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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 (show EME1 Proteins) endonuclease complexes are involved in DNA recombination and repair processes in Arabidopsis.
Mus81 knockdown improves the chemosensitivity of HCC (show FAM126A Proteins) cells by inducing S-phase arrest and promoting apoptosis through CHK1 (show CHEK1 Proteins) pathway, suggesting Mus81 as a novel therapeutic target for HCC (show FAM126A Proteins).
Using mice deficient in both Mus81 and the FA pathway protein FancC (show FANCC Proteins), we show both proteins cooperate in parallel pathways, as concomitant loss of FancC (show FANCC Proteins) 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.
FBH1 helicase 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 Proteins) is maintaining lymphocyte development and that dual inactivation of Chk2 (show CHEK2 Proteins) 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 (show EME1 Proteins)- and Rad54 (show RAD54L Proteins)-mediated homologous recombination are involved in the same DNA replication-dependent interstrand crosslinks repair pathway
Data suggest that Mus81 suppresses chromosomal instability by converting potentially detrimental replication-associated DNA structures into intermediates that are more amenable to DNA repair.
Analysis of meiotic progression in Mus81-nullizygous mice, and our results implicate the MUS81 pathway as a regulator of crossover frequency and placement in mammals.
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 (show EME1 Proteins) Protein by HIV-1 Viral Protein R (Vpr).
Mus81 sumoylation is important for normal mitotic chromosome congression.
Data suggest that the ATM (show ATM Proteins)/Chk2 (show CHEK2 Proteins) 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 Proteins)/Chk2 (show CHEK2 Proteins) pathway.
Avoiding damage formation through invalidation of Mus81-Eme2 (show EME2 Proteins) and Mre11 (show MRE11A Proteins), or preventing damage signaling by turning off the ATM (show ATM Proteins) pathway, suppresses the replication phenotypes of Chk1 (show CHEK1 Proteins)-deficient cells.
Mus81 regulates the rate of DNA replication during normal growth by promoting replication fork progression while reducing the frequency of replication initiation events.
Identification and characterization of MUS81 point mutations that abolish interaction with the SLX4 scaffold protein.MUS81 function in DNA interstrand crosslinks repair requires interaction with SLX4.
The data highlight the importance of Mus81 and Blm in DNA double-strand repair pathways, fertility, development and cancer.
Authors confirmed that HIV-1 Vpr induces degradation of Mus81 although, surprisingly, degradation is independent and genetically separable from Vprs ability to induce G2 arrest.
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