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spontaneous mitotic crossovers that occur when FANCM is missing are dependent on MUS312 and either MUS81 or SLX1.
did not find any role for MUS81-MMS4 in meiotic crossing over
SEND1 has at most a minor role in resolution of the Holliday junction but acts as an essential backup to MUS81 for resolution of toxic replication structures to ensure genome stability and to maintain telomere integrity.
Data show that DNA polymerase zeta catalytic subunit REV3 cooperates with ATP-dependent DNA helicase RECQ4A and e ndonuclease MUS81 to repair DNA interstrand cross links.
RECQ4A and MUS81 define RAD5A-independent pathways of DNA repair. RECQ4A and MUS81 act in parallel pathways presumably to resolve replication-associated DNA intermediates.
The role of AtMUS81 in meiotic and mitotic recombination.
AtMUS81 is involved in a secondary subset of meiotic crossovers that are interference insensitive.
The role of MUS81 in the reproduction and growth of A. thaliana, via its expression and metabolism during meiosis, is reported.
Both MUS81-EME1 endonuclease complexes are involved in DNA recombination and repair processes in Arabidopsis.
this study shows that immune rejection of prostate cancer cells relies on Mus81 and STING
Our study highlights the importance of the cooperation between Rad54 (show RAD54L ELISA Kits) and Mus81 for mediating DNA DSB repair and restraining chromosome missegregation.
Mus81 knockdown improves the chemosensitivity of HCC (show FAM126A ELISA Kits) cells by inducing S-phase arrest and promoting apoptosis through CHK1 (show CHEK1 ELISA Kits) pathway, suggesting Mus81 as a novel therapeutic target for HCC (show FAM126A ELISA Kits).
Using mice deficient in both Mus81 and the FA pathway protein FancC (show FANCC ELISA Kits), we show both proteins cooperate in parallel pathways, as concomitant loss of FancC (show FANCC ELISA Kits) and Mus81 triggered cell-type-specific proliferation arrest, apoptosis and DNA damage accumulation in utero.
Data indicate that SLX1 and MUS81-EME1 nucleases act together to resolve Holliday junctions (HJs) in a manner that requires tethering to SLX4 (show BTBD12 ELISA Kits).
FBH1 (show FBXO18 ELISA Kits) helicase (show DNA2 ELISA Kits) activity is required to eliminate cells with excessive replication stress through the generation of MUS81-induced DNA double-strand breaks.
data indicate that an important role for Chk2 (show CHEK2 ELISA Kits) is maintaining lymphocyte development and that dual inactivation of Chk2 (show CHEK2 ELISA Kits) and Mus81 remarkably inhibits cancer
studies demonstrate a critical role for the proper biallelic expression of the mammalian Mus81 in the maintenance of genomic integrity and tumor suppression
Mus81 acts at a late step in the repair of cross-link-induced lesions
Mus81-Eme1- and Rad54 (show RAD54L ELISA Kits)-mediated homologous recombination are involved in the same DNA replication-dependent interstrand crosslinks repair pathway
Low EZH2 (show EZH2 ELISA Kits) or MUS81 expression levels predict chemoresistance.
RECQ5 removes RAD51 filaments stabilizing stalled replication forks at common fragile sites and hence facilitates CFS cleavage by MUS81-EME1.
The mitotic DNA synthesis is RAD52 (show RAD52 ELISA Kits) dependent, and RAD52 (show RAD52 ELISA Kits) is required for the timely recruitment of MUS81 and POLD3 (show POLD3 ELISA Kits) to common fragile sites in early mitosis.
Data suggest that dimeric GEN1 binds with high affinity/selectivity to Holliday junctions, introducing two symmetrical hydrolytic cleavages of phosphodiester backbone; at present, less is known about SLX1-SLX4-MUS81-EME1 resolving enzyme complex. (GEN1 = Holliday junction 5' flap endonuclease; SLX = structure-specific endonuclease subunit; MUS81 = MUS81 endonuclease; EME1 = essential meiotic endonuclease 1) [REVIEW]
down-regulation of MUS81 expression in ovarian cancer cells inhibited cell proliferation and colony formation ability, and influenced cell cycle progression
SLX4-SLX1 Protein-independent Down-regulation of MUS81-EME1 Protein by HIV-1 Viral Protein R (Vpr).
Mus81 sumoylation is important for normal mitotic chromosome congression.
Data suggest that the ATM (show ATM ELISA Kits)/Chk2 (show CHEK2 ELISA Kits) may promote the repair of DNA damage caused by cisplatin by sustaining methyl methanesulfonate and ultraviolet-sensitive gene clone 81, and the double-strand breaks generated by methyl methanesulfonate and ultraviolet-sensitive gene clone 81 may activate the ATM (show ATM ELISA Kits)/Chk2 (show CHEK2 ELISA Kits) pathway.
Avoiding damage formation through invalidation of Mus81-Eme2 (show EME2 ELISA Kits) and Mre11 (show MRE11A ELISA Kits), or preventing damage signaling by turning off the ATM (show ATM ELISA Kits) pathway, suppresses the replication phenotypes of Chk1 (show CHEK1 ELISA Kits)-deficient cells.
Interacts with EME1 and EME2 to form a DNA structure- specific endonuclease with substrate preference for branched DNA structures with a 5'-end at the branch nick. Typical substrates include 3'-flap structures, replication forks and nicked Holliday junctions. May be required in mitosis for the processing of stalled or collapsed replication forks.
, crossover junction endonuclease MUS81
, MUS81 endonuclease homolog (S. cerevisiae)
, MUS81 endonuclease homolog
, MUS81 protein
, crossover junction endonuclease MUS81-like
, SLX3 structure-specific endonuclease subunit homolog
, hypothetical protein