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Epigenetics and Nuclear Signaling DNA / RNA DNA Damage & Repair Mismatch Repair
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Recombinant Human MLH1 protein (ab131924)

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SDS-PAGE - Recombinant Human MLH1 protein (ab131924)

    Key features and details

    • Expression system: Wheat germ
    • Suitable for: ELISA, SDS-PAGE, WB

    Description

    • Product name

      Recombinant Human MLH1 protein
    • Expression system

      Wheat germ
    • Accession

      P40692
    • Protein length

      Full length protein
    • Animal free

      No
    • Nature

      Recombinant
      • Species

        Human
      • Sequence

        MSFVAGVIRRLDETVVNRIAAGEVIQRPANAIKEMIENCLDAKSTSIQVI VKEGGLKLIQIQDNGTGIRKEDLDIVCERFTTSKLQSFEDLASISTYGFR GEALASISHVAHVTITTKTADGKCAYRASYSDGKLKAPPKPCAGNQGTQI TVEDLFYNIATRRKALKNPSEEYGKILEVVGRYSVHNAGISFSVKKQGET VADVRTLPNASTVDNIRSIFGNAVSRELIEIGCEDKTLAFKMNGYISNAN YSVKKCIFLLFINHRLVESTSLRKAIETVYAAYLPKNTHPFLYLSLEISP QNVDVNVHPTKHEVHFLHEESILERVQQHIESKLLGSNSSRMYFTQTLLP GLAGPSGEMVKSTTSLTSSSTSGSSDKVYAHQMVRTDSREQKLDAFLQPL SKPLSSQPQAIVTEDKTDISSGRARQQDEEMLELPAPAEVAAKNQSLEGD TTKGTSEMSEKRGPTSSNPRKRHREDSDVEMVEDDSRKEMTAACTPRRRI INLTSVLSLQEEINEQGHEVLREMLHNHSFVGCVNPQWALAQHQTKLYLL NTTKLSEELFYQILIYDFANFGVLRLSEPAPLFDLAMLALDSPESGWTEE DGPKEGLAEYIVEFLKKKAEMLADYFSLEIDEEGNLIGLPLLIDNYVPPL EGLPIFILRLATEVNWDEEKECFESLSKECAMFYSIRKQYISEESTLSGQ QSEVPGSIPNSWKWTVEHIVYKALRSHILPPKHFTEDGNILQLANLPDLY KVFERC
      • Predicted molecular weight

        109 kDa including tags
      • Amino acids

        1 to 756

    Associated products

    • Related Products

      • Anti-MLH1 antibody [EPR3893] (ab108622)
      • Anti-MLH1 antibody [G168-15] (ab14206)
      • Anti-MLH1 antibody [EPR3894] (ab92312)

    Specifications

    Our Abpromise guarantee covers the use of ab131924 in the following tested applications.

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

    • Applications

      ELISA

      SDS-PAGE

      Western blot

    • Form

      Liquid
    • Concentration information loading...

    Preparation and Storage

    • Stability and Storage

      Shipped on dry ice. Upon delivery aliquot and store at -80ºC. Avoid freeze / thaw cycles.

      pH: 8.00
      Constituents: 0.31% Glutathione, 0.79% Tris HCl

    General Info

    • Alternative names

      • COCA 2
      • COCA2
      • DNA mismatch repair protein Mlh1
      • FCC 2
      • FCC2
      • hMLH 1
      • hMLH1
      • HNPCC
      • HNPCC 2
      • HNPCC2
      • MGC5172
      • MLH 1
      • MLH1
      • MLH1_HUMAN
      • MutL homolog 1
      • MutL homolog 1 (E. coli)
      • MutL homolog 1 colon cancer nonpolyposis type 2
      • MutL homolog 1, colon cancer, nonpolyposis type 2 (E. coli)
      • MutL protein homolog 1
      • MutL, E. coli, homolog of, 1
      see all
    • Function

      Heterodimerizes with PMS2 to form MutL alpha, a component of the post-replicative DNA mismatch repair system (MMR). DNA repair is initiated by MutS alpha (MSH2-MSH6) or MutS beta (MSH2-MSH6) binding to a dsDNA mismatch, then MutL alpha is recruited to the heteroduplex. Assembly of the MutL-MutS-heteroduplex ternary complex in presence of RFC and PCNA is sufficient to activate endonuclease activity of PMS2. It introduces single-strand breaks near the mismatch and thus generates new entry points for the exonuclease EXO1 to degrade the strand containing the mismatch. DNA methylation would prevent cleavage and therefore assure that only the newly mutated DNA strand is going to be corrected. MutL alpha (MLH1-PMS2) interacts physically with the clamp loader subunits of DNA polymerase III, suggesting that it may play a role to recruit the DNA polymerase III to the site of the MMR. Also implicated in DNA damage signaling, a process which induces cell cycle arrest and can lead to apoptosis in case of major DNA damages. Heterodimerizes with MLH3 to form MutL gamma which plays a role in meiosis.
    • Tissue specificity

      Colon, lymphocytes, breast, lung, spleen, testis, prostate, thyroid, gall bladder and heart.
    • Involvement in disease

      Defects in MLH1 are the cause of hereditary non-polyposis colorectal cancer type 2 (HNPCC2) [MIM:609310]. 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, and accounts for 15% of all colon cancers. 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.
      Defects in MLH1 are a cause of mismatch repair cancer syndrome (MMRCS) [MIM:276300]; also known as Turcot syndrome or brain tumor-polyposis syndrome 1 (BTPS1). MMRCS is an autosomal dominant disorder characterized by malignant tumors of the brain associated with multiple colorectal adenomas. Skin features include sebaceous cysts, hyperpigmented and cafe au lait spots.
      Defects in MLH1 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.
      Note=Defects in MLH1 may contribute to lobular carcinoma in situ (LCIS), a non-invasive neoplastic disease of the breast.
      Defects in MLH1 are a cause of susceptibility to endometrial cancer (ENDMC) [MIM:608089].
      Note=Some epigenetic changes can be transmitted unchanged through the germline (termed 'epigenetic inheritance'). Evidence that this mechanism occurs in humans is provided by the identification of individuals in whom 1 allele of the MLH1 gene is epigenetically silenced throughout the soma (implying a germline event). These individuals are affected by HNPCC but does not have identifiable mutations in MLH1, even though it is silenced, which demonstrates that an epimutation can phenocopy a genetic disease.
    • Sequence similarities

      Belongs to the DNA mismatch repair mutL/hexB family.
    • Cellular localization

      Nucleus.
    • Target information above from: UniProt accession P40692 The UniProt Consortium
      The Universal Protein Resource (UniProt) in 2010
      Nucleic Acids Res. 38:D142-D148 (2010) .

      Information by UniProt

    Images

    • SDS-PAGE - Recombinant Human MLH1 protein (ab131924)
      SDS-PAGE - Recombinant Human MLH1 protein (ab131924)
      12.5% SDS-PAGE analysis of ab131924 stained with Coomassie Blue.

    Protocols

    To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.

    Click here to view the general protocols

    Datasheets and documents

    • SDS download

    • Datasheet download

      Download

    References (0)

    Publishing research using ab131924? Please let us know so that we can cite the reference in this datasheet.

    ab131924 has not yet been referenced specifically in any publications.

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