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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

MMS4 Mms4p

Eme1, Mms4
This gene encodes a protein that complexes with methyl methanesulfonate-sensitive UV-sensitive 81 protein to form an endonuclease complex. The encoded protein interacts with specifc DNA structures including nicked Holliday junctions, 3'-flap structures and aberrant replication fork structures. This protein may be involved in repairing DNA damage and in maintaining genomic stability. Alternative splicing results in multiple transcript variants.[provided by RefSeq, Oct 2009] (from NCBI)
Top mentioned proteins: Mus81, CAN, rad1, ERCC1, Blm
Papers on Eme1
Survivin contributes to DNA repair by homologous recombination in breast cancer cells.
Barillé-Nion et al., Nantes, France. In Breast Cancer Res Treat, Jan 2016
Survivin depletion decreases the transcription of a set of genes involved in HR, decreases RAD51 protein expression and impairs the endonuclease complex MUS81/EME1 involved in the resolution of Holliday junctions.
Replication stress activates DNA repair synthesis in mitosis.
Hickson et al., Copenhagen, Denmark. In Nature, Jan 2016
The MUS81-EME1 structure-specific endonuclease promotes the appearance of chromosome gaps or breaks at CFSs following replicative stress.
Resolution of Recombination Intermediates: Mechanisms and Regulation.
Wyatt et al., United Kingdom. In Cold Spring Harb Symp Quant Biol, Oct 2015
These involve (1) BLM-Topoisomerase IIIα-RMI1-RMI2 (BTR complex), (2) SLX1-SLX4-MUS81-EME1 (SLX-MUS complex), and (3) GEN1.
DNA repair defects ascribed to pby1 are caused by disruption of Holliday junction resolvase Mus81-Mms4.
Rass et al., Basel, Switzerland. In Dna Repair (amst), Sep 2015
On the basis of genetic interaction profile similarity, we pinpoint disruption of Holliday junction resolvase Mus81-Mms4 as the mutation responsible for DNA repair phenotypes currently ascribed to pby1.
System-wide Analysis of SUMOylation Dynamics in Response to Replication Stress Reveals Novel Small Ubiquitin-like Modified Target Proteins and Acceptor Lysines Relevant for Genome Stability.
Vertegaal et al., Leiden, Netherlands. In Mol Cell Proteomics, May 2015
A large subset of these identified proteins function in one network that consists of interacting replication factors, transcriptional regulators, DNA damage response factors including MDC1, ATR-interacting protein ATRIP, the Bloom syndrome protein and the BLM-binding partner RMI1, the crossover junction endonuclease EME1, BRCA1, and CHAF1A.
Controlling meiotic recombinational repair - specifying the roles of ZMMs, Sgs1 and Mus81/Mms4 in crossover formation.
Fung et al., San Francisco, United States. In Plos Genet, 2014
Our analysis suggests that Mus81/Mms4 (Eme1), rather than just being a minor resolvase for COs is crucial for both COs and NCOs in preventing chromosome entanglements by removing 3'- flaps to promote second-end capture.
Holliday junction processing enzymes as guardians of genome stability.
West et al., London, United Kingdom. In Trends Biochem Sci, 2014
In mammalian cells, HJs are processed by the BTR (BLM-topoisomerase IIIα-RMI1-RMI2) complex, the SLX-MUS (SLX1-SLX4-MUS81-EME1) complex, and the GEN1 resolvase.
Holliday junction resolution: regulation in space and time.
West et al., London, United Kingdom. In Dna Repair (amst), 2014
A conserved network of core cell-cycle kinases and phosphatases modulate HJ metabolism by exerting spatial and temporal control over the activities of two structure-selective nucleases: yeast Mus81-Mms4 (human MUS81-EME1) and Yen1 (human GEN1).
Premature activation of the SLX4 complex by Vpr promotes G2/M arrest and escape from innate immune sensing.
Benkirane et al., Montpellier, France. In Cell, 2014
Direct interaction of Vpr with SLX4 induced the recruitment of VPRBP and kinase-active PLK1, enhancing the cleavage of DNA by SLX4-associated MUS81-EME1 endonucleases.
Mus81-Mms4 and Yen1 resolve a novel anaphase bridge formed by noncanonical Holliday junctions.
Machín et al., Santa Cruz de Tenerife, Spain. In Nat Commun, 2013
Here we report that the overlapping actions of the structure-selective endonucleases (SSEs) Mus81-Mms4/EME1 and Yen1/GEN1, but not Slx1-Slx4, are also essential to prevent the formation of spontaneous SCBs that depend on the homologous recombination pathway.
Resolving branched DNA intermediates with structure-specific nucleases during replication in eukaryotes.
Rass, Basel, Switzerland. In Chromosoma, 2013
In eukaryotes, multiple structure-specific nucleases, including Mus81-Mms4/MUS81-EME1, Yen1/GEN1, and Slx1-Slx4/SLX1-SLX4 (FANCP) have been implicated in the resolution of branched DNA intermediates.
A blooming resolvase at chromosomal fragile sites.
Muzi-Falconi et al., In Nat Cell Biol, 2013
Now CFS expression is shown to reflect the activity of the MUS81-EME1 resolvase complex which cooperates with the dissolving action of the BLM helicase to prevent uncontrolled chromosome breakage and to promote genome integrity.
MUS81 promotes common fragile site expression.
Hickson et al., Oxford, United Kingdom. In Nat Cell Biol, 2013
Here, we report that the DNA structure-specific nuclease MUS81-EME1 localizes to CFS loci in early mitotic cells, and promotes the cytological appearance of characteristic gaps or breaks observed at CFSs in metaphase chromosomes.
ERCC1 and MUS81-EME1 promote sister chromatid separation by processing late replication intermediates at common fragile sites during mitosis.
Rosselli et al., Villejuif, France. In Nat Cell Biol, 2013
To decipher the mechanisms protecting CFSs in G2/M, we searched for proteins that co-localize with FANCD2 on mitotic chromosomes, and identified XPF-ERCC1 and MUS81-EME1, two structure-specific endonucleases.
Mus81-Mms4 functions as a single heterodimer to cleave nicked intermediates in recombinational DNA repair.
Heyer et al., Davis, United States. In Mol Cell Biol, 2012
data support a model in which Mus81-Mms4 cleaves nicked recombination intermediates such as displacement loops (D-loops), nicked Holliday junctions, or 3' flaps but not intact Holliday junctions with four uninterrupted strands
Orchestrating the nucleases involved in DNA interstrand cross-link (ICL) repair.
McHugh et al., Oxford, United Kingdom. In Cell Cycle, 2012
Here, we review recent work showing that the XPF-ERCC1 endonuclease and the hSNM1A exonuclease act in the same pathway, together with SLX4, to initiate ICL repair, with the MUS81-EME1 fork incision activity becoming important in the absence of the XPF-SNM1A-SLX4-dependent pathway.
Wee1 controls genomic stability during replication by regulating the Mus81-Eme1 endonuclease.
Freire et al., Santa Cruz de Tenerife, Spain. In J Cell Biol, 2011
Results demonstrate a novel role of Wee1 in controlling Mus81-Eme1 and DNA replication in human cells.
Structure-specific DNA endonuclease Mus81/Eme1 generates DNA damage caused by Chk1 inactivation.
Jackson et al., Cambridge, United Kingdom. In Plos One, 2010
Data show that Mus81/Eme1-dependent DNA damage--rather than a global increase in replication-fork stalling--is the cause of incomplete replication in Chk1-deficient cells.
Functional overlap between the structure-specific nucleases Yen1 and Mus81-Mms4 for DNA-damage repair in S. cerevisiae.
West et al., London, United Kingdom. In Dna Repair (amst), 2010
Functional overlap between the structure-specific nucleases Yen1 and Mus81-Mms4 for DNA-damage repair in S. cerevisiae
Functional evidence for Eme1 as a marker of cisplatin resistance.
Miyagawa et al., Tokyo, Japan. In Int J Cancer, 2009
Low Eme1 levels were more sensitive to the drug than tumors with high levels.
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