Anti - Mouse, MLH1 Clone ZM001
- Known as:
- Anti - Mouse, MLH1 Clone ZM001
- Catalog number:
- 60-0075-7
- Product Quantity:
- 7mL
- Category:
- -
- Supplier:
- Genemed
- Gene target:
- Anti - Mouse MLH1 Clone ZM001
Ask about this productRelated genes to: Anti - Mouse, MLH1 Clone ZM001
- Gene:
- MLH1 NIH gene
- Name:
- mutL homolog 1
- Previous symbol:
- COCA2
- Synonyms:
- HNPCC, FCC2, HNPCC2
- Chromosome:
- 3p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-24
- Date modifiied:
- 2019-04-23
Related products to: Anti - Mouse, MLH1 Clone ZM001
Related articles to: Anti - Mouse, MLH1 Clone ZM001
- 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 - 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
- Mismatch repair deficiency (MMRd) is identified in a small subset of prostate cancers and has implications for therapy selection and germline testing. The clinicopathologic spectrum of primary MMRd prostate cancer remains incompletely characterized. We evaluated 32 primary treatment-naive MMRd prostatic adenocarcinomas identified at a single institution. Grade group distribution included GG5 (n=12, 38%), GG4 (n=4, 13%), GG3 (n=7, 22%), and GG2 (n=9, 28%). Intraductal and/or invasive cribriform carcinoma was identified in 78% of cases overall and in 78% of GG2 tumors. MMR protein loss predominantly involved MSH2/MSH6 (78%), with isolated MSH6 loss in 16% and MLH1/PMS2 loss in 6%. Concordant pathogenic MMR gene alterations were identified on targeted NGS in all cases, while concurrent Tier 1/2 HRR gene alterations were present in 11 cases (35%), including ATM, BRCA1, and BRCA2. Germline testing performed in 15 cases identified Lynch syndrome in 5 (33%). MMR immunohistochemistry performed on multiple tissue blocks in 14 cases revealed discordant MMR status between tumor foci in 8 cases (57%), with MMR deficiency consistently restricted to the highest-grade focus and retained expression in spatially separate lower-grade foci. One additional case demonstrated apparent intratumoral heterogeneity within a single biopsy core, with MMR deficiency restricted to a higher-grade component and retained expression in the adjacent lower-grade tumor. These findings demonstrate a broader clinicopathologic spectrum of primary MMRd prostate cancer than previously recognized. Frequent discordance of MMR status between tumor foci highlights the importance of evaluating the highest-grade tumor focus when assessing multifocal primary prostate cancer. - Source: PubMed
Publication date: 2026/09/15
Martin DarrellCheung Carol CYang ChenBeauchamp LéonieMansoor MehdiGreen Sophia MSelvarajah ShaminiPrendeville Susan