Recombinant Human CASP10
- Known as:
- Recombinant Human CASP10
- Catalog number:
- CF93
- Product Quantity:
- 10ug
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Recombinant Human CASP10
Related genes to: Recombinant Human CASP10
- Gene:
- CASP10 NIH gene
- Name:
- caspase 10
- Previous symbol:
- -
- Synonyms:
- MCH4
- Chromosome:
- 2q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-21
- Date modifiied:
- 2019-04-23
Related products to: Recombinant Human CASP10
Related articles to: Recombinant Human CASP10
- We evaluated the immunohistochemical expression of ASCL1, NEUROD1, POU2F3, YAP1, INSM1, NFIB, SLFN11, and CASP10 in 94 resected primary small-cell lung cancer (SCLC) tumors and 32 matched regional lymph-node metastases (excluding combined SCLC and micro-metastases). We applied subtype assignments (SCLC-A, SCLC-N, SCLC-A/N, SCLC-P, SCLC-I), quantified intratumoral heterogeneity using Shannon Evenness Index, and assessed genomic alterations through targeted next-generation sequencing. Subtypes were dominated by ASCL1- and NEUROD1-driven programs, with one-third of tumors exhibiting mixed A/N expression. Cross-site comparison showed moderate concordance between primary tumors and lymph-node metastases; however, notable phenotypic discordance occurred in matched pairs (37.5%), frequently manifesting as a drift toward NEUROD1-dominant or mixed A/N phenotypes following dissemination. NEUROD1 correlated strongly with NFIB and INSM1, and NEUROD1 expression was high in paired regional lymph node metastases, supporting migratory or plastic phenotype associations. SLFN11 demonstrated high concordance between primary tumors and matched regional lymph node metastases, reinforcing its reliability as a predictive biomarker for chemotherapy sensitivity, owing to its stable expression during initial lymphatic dissemination. CASP10 was markedly downregulated in tumors relative to that in normal lung or lymphoid tissues. Genomic profiling confirmed canonical TP53/RB1 dual inactivation pattern alongside recurrent alterations in NOTCH1, PIK3CA, CREBBP, and KMT2D. Thus, SCLC subtyping shows significant spatiotemporal heterogeneity and organ-specific lineage plasticity. The observed discordance during regional nodal dissemination suggests that single site-dependent immunohistochemistry-based subtyping may be insufficient. Future frameworks incorporating multi-region analysis and liquid biopsy are essential to capture the dynamic evolution of SCLC and optimize personalized management for localized disease. - Source: PubMed
Publication date: 2026/03/21
Lin ZhihongLyu QiongLi JiaweiFan LeiWang PingWu YueLin XiaodongHe Ping - This study aimed to identify plasma proteins causally associated with pulmonary arterial hypertension (PAH) by using a proteome-wide Mendelian randomization (PWMR) approach. We integrated two large proteomic genome-wide association study (GWAS) data sets with two PAH GWAS data sets and applied PWMR, Bayesian colocalization, and SMR to prioritize candidate proteins. Drug prediction, molecular docking, single-cell RNA sequencing (scRNA-seq) profiling, and a phenome-wide association study (PheWAS) were further used to assess druggability and potential phenotypic associations. PWMR identified 271 PAH-associated proteins, which were refined to the following three targets: CASP10, NOTCH3, and NCAM2. Molecular docking showed strong predicted binding between CASP10 and usnic acid and masoprocol and between NOTCH3 and 2-mercaptobenzothiazole. scRNA-seq data revealed CASP10 expression in endothelial and inflammatory cells and NOTCH3 expression in smooth muscle cells and fibroblasts. The PheWAS did not detect any adverse associations that survived the false discovery rate (FDR) correction. Overall, this integrated analysis highlights CASP10 and NOTCH3 as potential therapeutic targets for PAH. CASP10, as supported by stronger predicted druggability and multiomics evidence, warrants priority for further experimental evaluation. - Source: PubMed
Publication date: 2026/03/03
Chen HuaningChen JintongHou ChengchengRui HongbingXie Liangdi - Introduction Monogenic neonatal diabetes mellitus (NDM) is a rare form of diabetes, presenting within the first six months of life and caused by pathogenic variants affecting pancreatic β-cell development or function. Because its initial presentation may overlap with type 1 diabetes, molecular diagnosis is crucial, as it directly influences prognosis and treatment - particularly the potential responsiveness to sulfonylureas in ATP-sensitive potassium (KATP)-channel-related NDM. This study reports a retrospective descriptive case series and aims to characterize the clinical and genetic features of infants with NDM, to improve therapeutic management and long-term outcomes. Materials and methods We conducted a retrospective descriptive case series of infants diagnosed with diabetes before six months of age, hospitalized in the Pediatric Endocrinology Unit of the Abderrahim Harouchi Mother-Child Hospital, Casablanca, Morocco, between January 2018 and December 2025. Clinical presentation, biochemical data, insulin requirements, genetic results, and outcomes were extracted from medical records. Genetic testing was performed through next-generation sequencing (NGS), or targeted Sanger sequencing when financially feasible. Results Ten infants were included (nine males and one female), with a mean age at diagnosis of 71 days. Diabetic ketoacidosis (DKA) was the presenting feature in all cases. Consanguinity was reported in 55% of families. Pathogenic or likely pathogenic variants were identified in six infants (60%), involving ABCC8, INS, EIF2AK3, CASP10, and chromosome 6q23-24 duplication, including two syndromic forms. Two infants with ABCC8 mutations achieved insulin independence with sulfonylurea therapy. Syndromic etiologies - Wolcott-Rallison syndrome, Donohue syndrome, and autoimmune lymphoproliferative syndrome type IIA (ALPS-type IIA) - were associated with severe multisystemic involvement. Three children had no identifiable pathogenic variant, despite clinical features consistent with NDM. Long-term outcomes varied widely, ranging from normal neurodevelopment to early mortality in Donohue syndrome. Conclusion This retrospective descriptive case series highlights the marked genetic heterogeneity and clinical variability of neonatal diabetes in a resource-limited setting. Genetic testing enabled precision therapy in infants harboring KATP-channel mutations and clarified prognosis in syndromic forms. Expanding access to molecular diagnostics remains essential to improve equity in care, optimize metabolic outcomes, and support individualized management strategies. - Source: PubMed
Publication date: 2026/01/29
Yakine FatimazahraBouarab IlhamAlaoui-Inboui Fatima ZahraEch-Charafi MeryemBenmohamed HoudaJennane FaridaSlaoui Bouchra - Atherosclerosis (AS) is a chronic inflammatory disease driven by endothelial dysfunction and plaque instability. The DNA damage response (DDR) has been implicated in endothelial cell fate; its precise role in AS remains unclear. This study aims to identify DDR-related biomarkers associated with AS and elucidate their mechanisms in endothelial pyroptosis. Our analysis identified 66 DDR-related genes, which achieved over 80% accuracy in discriminating early from advanced lesions and hemorrhagic from non-hemorrhagic plaques in external datasets, and reached 100% accuracy in differentiating plaque stability. CASP10 emerged as a top diagnostic biomarker (AUC = 0.991) compared to other DDR genes. Single-cell analysis confirmed elevated CASP10 expression in endothelial cells of AS plaques. Functional experiments revealed that CASP10 is both necessary and sufficient for ox-LDL-induced DNA damage and pyroptosis in HUVECs. CASP10 overexpression exacerbated γHAX accumulation, NLRP3 expression, GSDMD-N cleavage and IL-1β release, while CASP10 knockdown attenuated these effects. Overall, CASP10 serves as a reliable biomarker for identifying unstable plaques and functions as a pivotal mediator linking DNA damage to endothelial pyroptosis. Targeting CASP10 may represent a novel therapeutic strategy to reduce endothelial cell death and stabilise atherosclerotic plaques. - Source: PubMed
Meng XiangrongZhang KejianXi YuWang ZhuozhongZhu XinyuZhang Wenjing - Malignant melanoma is a highly aggressive skin malignancy characterised by metastatic properties and resistance to conventional therapies. This indicates a necessity to explore novel, efficacious treatment modalities. Atranorin, a secondary metabolite derived from lichen, has demonstrated a diverse range of bioactivities. However, the antineoplastic mechanisms of atranorin in melanoma remain underexplored. - Source: PubMed
Publication date: 2026/01/15
Ensoy MineCansaran-Duman Demet