Anti-MSH6 antibody [SP93], prediluted (ab99890)


  • Product name
    Anti-MSH6 antibody [SP93], prediluted
    See all MSH6 primary antibodies
  • Description
    Rabbit monoclonal [SP93] to MSH6, prediluted
  • Host species
  • Tested applications
    Suitable for: WB, IHC-Pmore details
  • Species reactivity
    Reacts with: Human
  • Immunogen

    A synthetic peptide corresponding to internal region of Human MSH6.

  • Positive control
    • Human Rectal Carcinoma
  • General notes

    This product is a recombinant rabbit monoclonal antibody.


  • Form
  • Storage instructions
    Shipped at 4°C. Store at +4°C.
  • Storage buffer
    Preservative: 0.1% Sodium Azide
    Constituents: 1% BSA, 50mM Tris, pH 7.6
  • Concentration information loading...
  • Purification notes
    Purified from TCS by protein A/G.
  • Clonality
  • Clone number
  • Isotype
  • Research areas

Associated products


Our Abpromise guarantee covers the use of ab99890 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
WB 1/1.
IHC-P 1/1. Boil tissue section in 1mM EDTA, pH 8.0 for 10 min followed by cooling at RT for 20 min.


  • Function
    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. When bound, MutS alpha bends the DNA helix and shields approximately 20 base pairs, and recognizes single base mismatches and dinucleotide insertion-deletion loops (IDL) in the DNA. 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 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.
  • Involvement in disease
    Defects in MSH6 are the cause of hereditary non-polyposis colorectal cancer type 5 (HNPCC5) [MIM:600678]. 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. MSH6 mutations appear to be associated with atypical HNPCC and in particular with development of endometrial carcinoma or atypical endometrial hyperplasia, the presumed precursor of endometrial cancer. Defects in MSH6 are also found in familial colorectal cancers (suspected or incomplete HNPCC) that do not fulfill the Amsterdam criteria for HNPCC.
    Defects in MSH6 are a cause of susceptibility to endometrial cancer (ENDMC) [MIM:608089].
  • Sequence similarities
    Belongs to the DNA mismatch repair mutS family.
    Contains 1 PWWP domain.
  • Post-translational
    The N-terminus is blocked.
    Phosphorylated upon DNA damage, probably by ATM or ATR.
    Phosphorylated by PRKCZ, which may prevent MutS alpha degradation by the ubiquitin-proteasome pathway.
  • Cellular localization
  • Information by UniProt
  • Database links
  • Alternative names
    • DNA mismatch repair protein Msh6 antibody
    • G/T mismatch binding protein antibody
    • G/T mismatch-binding protein antibody
    • GTBP antibody
    • GTMBP antibody
    • hMSH6 antibody
    • HNPCC 5 antibody
    • HNPCC5 antibody
    • HSAP antibody
    • MSH 6 antibody
    • MSH6 antibody
    • MSH6_HUMAN antibody
    • mutS (E. coli) homolog 6 antibody
    • MutS alpha 160 kDa subunit antibody
    • MutS homolog 6 (E. coli) antibody
    • mutS homolog 6 antibody
    • MutS-alpha 160 kDa subunit antibody
    • p160 antibody
    • Sperm associated protein antibody
    see all


  • Staining of Human MSH6 in a Formalin/PFA-fixed paraffin-embedded section of Human Rectal Carcinoma using prediluted ab99890.
  • Anti-MSH6 antibody [SP93] (ab99889) at 1/100 dilution + lysate prepared from A431 cells

    Observed band size: 170 kDa (why is the actual band size different from the predicted?)

    ab99889 used in the image is the undiluted version of ab99890.


This product has been referenced in:
  • Sekine S  et al. Mismatch repair deficiency commonly precedes adenoma formation in Lynch Syndrome-Associated colorectal tumorigenesis. Mod Pathol 30:1144-1151 (2017). Read more (PubMed: 28548127) »

See 1 Publication for this product

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