Anti-MSH2 antibody,Abcam,AB70270

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Host

Rabbit

Reactivity

Mouse, Human

Application

IHC-P, ICC/IF, WB, IP

Platform ID

BAB577300907

Abcam

Headquarters

Discovery Drive Cambridge Biomedical Campus Cambridge CB2 0AX UK

Contact

Tel: +44 (0)1223 696000
Fax: +44 (0)1223 215 215

Product Specifications
Scientific Background

Specifications

NameAnti-MSH2 antibody
Cat. No.AB70270
HostRabbit
IsotypeIgG
ReactivityMouse, Human
ApplicationIHC-P, ICC/IF, WB, IP
ClonalityPolyclonal
Concentration1 mg/mL Batch dependent concentration
ImmunogenSynthetic Peptide within Human MSH2 aa 850 to C-terminus. The exact immunogen used to generate this antibody is proprietary information.
PurityAffinity purification Immunogen
Appearance/FormLiquid
ShippingBlue Ice
FormulationpH: 7 - 8 Preservative: 0.09% Sodium azide Constituents: PBS, 1.815% Tris, 1.764% Sodium citrate
Storage+4°C
Regulatory StatusResearch Use Only

Scientific Background

Target data Component of the post-replicative DNA mismatch repair system (MMR). Forms two different heterodimers : MutS alpha (MSH2-MSH6 heterodimer) and MutS beta (MSH2-MSH3 heterodimer) which binds to DNA mismatches thereby initiating DNA repair. When bound, heterodimers bend the DNA helix and shields approximately 20 base pairs. MutS alpha recognizes single base mismatches and dinucleotide insertion-deletion loops (IDL) in the DNA. MutS beta recognizes larger insertion-deletion loops up to 13 nucleotides long. After mismatch binding, MutS alpha or beta 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. Recruits DNA helicase MCM9 to chromatin which unwinds the mismatch containing DNA strand (PubMed : 26300262). ATP binding and hydrolysis play a pivotal role in mismatch repair functions. The ATPase activity associated with MutS alpha regulates binding similar to a molecular switch : mismatched DNA provokes ADP-->ATP exchange, resulting in a discernible conformational transition that converts MutS alpha into a sliding clamp capable of hydrolysis-independent diffusion along the DNA backbone. This transition is crucial for mismatch repair. MutS alpha may also play a role in DNA homologous recombination repair. In melanocytes may modulate both UV-B-induced cell cycle regulation and apoptosis. See full target information MSH2

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