Monoclonal Anti-Mus81 (mouse IgG2a isotype) is derived from the hybridoma MTA30 2G10/3 produced by the fusion of mouse myeloma cells (Sp2/0 Ag.14 cells) and splenocytes from BALB/c mice immunized with Mus81 protein. Crossover junction endonuclease Mus81 protein was identified by screening a human cerebellum cDNA library with a probe from the yeast Mus81. The human Mus81 has 551 amino acids with a molecular mass of 59 kDa. The highest sequence similarity between different species is around the VERKX3D motif. This motif is conserved in the endonuclease family (XPF) family of nucleases. The protein has helix-hairpin-helix DNA-binding domains in the N- and C-termini of the protein that are also conserved.
Immunogen
Mus81 protein.
Application
Anti-Mus81 antibody, Mouse monoclonal has been used in immunofluorescence, immunoblotting and immunoprecipitation.
Biochem/physiol Actions
Crossover junction endonuclease Mus81 is elevated in cells exposed to agents that block DNA replication. Knockout mice that are homozygous Mus81-/-, or their heterozygous cohorts Mus81-/+, are susceptible to spontaneous chromosomal damage and cancer predisposition suggesting that this protein is important for genomic integrity and tumor suppression
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Interstrand cross-link (ICL) hypersensitivity is a characteristic trait of Fanconi anemia (FA). Although FANCD2-associated nuclease 1 (FAN1) contributes to ICL repair, FAN1 mutations predispose to karyomegalic interstitial nephritis (KIN) and cancer rather than to FA. Thus, the biological role of
The Mus81 solution to resolution: generating meiotic crossovers without Holliday junctions
A major driver of cancer chromosomal instability is replication stress, the slowing or stalling of DNA replication. How replication stress and genomic instability are connected is not known. Aphidicolin-induced replication stress induces breakages at common fragile sites, but the exact
Oncogenes induce genotoxic stress by mitotic processing of unusual replication intermediates
Neelsen KJ, et al.
The Journal of Cell Biology, 200(6), 699-708 (2013)
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