Made-to-order (14-16 weeks)
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
Value-added Deliverables
① 200ug * antigen (positive control); ② 1ml * Pre-immune serum (negative control);
Quality Guarantee
① Antibody purity can be guaranteed above 90% by SDS-PAGE detection; ② ELISA titer can be guaranteed 1: 64,000; ③ WB validation with antigen can be guaranteed positive;
Component of the post-replicative DNA mismatch repair system (MMR). Heterodimerizes with MSH2 to form MutS alpha, which binds to DNA mismatches thereby initiating DNA repair. MSH6 provides substrate-binding and substrate specificity to the complex. When bound, MutS alpha bends the DNA helix and shields approximately 20 base pairs. Acts mainly to repair base-base and single insertion-deletion mismatches that occur during replication, but can also repair longer insertion-deletion loops (IDLs), although with decreasing efficiency as the size of the extrahelical loop increases. After mismatch binding, forms a ternary complex with the MutL alpha heterodimer, which is thought to be responsible for directing the downstream MMR events, including strand discrimination, excision, and resynthesis. ATP binding and hydrolysis by the MutS alpha complex is crucial for MMR. Both subunits bind ATP, but with differing affinities, and their ATPase kinetics are also very different. MSH6 binds and hydrolyzes ATP rapidly, whereas MSH2 catalyzes ATP at a substantially slower rate. Binding to a mismatched base pair suppresses MSH6-catalyzed ATP hydrolysis, but not the activity of MSH2. ATP binding to both subunits is necessary to trigger a change in MutS alpha interaction with mismatched DNA, converting MutS alpha into a sliding clamp capable of hydrolysis-independent movement along DNA, and also facilitates formation of ternary complexes containing MutS and MutL proteins and the mismatch. May also be involved in resolution of recombination intermediates.
Gene References into Functions
MSH6 overexpression affected the integrity of the DNA replication fork, causing genome instability phenotypes.PMID:29654124
Msh2-Msh6 slides without hopping and is largely blocked by protein roadblocks.PMID:26837705
Msh2-Msh6 localizes PCNA to repair sites after mispair recognition.PMID:24981171
analysis of the interaction between the Msh2 and Msh6 nucleotide-binding sites in the Saccharomyces cerevisiae Msh2-Msh6 complexPMID:20089866
results suggest that MSH2-MSH6 binding to homoduplex regions of DNA recruits NHP6A, which then prevents further binding of MSH2-MSH6 to these sites unless a mismatch is present.PMID:19843605
genetic analysis of the interaction between the Saccharomyces cerevisiae MSH2-MSH6 and MLH1-PMS1 complexes with DNAPMID:15811858
Msh2 and Msh6 subunits have roles in the asymmetric ATPase and DNA mismatch binding activities of Saccharomyces cerevisiae Msh2-Msh6 mismatch repair proteinPMID:16214425
A detailed biochemical analysis of four dominant mutant Msh2-Msh6 complexes is presentedPMID:16407100
Glu339 in Msh6 may have a specialized role in repairing mismatches containing oxidized bases.PMID:17141577
The N-terminal repeat is involved in mismatch repair that is partially redundant with PCNA binding.PMID:17531814
communication between the mispair-binding domain and the ATPase domain is conserved between Msh2-Msh3 and Msh2-Msh6PMID:17573527
Interactions between Msh2-Msh6 and DNA are dominated by lateral movement of the protein along the helical axis and have implications for how MutS family members travel along DNA at different stages of the mismatch repair reaction.PMID:17996701