Anti - Mouse, MSH2 Clone FE11
- Known as:
- Anti - Mouse, MSH2 Clone FE11
- Catalog number:
- 60-0046-7
- Product Quantity:
- 7mL
- Category:
- -
- Supplier:
- Genemed
- Gene target:
- Anti - Mouse MSH2 Clone FE11
Related genes to: Anti - Mouse, MSH2 Clone FE11
- Gene:
- MSH2 NIH gene
- Name:
- mutS homolog 2
- Previous symbol:
- COCA1
- Synonyms:
- HNPCC, HNPCC1
- Chromosome:
- 2p21-p16.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-07-28
- Date modifiied:
- 2019-04-23
Related products to: Anti - Mouse, MSH2 Clone FE11
Related articles to: Anti - Mouse, MSH2 Clone FE11
- DNA mismatch repair (MMR) maintains genomic stability, and defects in MMR genes such as MLH1 and MSH2 predispose to cancer. Unlike other MMR components, MLH1 has unexplained roles in development, as Mlh1-deficient male mice exhibit severe testicular hypoplasia and sterility. Here, we uncover that MLH1 regulates testis development through the Hippo-Yes-associated protein (YAP) pathway. MLH1 directly binds YAP via its C-terminal domain and the WW domains of YAP, competitively inhibiting LATS1-mediated YAP phosphorylation. This interaction stabilizes YAP by suppressing ubiquitination and promotes its nuclear translocation dependent on MLH1's nuclear localization signal. Additionally, MLH1 facilitates YAP-TEAD complex formation, enabling expression of testicular development genes, including Wt1, Sox9, and Ctgf. These functions are independent of the MMR activity of MLH1. Mlh1-deficient mice show elevated YAP phosphorylation, reduced target gene expression, and impaired proliferation in developing testes. Pharmacological inhibition of the Hippo pathway kinases MST1/2 partially rescues testis hypoplasia in Mlh1-/- mice. These findings establish MLH1 as a Hippo pathway regulator and resolve its long-standing role in male gonad development. - Source: PubMed
Li XueyingYang JiajunLi Guo-Min - Cancer of unknown primary (CUP) is aggressive, with limited options and poor prognosis. Mismatch repair-deficient (dMMR) CUP is rare, and reports of its response to immunotherapy are scarce. - Source: PubMed
Publication date: 2026/08/20
Turker MehmetDusgun AlpayTurker AliSelvi SeherAlisan IrfanBuyuksimsek Mahmut - Immune checkpoint inhibitors (ICIs) are important therapeutic options for metastatic colorectal cancer showing microsatellite instability-high (MSI-H)/mismatch repair deficiency (dMMR). We report a case of rectal adenocarcinoma with liver metastases diagnosed as dMMR cancer that was resistant to ICI therapy, leading us to conduct an additional pathological analysis to uncover the reasons underlying ICI resistance. - Source: PubMed
Publication date: 2026/09/01
Okura KoheiTakenaka HarukaFujita HiroshiHanada NorihisaKomohara Yoshihiro - To create a non-invasive model for forecasting microsatellite instability (MSI) status in colorectal cancer (CRC) using preoperative F-FDG PET/CT metabolic parameters, guiding personalized treatment. - Source: PubMed
Publication date: 2026/08/31
Chen RDeng LWang JLin CGong Q - LINE-1 (L1) retrotransposition is common in human cancers and rearrangements at insertion sites can contribute to cancer-driving oncogene amplifications and promote genome instability. However, the mechanisms underlying rearrangements of L1 retrotransposition intermediates are poorly understood. To address this gap, we developed GFP-based recombination reporter assays to study the formation of L1 retrotransposition-mediated rearrangements. Using these reporters combined with long-read sequencing, we find that L1 retrotransposition cDNA intermediates can recombine with distal DNA breaks to generate chromosomal rearrangements. We also find that two independent L1 insertion cDNA intermediates on distinct genomic loci can recombine with each other to generate chromosomal rearrangements. Both types of rearrangements depend on L1-encoded ORF2p endonuclease and reverse transcriptase activities. Using these reporters, we discover that L1 retrotransposition-mediated rearrangements are robustly induced when the recombining sequences share extensive homology and that their formation requires the homologous recombination factor BRCA1. In contrast, we find L1 retrotransposition-mediated rearrangements are suppressed by the mismatch repair factor MSH2 when the recombining sequences contain mismatches. Given the repetitive nature of our genome, these findings highlight the risk of L1 insertion intermediates becoming substrates for aberrant recombination and promoting genome instability. - Source: PubMed
Publication date: 2026/08/01
Mendez-Dorantes CarlosKalinowski Jupiter CBurn AidanSchofield PhillipLaw Cheuk-TingIsik EsinBurns Kathleen H