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Key Specifications Table
| Species Reactivity | Key Applications | Host | Format | Antibody Type |
|---|---|---|---|---|
| H | WB, IHC | M | Purified | Monoclonal Antibody |
| Description | |
|---|---|
| Catalogue Number | MABE284 |
| Description | Anti-MSH2 Antibody, clone FE11 |
| Alternate Names |
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| Background Information | MSH2 is a ubiquitously expressed nuclear protein that is involved in DNA repair processes. MSH2 is active as a heterodimer of MutS alpha and beta subunits that bind DNA at mismatched strands. The MutS alpha subunit binds to single base mismatches and dinucleotide insertion-deletion loops, whereas MutS beta detects longer insertion-deletion loops. Bound MutS subunits then form complexes with MutL alpha dimers, to coordinate downstream DNA-mismatch–repair processes. Abnormal expression of MSH2 has been linked to hereditary non-polyposis colorectal cancer type 1 and Muir-Torre syndrome. |
| Product Information | |
|---|---|
| Format | Purified |
| Control |
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| Presentation | Purified mouse monoclonal IgG1κ in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide. |
| Quality Level | MQ100 |
| Applications | |
|---|---|
| Application | Anti-MSH2 Antibody, clone FE11 is a Mouse Monoclonal Antibody for detection of MSH2 also known as DNA mismatch repair protein Msh2, hMSH2, MutS protein homolog 2 & has been validated in WB & IHC. |
| Key Applications |
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| Application Notes | Immunohistochemistry Analysis: A representative lot from an independent laboratory detected SW-480 in human normal colonic tissue and in human adenocarcinoma tissue (Thibodeau, S. N., et al. (1996). 56(21):4836-4840.). |
| Biological Information | |
|---|---|
| Immunogen | Recombinant protein corresponding to the C-terminus of human MSH2. |
| Epitope | C-terminus |
| Clone | FE11 |
| Concentration | Please refer to the Certificate of Analysis for the lot-specific concentration. |
| Host | Mouse |
| Specificity | This antibody recognizes the C-terminus of MSH2. |
| Isotype | IgG1κ |
| Species Reactivity |
|
| Antibody Type | Monoclonal Antibody |
| Entrez Gene Number |
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| Entrez Gene Summary | MSH2 was identified as a locus frequently mutated in hereditary nonpolyposis colon cancer (HNPCC). When cloned, it was discovered to be a human homolog of the E. coli mismatch repair gene mutS, consistent with the characteristic alterations in microsatellite sequences (RER+ phenotype) found in HNPCC. |
| Gene Symbol |
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| Purification Method | Protein G Purified |
| UniProt Number |
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| UniProt Summary | FUNCTION: 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. 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. SUBUNIT STRUCTURE: Heterodimer consisting of MSH2-MSH6 (MutS alpha) or MSH2-MSH3 (MutS beta). Both heterodimer form a ternary complex with MutL alpha (MLH1-PMS1). Interacts with EXO1. Part of the BRCA1-associated genome surveillance complex (BASC), which contains BRCA1, MSH2, MSH6, MLH1, ATM, BLM, PMS2 and the RAD50-MRE11-NBS1 protein complex. This association could be a dynamic process changing throughout the cell cycle and within subnuclear domains. Interacts with ATR. Interacts with SLX4/BTBD12; this interaction is direct and links MutS beta to SLX4, a subunit of different structure-specific endonucleases. Interacts with SMARCAD1. SUBCELLULAR LOCATION: Nucleus. TISSUE SPECIFICITY: Phosphorylated by PRKCZ, which may prevent MutS alpha degradation by the ubiquitin-proteasome pathway. Phosphorylated upon DNA damage, probably by ATM or ATR. INVOLVEMENT IN DISEASE: Defects in MSH2 are the cause of hereditary non-polyposis colorectal cancer type 1 (HNPCC1). 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 (MRTES). Rare autosomal dominant disorder characterized by sebaceous neoplasms and visceral malignancy. Defects in MSH2 are a cause of susceptibility to endometrial cancer (ENDMC). Defects in MSH2 are a cause of hereditary non-polyposis colorectal cancer type 8 (HNPCC8). 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 SIMILARITIES: Belongs to the DNA mismatch repair mutS family. SEQUENCE CAUTION: The sequence AAC27930.1 differs from that shown. Reason: Frameshift at position 417. The frameshift is caused by a single nucleotide deletion which is found in a HNPCC kindred. |
| Molecular Weight | ~104 kDa observed |
| Product Usage Statements | |
|---|---|
| Quality Assurance | Evaluated by Western Blot in SW-480 cell lysate. Western Blot Analysis: 1 µg/mL of this antibody detected MSH2 in 10 µg of SW-480 cell lysate. |
| Usage Statement |
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| Storage and Shipping Information | |
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| Storage Conditions | Stable for 1 year at 2-8°C from date of receipt. |
| Packaging Information | |
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| Material Size | 100 µg |