Key features and details
- Produced recombinantly (animal-free) for high batch-to-batch consistency and long term security of supply
- Rabbit monoclonal [EPR3943] to MSH2
- Suitable for: WB
- Knockout validated
- Reacts with: Human
Product nameAnti-MSH2 antibody [EPR3943]
See all MSH2 primary antibodies
DescriptionRabbit monoclonal [EPR3943] to MSH2
Tested applicationsSuitable for: WBmore details
Unsuitable for: Flow Cyt,ICC/IF or IP
Species reactivityReacts with: Human
Synthetic peptide within Human MSH2 aa 1-100 (N terminal). The exact sequence is proprietary.
- WB: A375, A431, SW480 and HeLa whole cell lysate (ab150035) IHC-P: Human colonic adenocarcinoma ICC/IF: HeLa cells
To see more of the key markers and tools you need to study the hallmarks of cancer, including genome instability and mutation, please visit the following page.
Mouse, Rat: We have preliminary internal testing data to indicate this antibody may not react with these species. Please contact us for more information.
This product is a recombinant monoclonal antibody, which offers several advantages including:
- - High batch-to-batch consistency and reproducibility
- - Improved sensitivity and specificity
- - Long-term security of supply
- - Animal-free production
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.
We are constantly working hard to ensure we provide our customers with best in class antibodies. As a result of this work we are pleased to now offer this antibody in purified format. We are in the process of updating our datasheets. The purified format is designated 'PUR' on our product labels. If you have any questions regarding this update, please contact our Scientific Support team.
Storage instructionsShipped at 4°C. Store at -20°C. Stable for 12 months at -20°C.
Storage bufferpH: 7.20
Preservative: 0.01% Sodium azide
Constituents: 0.31% Sodium citrate, 0.175% Sodium chloride, 0.0172% EDTA disodium salt, 59% PBS, 40% Glycerol, 0.05% BSA
Concentration information loading...
PurityProtein A purified
Our Abpromise guarantee covers the use of ab92473 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/1000 - 1/10000. Predicted molecular weight: 105 kDa.|
FunctionComponent 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. 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.
Tissue specificityUbiquitously expressed.
Involvement in diseaseDefects in MSH2 are the cause of hereditary non-polyposis colorectal cancer type 1 (HNPCC1) [MIM:120435]. Mutations in more than one gene locus can be involved alone or in combination in the production of the HNPCC phenotype (also called Lynch syndrome). Most families with clinically recognized HNPCC have mutations in either MLH1 or MSH2 genes. HNPCC is an autosomal, dominantly inherited disease associated with marked increase in cancer susceptibility. It is characterized by a familial predisposition to early onset colorectal carcinoma (CRC) and extra-colonic cancers of the gastrointestinal, urological and female reproductive tracts. HNPCC is reported to be the most common form of inherited colorectal cancer in the Western world. Cancers in HNPCC originate within benign neoplastic polyps termed adenomas. Clinically, HNPCC is often divided into two subgroups. Type I: hereditary predisposition to colorectal cancer, a young age of onset, and carcinoma observed in the proximal colon. Type II: patients have an increased risk for cancers in certain tissues such as the uterus, ovary, breast, stomach, small intestine, skin, and larynx in addition to the colon. Diagnosis of classical HNPCC is based on the Amsterdam criteria: 3 or more relatives affected by colorectal cancer, one a first degree relative of the other two; 2 or more generation affected; 1 or more colorectal cancers presenting before 50 years of age; exclusion of hereditary polyposis syndromes. The term "suspected HNPCC" or "incomplete HNPCC" can be used to describe families who do not or only partially fulfill the Amsterdam criteria, but in whom a genetic basis for colon cancer is strongly suspected. MSH2 mutations may predispose to hematological malignancies and multiple cafe-au-lait spots.
Defects in MSH2 are a cause of Muir-Torre syndrome (MuToS) [MIM:158320]; also abbreviated MTS. MuToS is a rare autosomal dominant disorder characterized by sebaceous neoplasms and visceral malignancy.
Defects in MSH2 are a cause of susceptibility to endometrial cancer (ENDMC) [MIM:608089].
Defects in MSH2 are a cause of hereditary non-polyposis colorectal cancer type 8 (HNPCC8) [MIM:613244]. HNPCC is a disease associated with marked increase in cancer susceptibility. It is characterized by a familial predisposition to early-onset colorectal carcinoma (CRC) and extra-colonic tumors of the gastrointestinal, urological and female reproductive tracts. HNPCC is reported to be the most common form of inherited colorectal cancer in the Western world. Clinically, HNPCC is often divided into two subgroups. Type I is characterized by hereditary predisposition to colorectal cancer, a young age of onset, and carcinoma observed in the proximal colon. Type II is characterized by increased risk for cancers in certain tissues such as the uterus, ovary, breast, stomach, small intestine, skin, and larynx in addition to the colon. Diagnosis of classical HNPCC is based on the Amsterdam criteria: 3 or more relatives affected by colorectal cancer, one a first degree relative of the other two; 2 or more generation affected; 1 or more colorectal cancers presenting before 50 years of age; exclusion of hereditary polyposis syndromes. The term 'suspected HNPCC' or 'incomplete HNPCC' can be used to describe families who do not or only partially fulfill the Amsterdam criteria, but in whom a genetic basis for colon cancer is strongly suspected. Note=HNPCC8 results from heterozygous deletion of 3-prime exons of EPCAM and intergenic regions directly upstream of MSH2, resulting in transcriptional read-through and epigenetic silencing of MSH2 in tissues expressing EPCAM.
Sequence similaritiesBelongs to the DNA mismatch repair mutS family.
modificationsPhosphorylated by PRKCZ, which may prevent MutS alpha degradation by the ubiquitin-proteasome pathway.
Phosphorylated upon DNA damage, probably by ATM or ATR.
- Information by UniProt
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Lane 1: Wild-type HAP1 cell lysate (20 µg)
Lane 2: MSH2 knockout HAP1 cell lysate (20 µg)
Lane 3: HeLa cell lysate (20 µg)
Lane 4: A375 cell lysate (20 µg)
Lanes 1 - 4: Merged signal (red and green). Green - ab92473 observed at 115 kDa. Red - loading control, ab8245, observed at 37 kDa.
ab92473 was shown to recognize MSH2 when MSH2 knockout samples were used, along with additional cross-reactive bands. Wild-type and MSH2 knockout samples were subjected to SDS-PAGE. ab92473 and ab8245 (loading control to GAPDH) were diluted 1/1000 and 1/2000 respectively and incubated overnight at 4°C. Blots were developed with Goat anti-Rabbit IgG H&L (IRDye® 800CW) preadsorbed (ab216773) and Goat anti-Mouse IgG H&L (IRDye® 680RD) preadsorbed (ab216776) secondary antibodies at 1/10000 dilution for 1 h at room temperature before imaging.
All lanes : Anti-MSH2 antibody [EPR3943] (ab92473) at 1/1000 dilution
Lane 1 : A375 cell lysate
Lane 2 : A431 cell lysate
Lane 3 : SW480 cell lysate
Lane 4 : HeLa cell lysate
Lysates/proteins at 10 µg per lane.
All lanes : HRP labelled goat anti-rabbit antibody at 1/2000 dilution
Predicted band size: 105 kDa
ab92473 has been referenced in 3 publications.
- Tian H et al. Hypermethylation of mismatch repair gene hMSH2 associates with platinum-resistant disease in epithelial ovarian cancer. Clin Epigenetics 11:153 (2019). PubMed: 31666131
- Grassi T et al. Mismatch repair system in endometriotic tissue and eutopic endometrium of unaffected women. Int J Clin Exp Pathol 8:1867-77 (2015). PubMed: 25973079
- Nelson GS et al. MMR deficiency is common in high-grade endometrioid carcinomas and is associated with an unfavorable outcome. Gynecol Oncol 131:309-14 (2013). ICC/IF ; Human . PubMed: 23938375