Anti - Mouse, MSH6 Clone GM009
- Known as:
- Anti - Mouse, MSH6 Clone GM009
- Catalog number:
- 60-0047-7
- Product Quantity:
- 7mL
- Category:
- -
- Supplier:
- Genemed
- Gene target:
- Anti - Mouse MSH6 Clone GM009
Related genes to: Anti - Mouse, MSH6 Clone GM009
- Gene:
- MSH6 NIH gene
- Name:
- mutS homolog 6
- Previous symbol:
- GTBP
- Synonyms:
- -
- Chromosome:
- 2p16.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-08-29
- Date modifiied:
- 2019-04-23
Related products to: Anti - Mouse, MSH6 Clone GM009
Related articles to: Anti - Mouse, MSH6 Clone GM009
- DNA mismatch repair (MMR) corrects DNA replication errors, some forms of chemical damage to DNA bases, and acts in processes such as heteroduplex rejection, triplet repeat expansion, antibody maturation and cytotoxicity of alkylating agents. During MMR, the newly synthesized DNA strand containing the error must be removed and resynthesized to prevent mutations. In bacteria, this strand is displaced by the UvrD DNA helicase. In eukaryotes, this strand is excised by redundant pathways. In the first excision pathway identified, Msh2-Msh6 (or Msh2-Msh3) and/or Mlh1-Pms1 (human MLH1-PMS2) recruit Exo1 to 5' nicks, and 5'-to-3' excision by Exo1 excises the daughter strand containing the mispair to generate a single-stranded gap. The Mlh1-Pms1 endonuclease also mediates excision through extensive nicking of the daughter strand to generate single-stranded gaps. In coupled strand-displacement synthesis coordinated by Msh2-Msh6 (or Msh2-Msh3), DNA polymerase delta and Rad27 (human FEN1)-mediated 5' flap cleavage excise the mispair and resynthesize the daughter strand. Resynthesis in the Exo1- and Mlh1-Pms1-mediated pathways can be performed by both DNA polymerase delta and epsilon, and in all excision pathways the nicked product can be sealed by DNA ligase. Genetic analysis in suggests that these three pathways correspond to all or at least the major excision pathways; however, other factors such as Fan1, Artemis, Mre11, Dna2, Fun30, and the RSC complex have been implicated in eukaryotic MMR but are less well understood. The roles of excision and its redundant pathways have also been less well characterized for other processes involving MMR proteins. - Source: PubMed
Publication date: 2026/10/04
Putnam Christopher DKolodner Richard D - Early-onset colorectal cancer (EOCRC), defined as CRC diagnosed before age 50, is rising globally. The genomic landscape of EOCRC has been characterized in several prior studies, but the reproducibility of findings across independent cohorts, the impact of adjustment for tumor stage and sample type, and the specificity of prognostic biomarkers to the EOCRC subgroup remain incompletely defined. Furthermore, BRAF mutation frequency is strongly modified by tumor location, which is often not considered in prior analyses. - Source: PubMed
Publication date: 2026/10/01
Sertesen Çamöz ElifKaya Osman BilgeErçelebi HakanKaraçin CengizTerzi Yunus KasımYılmaz Çelik Zerrin - To assess the prevalence of pathogenic germline variants (gPVs) and indications for testing in a diverse community-based endometrial cancer population. - Source: PubMed
Publication date: 2026/10/01
Suh-Burgmann ElizabethFinertie HollyHung Yun-YiHoodfar ElizabethCarwana HollyZhong HaoyuanNau ClaudiaSchmittdiel Julie - Lynch syndrome (LS) is an autosomal dominant cancer predisposition syndrome caused by germline mutations in DNA mismatch repair genes or, less commonly, EPCAM deletions. LS-associated colorectal carcinomas often present at a young age and may show unusual histomorphological patterns, posing diagnostic challenges. We report a rare case of a 29-year-old female with EPCAM-mutated LS presenting as colonic adenocarcinoma with neuroendocrine-like rosette formation. The tumor initially mimicked mixed adenoneuroendocrine carcinoma (MANEC) due to biphasic histology and the presence of multiple rosettes. However, immunohistochemistry demonstrated negativity for synaptophysin and chromogranin, excluding true neuroendocrine differentiation with diffuse Pan CK and focal CDX2, CK20 positivity along with loss of MSH2 and MSH6. Further molecular analyses confirmed EPCAM exon 5-9 deletion. The tumor was ultimately classified as an MMR-deficient adenocarcinoma with pseudoendocrine morphology. This case broadens the histomorphological spectrum of LS-associated colorectal carcinomas and introduces the concept of a possible pseudoendocrine carcinoma arising in an epithelial malignancy. Recognition of this pattern is crucial to prevent misdiagnosis as MANEC, to guide appropriate management, facilitate familial screening, and highlight that not every rosette signifies neuroendocrine differentiation; some may represent LS in disguise. - Source: PubMed
Publication date: 2026/09/28
Bandyopadhyay ArghyaChakrabarti AsmitaMondal AmbalikaMaji RatnaprabhaBarui Gopinath - Appendiceal neoplasms are a group of rare, heterogeneous tumors that exhibit varying malignant potential. Systemic treatment options for disseminated appendiceal cancer are limited. We sought to review rates of mutations that may indicate potential roles for routine next-generation sequencing to identify targetable therapies. - Source: PubMed
Publication date: 2026/09/29
Zheng-Pywell RuiLumia Salvatore JFelipe Heidy CosGironda Daniel JMiller Lance DLevine Edward A