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

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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UNIGENE: Mm.4619

KEGG: mmu:17685

STRING: 10090.ENSMUSP00000024967