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
- Termite reproductives provide a useful system for examining molecular changes associated with reproductive differentiation because secondary reproductives can arise from worker-like individuals. Here, we compared workers and worker-derived ergatoids of Reticulitermes chinensis to characterize transcriptional changes associated with the acquisition of reproductive status. Histological observations revealed developed gonads containing vitellogenic oocytes in female 10-day post-differentiation ergatoids and spermatids and spermatozoa in male 10-day post-differentiation ergatoids. Transcriptome sequencing, targeted gene set enrichment analysis, weighted gene co-expression network analysis, and RT-qPCR revealed caste-associated changes in the expression of genes annotated to DNA repair-related pathways. Gene sets associated with homologous recombination, p53/checkpoint signaling and mismatch repair were significantly positively enriched toward the ergatoid-associated end of the ranked gene list, whereas the Fanconi anemia-related repair gene set showed a positive but non-significant enrichment trend. Several mismatch repair genes, including MSH2, MSH6, and MLH1, showed higher transcript abundance in ergatoids, and MLH1 retained conserved sequence and domain features across representative insects. These findings indicate that worker-to-ergatoid differentiation is associated with reproductive maturation and coordinated transcriptional remodeling of DNA repair-related genes. This study identifies candidate genes and pathways for future functional investigations of genome-maintenance-related processes during reproductive differentiation in termites. - Source: PubMed
Publication date: 2026/09/17
Wu JiaWang YonghuiDong YananDu BeiYu Shuxin - BackgroundThe fidelity of the DNA mismatch repair (MMR) system is routinely evaluated using MMR immunohistochemistry (IHC). The MMR IHC is interpreted based on obligate heterodimeric relationships (MLH1-PMS2; MSH2-MSH6). MSH2 loss typically results in concurrent MSH6 loss. Atypical non-dimer patterns, such as isolated loss of MSH2 with retained or patchy MSH6, complicate reflex testing and genotype inference.Patient presentationPatient 1 was a 90-year-old woman with an ascending colon mass. Biopsy showed invasive moderately differentiated colorectal adenocarcinoma. MMR IHC demonstrated isolated loss of MSH2 with heterogeneous/patchy MSH6 retention. Polymerase chain reaction (PCR)-based microsatellite instability (MSI) testing was reported as microsatellite stable (MSS). Targeted testing showed no / or mutations. Patient 2 was a 70-year-old man with recurrent high-grade prostatic carcinoma sampled by transurethral resection of the prostate (TURP) from the pelvic bed. MMR IHC demonstrated intact MLH1/PMS2/MSH6 with isolated loss of nuclear MSH2, accompanied by very faint cytoplasmic staining. These IHC findings were reproduced on an additional block. MSI testing was reported as MSI-High (MSI-H).ConclusionA focused literature review identified this non-dimeric pattern of isolated MSH2 loss across multiple tumor types, most commonly colorectal, prostate, and endometrial carcinomas. Our paired findings illustrate that this non-dimeric pattern may coexist with either MSS or MSI-H status, underscoring that MMR IHC patterns should be confirmed for repeatability and interpreted in the context of clinicopathologic and molecular correlation. - Source: PubMed
Publication date: 2026/09/18
Kakodkar PramathWang Hui - Numerous studies have demonstrated that Ashkenazi Jewish individuals heterozygous for APC c.3902T > A; p.Ile1307Lys have 1.7-fold increased odds of colorectal adenocarcinoma (CRC). The cancer risk for homozygotes is unknown, and published data is based on small sample sizes. Here, we aim to quantitatively evaluate the odds of CRC in homozygotes from a clinical diagnostic setting. Analyses comparing the demographic and clinical histories among heterozygotes (n = 340) or homozygotes (n = 74) were compared to individuals with MSH6-associated Lynch syndrome (n = 372) and individuals from a pan-cancer panel of up to 90 genes who were negative for APC I1307K, MSH6 (likely) pathogenic (LP/P) variants, and other reportable LP/P variants after exclusions, henceforth referred to as wildtype (WT, n = 19,809). Comparisons included Fisher's exact or two-sample t-test and multivariate logistic regression. Homozygotes demonstrated a trend toward increased odds of CRC compared to WT (OR: 2.48; p = 0.074), and there was no difference between heterozygotes and WT (OR: 0.94; p = 0.83). MSH6-positive individuals had increased odds of CRC relative to homozygotes (OR: 3.54; p < 0.0001) but this was not significant in the logistic regression (OR: 1.19; p = 0.78). While homozygotes but not heterozygotes demonstrated an increase in CRC OR compared to WT, there was no statistically distinct odds of CRC between heterozygotes and homozygotes in this cohort. While the ORs herein support that the observed increase in CRC for homozygotes was more modest than that observed for MSH6-related Lynch syndrome in this cohort, current sample size and selection bias limit precise risk estimation and do not allow for distinction between modestly increased risk and no risk of CRC. - Source: PubMed
Publication date: 2026/09/17
Zaretsky LeahRichardson Marcy EColeman TaylorHorton CarrieTrottier MaganFeng MaggiePolfus Linda MLucas Aimee L - A 53-year-old man underwent resection of a nonfunctional 9 cm oncocytic adrenal cortical carcinoma (ACC) with focal high-grade features. Two years later he presented again, with gynecomastia and elevated levels of estradiol, 11-deoxycortisol, and serum calcium (10.5 mg/dL, SI: 2.62 mmol/L) (reference range 8.4-10.2 mg/dL [SI: 2.10-2.55 mmol/L]). Imaging demonstrated locally recurrent ACC, which was resected. Steroid excess resolved and he started mitotane. Months after, his calcium was 11.9 mg/dL (SI: 2.97 mmol/L), parathyroid hormone (PTH) 209 pg/mL (SI: 22.0 pmol/L) (reference range 15-65 pg/mL [SI: 1.6-6.9 pmol/L]), and parathyroid hormone-related peptide (PTHrp) was undetectable. Germline genetic testing ( and ) was negative; localizing imaging demonstrated possible right inferior parathyroid adenoma. He underwent 4-gland parathyroid exploration. Right inferior parathyroid (460 mg) was excised, superior parathyroids appeared normal, and left inferior parathyroid was not identified. Intraoperative parathyroid hormone (IOPTH) did not drop appropriately. Follow-up calcium rose to 13.1 mg/dL (SI: 3.27 mmol/L) and PTH to 336 pg/mL (SI: 35.6 pmol/L). Repeat imaging demonstrated ACC recurrence. After cytoreductive surgery (nephrectomy and omentectomy) and heated intraperitoneal chemotherapy (HIPEC), calcium and PTH normalized. Staining of the recurrent ACC demonstrated PTH positivity. This is a novel case of PTH-secreting ACC and concomitant parathyroid adenoma. - Source: PubMed
Publication date: 2026/09/16
Moreno Natalie AHamrahian Amir HMeyer Christian FMangone CieraBaraban EzraMorris-Wiseman Lilah F
- Source: PubMed