complex perturbation; protein level quantification The Journal of biological chemistry Medium 27354282
2016 Gen1 and Eme1 play redundant roles in HJ resolution, DNA repair, and meiotic recombination in mice; combined homozygous Gen1 and Eme1 mutations cause synthetic lethality during early embryonic development. Mouse genetics; MEF cell survival assays with DNA-damaging agents; meiotic recombination analysis in double mutants DNA and cell biology Medium 27383418
2018 CK2 kinase phosphorylates MUS81 at Serine 87 in late-G2/mitosis and upon mild replication stress; this phosphorylation promotes MUS81 interaction with SLX4, enhancing MUS81 complex function; S87 phosphorylation is suppressed in S-phase and is mainly detected in MUS81 molecules associated with EME1. Phosphorylation site mapping; phosphomimic and phosphoablative MUS81 mutants; co-immunoprecipitation (MUS81-SLX4); cell cycle analysis; DSB detection Nucleic acids research Medium 29850896
2020 Mus81-Eme1 aberrantly cleaves under-replicated DNA engaged in mitotic DNA synthesis when Chk1 is depleted, causing chromosome segregation defects; supplementing cells with nucleosides to complete mitotic DNA synthesis restrains this Mus81-Eme1-dependent DNA damage. Chk1 depletion with RNAi; Mus81-Eme1 co-depletion epistasis; nucleoside supplementation rescue; chromosome segregation quantification Science advances Medium 33298441
2022 In fission yeast, direct phosphorylation of Eme1 by the Rad3(ATR) checkpoint kinase is essential for catalytic stimulation of Mus81-Eme1; Chk1-mediated phosphorylation also contributes when combined with Rad3ATR phosphorylation; two SUMO-interacting motifs (SIMs) in the N-terminal domain of Eme1 are also required for cell survival in the absence of Rqh1BLM; abrogating bimodal phosphorylation plus mutating the SIMs is incompatible with rqh1Δ cell viability. Rad3ATR phosphorylation site identification and mutagenesis; in vitro kinase assay; endonuclease activity assay; SIM mutant analysis; genetic viability assays PLoS genetics High 35452455
2022 CDK1-cyclin B phosphorylates SLX4 residues T1544, T1561, and T1571 in the MUS81-binding region (SLX4MBR); phosphorylated SLX4MBR drives folding of an SAP domain which mediates high-affinity interaction with MUS81-EME1 and relaxes the substrate specificity of MUS81-EME1 to stimulate cleavage of replication and recombination structures. In vitro CDK1-cyclin B kinase assay; structural analysis of phospho-SLX4MBR; biochemical MUS81-EME1 cleavage assay; co-immunoprecipitation Cell reports High 36288699
2025 SETD1A-dependent transcription of EME1 correlates with sensitivity to PARP inhibitor Olaparib in BRCA1- or ATM-deficient cancer cells; loss of SETD1A or EME1 drives resistance to Olaparib and partially restores homologous recombination. siRNA/CRISPR depletion of SETD1A and EME1; HR assay; Olaparib cell viability; RNAseq British journal of cancer Medium 39994444

Source papers

Stage 0 corpus · 47 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2001 Mus81-Eme1 are essential components of a Holliday junction resolvase. Cell 455 11719193
2013 Coordinated actions of SLX1-SLX4 and MUS81-EME1 for Holliday junction resolution in human cells. Molecular cell 261 24076221
2003 Generating crossovers by resolution of nicked Holliday junctions: a role for Mus81-Eme1 in meiosis. Molecular cell 259 14527420
2006 The structure-specific endonuclease Mus81-Eme1 promotes conversion of interstrand DNA crosslinks into double-strands breaks. The EMBO journal 245 17036055
2013 ERCC1 and MUS81-EME1 promote sister chromatid separation by processing late replication intermediates at common fragile sites during mitosis. Nature cell biology 236 23811686
2002 Mus81-Eme1 and Rqh1 involvement in processing stalled and collapsed replication forks. The Journal of biological chemistry 203 12084712
2003 Identification and characterization of the human mus81-eme1 endonuclease. The Journal of biological chemistry 175 12721304
2011 Wee1 controls genomic stability during replication by regulating the Mus81-Eme1 endonuclease. The Journal of cell biology 162 21859861
2003 The endogenous Mus81-Eme1 complex resolves Holliday junctions by a nick and counternick mechanism. Molecular cell 149 14527419
2013 Cooperative control of holliday junction resolution and DNA repair by the SLX1 and MUS81-EME1 nucleases. Molecular cell 127 24076219
2014 Roles of SLX1-SLX4, MUS81-EME1, and GEN1 in avoiding genome instability and mitotic catastrophe. Genes & development 116 24831703
2007 Exploring the roles of Mus81-Eme1/Mms4 at perturbed replication forks. DNA repair 114 17409028
2003 Eme1 is involved in DNA damage processing and maintenance of genomic stability in mammalian cells. The EMBO journal 114 14609959
2012 Cell cycle-dependent regulation of the nuclease activity of Mus81-Eme1/Mms4. Nucleic acids research 106 22730299
2002 Cleavage of model replication forks by fission yeast Mus81-Eme1 and budding yeast Mus81-Mms4. The Journal of biological chemistry 102 12473680
2003 Fission yeast Mus81.Eme1 Holliday junction resolvase is required for meiotic crossing over but not for gene conversion. Genetics 100 14704204
2011 Structure-specific DNA endonuclease Mus81/Eme1 generates DNA damage caused by Chk1 inactivation. PloS one 96 21858151
2007 Cleavage of stalled forks by fission yeast Mus81/Eme1 in absence of DNA replication checkpoint. Molecular biology of the cell 68 18032583
2008 Cleavage mechanism of human Mus81-Eme1 acting on Holliday-junction structures. Proceedings of the National Academy of Sciences of the United States of America 60 18310322
2006 Haploinsufficiency of the Mus81-Eme1 endonuclease activates the intra-S-phase and G2/M checkpoints and promotes rereplication in human cells. Nucleic acids research 59 16456034
2013 Regulation of Mus81-Eme1 Holliday junction resolvase in response to DNA damage. Nature structural & molecular biology 54 23584455
2008 Crystal structure of the Mus81-Eme1 complex. Genes & development 54 18413719
2008 The EGFR-STAT3 oncogenic pathway up-regulates the Eme1 endonuclease to reduce DNA damage after topoisomerase I inhibition. Cancer research 52 18245483
2016 SLX4-SLX1 Protein-independent Down-regulation of MUS81-EME1 Protein by HIV-1 Viral Protein R (Vpr). The Journal of biological chemistry 34 27354282
2008 Human Rad54 protein stimulates human Mus81-Eme1 endonuclease. Proceedings of the National Academy of Sciences of the United States of America 34 19017809
2014 Crystal structures of the structure-selective nuclease Mus81-Eme1 bound to flap DNA substrates. The EMBO journal 33 24733841
2020 Mus81-Eme1-dependent aberrant processing of DNA replication intermediates in mitosis impairs genome integrity. Science advances 31 33298441
2018 Phosphorylation by CK2 regulates MUS81/EME1 in mitosis and after replication stress. Nucleic acids research 25 29850896
2007 Mus81-Eme1-dependent and -independent crossovers form in mitotic cells during double-strand break repair in Schizosaccharomyces pombe. Molecular and cellular biology 23 17353272
2022 Phosphorylation of the DNA repair scaffold SLX4 drives folding of the SAP domain and activation of the MUS81-EME1 endonuclease. Cell reports 21 36288699
2009 Functional evidence for Eme1 as a marker of cisplatin resistance. International journal of cancer 20 19267403
2011 Novel insights into maintaining genomic integrity: Wee1 regulating Mus81/Eme1. Cell division 19 22152133
2008 Interplay between Np95 and Eme1 in the DNA damage response. Biochemical and biophysical research communications 17 18692478
2021 Essential meiotic structure-specific endonuclease1 (EME1) promotes malignant features in gastric cancer cells via the Akt/GSK3B/CCND1 pathway. Bioengineered 12 34719326
2016 Gen1 and Eme1 Play Redundant Roles in DNA Repair and Meiotic Recombination in Mice. DNA and cell biology 12 27383418
2013 Damage-dependent regulation of MUS81-EME1 by Fanconi anemia complementation group A protein. Nucleic acids research 12 24170812
2023 FIBP interacts with transcription factor STAT3 to induce EME1 expression and drive radioresistance in lung adenocarcinoma. International journal of biological sciences 10 37564211
2014 Cetuximab induces eme1-mediated DNA repair: a novel mechanism for cetuximab resistance. Neoplasia (New York, N.Y.) 10 24731284
2023 Identification of small-molecule inhibitors of human MUS81-EME1/2 by FRET-based high-throughput screening. Bioorganic & medicinal chemistry 7 37352577
2022 Regulation of Mus81-Eme1 structure-specific endonuclease by Eme1 SUMO-binding and Rad3ATR kinase is essential in the absence of Rqh1BLM helicase. PLoS genetics 4 35452455
2013 Effect of EME1 exon variant Ile350Thr on risk and early onset of breast cancer in southern Chinese women. Journal of biomedical research 4 23720674
2022 A protocol to determine the activities of human MUS81-EME1&2 endonucleases. STAR protocols 3 35819885
2025 SETD1A-dependent EME1 transcription drives PARPi sensitivity in HR deficient tumour cells. British journal of cancer 2 39994444
2025 Oncogenic EME1 promotes tumor progression and immune modulation in human cancers with therapeutic targeting potential. Discover oncology 1 41082058
2022 The Glu69Asp Polymorphism of EME1 Gene is Associated with an Increased Risk of Hepatocellular Carcinoma in Guangxi Population, China. International journal of general medicine 1 36281338
2026 Targeting EME1 Increases the Sensitivity of Camptothecin in Nasopharyngeal Carcinoma Cells. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 0 41532283
2025 LncRNA-EME1 enhances BRCA1 recruitment and alters repair of DNA damage in cervical cancer radioresistance. Non-coding RNA research 0 41113473

Missed literature

Know a paper Affinage missed for EME1? Flag it for the maintainers and the community.

No submissions yet.