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

MUS81 Mus81p

Encodes an Arabidopsis homolog of the endonuclease MSU81. T-DNA insertion lines of AtMSU81 have a deficiency in homologous recombination in somatic cells but only after genotoxic stress. Crosses with a hyperrecombinogenic mutant of the AtRecQ4A helicase resulted in synthetic lethality in the double mutant. (from NCBI)
Top mentioned proteins: Eme1, rad1, CAN, ERCC1, Blm
Papers on Mus81
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.
MUS81 and SEND1 are essential for telomere stability in Arabidopsis.
Gallego et al., Clermont-Ferrand, France. In Plant Cell, Jan 2016
Combined absence of MUS81 and SEND1 however results in severe developmental defects, spontaneous cell death and genome instability.
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.
The Translesion Polymerase ζ Has Roles Dependent on and Independent of the Nuclease MUS81 and the Helicase RECQ4A in DNA Damage Repair in Arabidopsis.
Puchta et al., Karlsruhe, Germany. In Plant Physiol, Dec 2015
DNA polymerase zeta catalytic subunit REV3 is known to play an important role in the repair of DNA damage induced by cross-linking and methylating agents.
Cellular Recognition and Repair of Monofunctional-Intercalative Platinum-DNA Adducts.
Bierbach et al., Winston-Salem, United States. In Chem Res Toxicol, Dec 2015
At the same dose, P1-A1, but not cisplatin, elicited a distinct requirement for DNA double-strand break repair and stalled replication fork repair, which caused nuclear fluorescent staining related to high levels of MUS81, a specialized repair endonuclease, and phosphorylated histone protein γ-H2AX.
Acute MUS81 depletion leads to replication fork slowing and a constitutive DNA damage response.
Ying et al., Hangzhou, China. In Oncotarget, Dec 2015
The MUS81 protein belongs to a conserved family of DNA structure-specific nucleases that play important roles in DNA replication and repair.
DNA replication restart and cellular dynamics of Hef helicase/nuclease protein in Haloferax volcanii.
Myllykallio et al., Palaiseau, France. In Biochimie, Nov 2015
Here we will described how genetic and imaging studies have revealed the central role of the archaeal helicase/nuclease Hef belonging to the XPF/MUS81/FANCM family of endonucleases in repair of arrested replication forks.
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.
Hold your horSSEs: controlling structure-selective endonucleases MUS81 and Yen1/GEN1.
Matos et al., Santiago de Compostela, Spain. In Front Genet, 2014
Recent studies on two conserved SSEs - MUS81 and Yen1/GEN1- uncovered multiple layers of regulation that operate to carefully tailor JM-processing according to specific cellular needs.
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.
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.
Mus81-mediated DNA cleavage resolves replication forks stalled by topoisomerase I-DNA complexes.
Pommier et al., Bethesda, United States. In J Cell Biol, 2011
Mus81 cleaves stalled replication forks, which allows dissipation of the excessive supercoiling resulting from Top1 inhibition, spontaneous reversal of Top1cc, and replication fork progression.
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.
Inactivation of chk2 and mus81 leads to impaired lymphocytes development, reduced genomic instability, and suppression of cancer.
Hakem et al., Toronto, Canada. In Plos Genet, 2011
data indicate that an important role for Chk2 is maintaining lymphocyte development and that dual inactivation of Chk2 and Mus81 remarkably inhibits cancer
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.
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