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Gene Ontology Classifications
mutS homolog 6 (E. coli)

Go Annotations as Summary Text (Tabular View) (GO Graph)

GO curators for mouse genes have assigned the following annotations to the gene product of Msh6. (This text reflects annotations as of Tuesday, May 26, 2015.) MGI curation of this mouse gene is considered complete, including annotations derived from the biomedical literature as of May 3, 2007. If you know of any additional information regarding this mouse gene please let us know. Please supply mouse gene symbol and a PubMed ID.
Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene encodes a member of the DNA mismatch repair MutS family. In E. coli, the MutS protein helps in the recognition of mismatched nucleotides prior to their repair. A highly conserved region of approximately 150 aa, called the Walker-A adenine nucleotide binding motif, exists in MutS homologs. The encoded protein heterodimerizes with MSH2 to form a mismatch recognition complex that functions as a bidirectional molecular switch that exchanges ADP and ATP as DNA mismatches are bound and dissociated. Mutations in this gene may be associated with hereditary nonpolyposis colon cancer, colorectal cancer, and endometrial cancer. Transcripts variants encoding different isoforms have been described. [provided by RefSeq, Jul 2013]
Summary text based on GO annotations supported by experimental evidence in mouse
Summary text based on GO annotations supported by experimental evidence in other organisms
Summary text for additional MGI annotations
  1. Bourn RL et al. (2012) Pms2 suppresses large expansions of the (GAA.TTC)n sequence in neuronal tissues. PLoS One, 7:e47085. (PubMed:23071719)
  2. de Wind N et al. (1999) HNPCC-like cancer predisposition in mice through simultaneous loss of Msh3 and Msh6 mismatch-repair protein functions. Nat Genet, 23:359-62. (PubMed:10545954)
  3. Edelmann W et al. (1997) Mutation in the mismatch repair gene Msh6 causes cancer susceptibility. Cell, 91:467-77. (PubMed:9390556)
  4. Hegan DC et al. (2006) Differing patterns of genetic instability in mice deficient in the mismatch repair genes Pms2, Mlh1, Msh2, Msh3 and Msh6. Carcinogenesis, 27:2402-8. (PubMed:16728433)
  5. Kuraguchi M et al. (2001) The Distinct Spectra of Tumor-associated Apc Mutations in Mismatch Repair-deficient Apc(1638N) Mice Define the Roles of MSH3 and MSH6 in DNA Repair and Intestinal Tumorigenesis. Cancer Res, 61:7934-42. (PubMed:11691815)
  6. Li Z et al. (2004) Examination of Msh6- and Msh3-deficient Mice in Class Switching Reveals Overlapping and Distinct Roles of MutS Homologues in Antibody Diversification. J Exp Med, 200:47-59. (PubMed:15238604)
  7. Li Z et al. (2006) The mismatch repair protein Msh6 influences the in vivo AID targeting to the Ig locus. Immunity, 24:393-403. (PubMed:16618598)
  8. Mark SC et al. (2002) Elevated mutant frequencies and predominance of G:C to A:T transition mutations in Msh6(-/-) small intestinal epithelium. Oncogene, 21:7126-30. (PubMed:12370835)
  9. Wiesendanger M et al. (2000) Somatic hypermutation in MutS homologue (MSH)3-, MSH6-, and MSH3/MSH6-deficient mice reveals a role for the MSH2-MSH6 heterodimer in modulating the base substitution pattern. J Exp Med, 191:579-84. (PubMed:10662804)
  10. Yang G et al. (2004) Dominant effects of an Msh6 missense mutation on DNA repair and cancer susceptibility. Cancer Cell, 6:139-50. (PubMed:15324697)
  11. Yoshioka K et al. (2006) ATR kinase activation mediated by MutSalpha and MutLalpha in response to cytotoxic O6-methylguanine adducts. Mol Cell, 22:501-10. (PubMed:16713580)
  12. Young LC et al. (2003) DNA mismatch repair protein Msh6 is required for optimal levels of ultraviolet-B-induced apoptosis in primary mouse fibroblasts. J Invest Dermatol, 121:876-80. (PubMed:14632208)

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Gene Ontology Evidence Code Abbreviations:

  EXP Inferred from experiment
  IAS Inferred from ancestral sequence
  IBA Inferred from biological aspect of ancestor
  IBD Inferred from biological aspect of descendant
  IC Inferred by curator
  IDA Inferred from direct assay
  IEA Inferred from electronic annotation
  IGI Inferred from genetic interaction
  IKR Inferred from key residues
  IMP Inferred from mutant phenotype
  IMR Inferred from missing residues
  IPI Inferred from physical interaction
  IRD Inferred from rapid divergence
  ISS Inferred from sequence or structural similarity
  ISO Inferred from sequence orthology
  ISA Inferred from sequence alignment
  ISM Inferred from sequence model
  NAS Non-traceable author statement
  ND No biological data available
  RCA Reviewed computational analysis
  TAS Traceable author statement


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