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  4. Recombinant Mouse DNA mismatch repair protein Msh2 (Msh2), partial

Recombinant Mouse DNA mismatch repair protein Msh2 (Msh2), partial

  • 中文名称：
    小鼠Msh2重组蛋白
  • 货号：
    CSB-YP015028MO
  • 规格：
  • 来源：
    Yeast
  • 其他：
  • 中文名称：
    小鼠Msh2重组蛋白
  • 货号：
    CSB-EP015028MO
  • 规格：
  • 来源：
    E.coli
  • 其他：
  • 中文名称：
    小鼠Msh2重组蛋白
  • 货号：
    CSB-EP015028MO-B
  • 规格：
  • 来源：
    E.coli
  • 共轭：
    Avi-tag Biotinylated

    E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.

  • 其他：
  • 中文名称：
    小鼠Msh2重组蛋白
  • 货号：
    CSB-BP015028MO
  • 规格：
  • 来源：
    Baculovirus
  • 其他：
  • 中文名称：
    小鼠Msh2重组蛋白
  • 货号：
    CSB-MP015028MO
  • 规格：
  • 来源：
    Mammalian cell
  • 其他：

产品详情

  • 纯度：
    >85% (SDS-PAGE)
  • 基因名：
    Msh2
  • Uniprot No.：
    P43247
  • 别名：
    Msh2; DNA mismatch repair protein Msh2; MutS protein homolog 2
  • 种属：
    Mus musculus (Mouse)
  • 蛋白长度：
    Partial
  • 蛋白标签：
    Tag type will be determined during the manufacturing process.
    The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
  • 产品提供形式：
    Lyophilized powder
    Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
  • 复溶：
    We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
  • 储存条件：
    Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
  • 保质期：
    The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
    Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
  • 货期：
    Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
    Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
  • 注意事项：
    Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
  • Datasheet ：
    Please contact us to get it.

产品评价

靶点详情

  • 功能：
    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. 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.
  • 基因功能参考文献：
    1. Msh2 deficiency causes dysmyelination of the axonal projections in the corpus callosum. Evoked action potentials in the myelinated corpus callosum projections of Msh2-null mice were smaller than wild-type mice, whereas unmyelinated axons showed no difference. PMID: 27476972
    2. Deletion of the MSH2 C-terminus severely affected the stability of the MSH2/MSH6 heterodimer and consequently strongly attenuated DNA mismatch repair. The C-terminal truncation MSH2 mutant predisposed mice to tumor formation.Mutations deleting the MSH2 C-terminus can therefore unambiguously be considered as pathogenic and a cause of Lynch syndrome. PMID: 27873144
    3. Normal Msh2-deficient organoids showed increased inheritable transient cyst-like growth, which became independent of R-spondin. intestinal stem cell (ISC) proceeded faster in vitro than in vivo independent of the underlying genotype but more under Mutations in mismatch repair deficiency. PMID: 27941880
    4. Study shows that MSH2-/- mice develop spontaneous thymic lymphomas. PMID: 28767666
    5. Data show that in mutS homolog 2 protein Msh2(+/-) mice, azathioprine (Aza) induced a high incidence of microsatellite instability (MSI) lymphomas in a dose-dependent manner. PMID: 26327213
    6. In Msh2-/- mice, red meat enhanced survival compared to control (p<0.01) and lowered total tumour burden compared to resistant starch (p<0.167). PMID: 26022687
    7. Angptl2-induced inflammation increases susceptibility to microenvironmental changes, allowing increased oxidative stress and decreased Msh2 expression. PMID: 24258150
    8. Gut microbes did not induce colorectal cancer in APC(Min/+)MSH2(-/-) mice through an inflammatory response or the production of DNA mutagens but rather by providing carbohydrate-derived metabolites such as butyrate that fuel hyperproliferation of MSH2(-/-) colon epithelial cells. PMID: 25036629
    9. MSH2-MSH3 suppresses chromosomal instability and modulates the tumor spectrum in p53-deficient tumorigenesis. PMID: 24013230
    10. Results suggest that MSH2 is rate limiting for expansion in fragile X premutation mouse model and that MSH2 levels may be a key factor that accounts for tissue-specific differences in expansion risk. PMID: 24130133
    11. Toxicity, induced by tert-butyl-hydroperoxide and potassium bromate, differs in base excision repair proficient (Mpg (+/+), Nth1 (+/+)) and deficient (Mpg (-/-), Nth1 (-/-)) mouse embryonic fibroblasts following Msh2 knockdown, was examined. PMID: 23984319
    12. Medium-spiny striatal neurons-specific deletion of Msh2 was sufficient to eliminate the vast majority of striatal HTT CAG expansions in HTT CAG knock-in mice. PMID: 22970194
    13. elevated mutation levels have little effect on the development of the fetus, even if a mutator phenotype appears at the organogenesis stage. PMID: 22465156
    14. Enhanced occupancy of Msh2 and Msh3 proteins is detected downstream of the FXN expanded GAA repeat, suggesting a model in which Msh2/3 dimers are recruited to this region to repair mismatches. PMID: 22289650
    15. we show that AID binds cooperatively with UNG and the mismatch repair proteins Msh2-Msh6 to Ig Smu and Sgamma3 regions PMID: 21804017
    16. hMSH2 recruits ATR to DNA damage sites for activation during DNA damage-induced apoptosis. PMID: 21285353
    17. MSH2 is all important for efficient alternative end-joining-mediated class-switch recombination region DNA breaks in B cells. PMID: 21242524
    18. Azathioprine-induced carcinogenesis in mice depends on the number of functional copies of the Msh2 gene. PMID: 20923998
    19. similar defects on switching in Msh2(-/-), Msh2(-/-)Msh6(-/-) and Msh2(-/-)Msh6(-/-)Msh3(-/-) mice confirm that MutSalpha but not MutSbeta plays an important role in class switch recombination PMID: 20567595
    20. Msh2(LoxP/LoxP) mice in combination with appropriate Cre recombinase transgenes have excellent potential for preclinical modeling of Lynch syndrome. PMID: 19931261
    21. mice deficient in this display an increase in mutaion frequency and an altered mutational spectrum PMID: 11890935
    22. analysis of Msh2 mutations in mice PMID: 12489114
    23. Mice defective in the mismatch repair (MMR) gene Msh2 manifest an enhanced predisposition to skin cancer associated with exposure to ultraviolet radiation PMID: 12531020
    24. MSH2-deficiency caused a high incidence of spontaneous and UVB-induced skin tumorigenesis and the XPA and MSH2 genes have additive roles in the ultraviolet-induced skin tumorigenesis PMID: 12531021
    25. deficiency enhances somatic Apc and p53 mutations in Apc+/-Msh2-/- mice PMID: 12584170
    26. Our data suggest that an active MSH2 is required for a correct response to ionizing radiation-induced DNA damage in the G2 phase of the cell cycle, possibly connecting DSB repair to checkpoint signalling. PMID: 12687013
    27. These results indicate that Msh2 adenosine triphosphatase activity is required for A-T mutations, and suggest that Msh2 has more than one role in CSR. PMID: 14568978
    28. Msh2 primarily acts to delay mitotic entry of cells already in G2, that is, DNA damage incurred during G2 does not influence the cell once committed to mitotic traverse. PMID: 14576827
    29. germinal expansions are produced at the beginning of spermatogenesis, in spermatogonia, by a meiosis-independent mechanism involving MSH2 PMID: 14701736
    30. Msh2-mediated apoptosis is an important component of tumor suppression and certain MSH2 missense mutations can cause mismatch repair deficiency. PMID: 14744764
    31. Results link for the first time microtubule-integrity with intra-nuclear Msh2 protein dynamics. PMID: 15044851
    32. Mismatch repair protein Msh2 plays a role in UVB-induced S-phase arrest. PMID: 15533840
    33. MutSalpha interacts with the immunoglobulin S regions in switching B cells to promote DNA synapsis and recombination. PMID: 15753043
    34. Msh2 affects antibody gene switch region site location because of the requirement Msh2-directed processing to allow class switch recombination joining. PMID: 15955838
    35. Msh2 deficiency leads to chromosomal abnormalities, centrosome amplification, and telomere capping defect PMID: 16331258
    36. Msh2 deficiency accelerates benzo(a)pyrene-induced development of lymphomas PMID: 16381012
    37. Msh2 plays a suppressive role in the mammalian targeted nucleotide exchange reaction by either precluding oligonucleotide annealing to the target gene or by maintenance of a cell cycle checkpoint induced by the modified single-stranded oligonucleotides. PMID: 17113727
    38. Data show that Msh2 promoter hypermethylation correlates to aging, and suggesting that increased methylation in old retired breeders might account for further epigenetic changes that could additionally promote the aging process. PMID: 18461468
    39. A large fraction of the cancer-prone phenotype of Msh2 deficient mice depends on Mutyh activity. PMID: 19435918
    40. ATPase domain mutation of MSH2 strongly affects the formation of CTG expansions and leads instead to transmitted contractions, similar to a Msh2-null or Msh3-null deficiency. PMID: 19436705
    41. when the SmuTR region is present, deficiency of Msh2 does not lead to the increased microhomology seen with Mlh1 or Exo1 deficiencies, suggesting that Msh2 might have an additional function in class switch recombination PMID: 19553545
    42. The concerted action of Msh2 and UNG in stimulating A . T mutations also may have implications for mutagenesis at sites of spontaneous cytidine deamination. PMID: 19596785
    43. Msh2-dependent mismatch repair function actively suppresses c-Myc-associated oncogenesis during early B cell development. PMID: 19837692
    44. Dependence of nucleotide substitutions on Ung2, Msh2, and PCNA-Ub during somatic hypermutation. PMID: 19901081

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  • 亚细胞定位：
    Nucleus. Chromosome.
  • 蛋白家族：
    DNA mismatch repair MutS family
  • 数据库链接：

    KEGG: mmu:17685

    STRING: 10090.ENSMUSP00000024967

    UniGene: Mm.4619

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