CTSH MaxPab Mouse Polyclonal Antibody
- Known as:
- CTSH MaxPab Mouse Polyclonal Antibody
- Catalog number:
- BIN-001512-B01
- Product Quantity:
- 0.05ml
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- CTSH MaxPab Mouse Polyclonal Antibody
Related genes to: CTSH MaxPab Mouse Polyclonal Antibody
- Gene:
- CTSH NIH gene
- Name:
- cathepsin H
- Previous symbol:
- CPSB
- Synonyms:
- ACC-4, ACC-5, ACC4, ACC5
- Chromosome:
- 15q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2015-02-16
Related products to: CTSH MaxPab Mouse Polyclonal Antibody
Related articles to: CTSH MaxPab Mouse Polyclonal Antibody
- Cathepsins play critical roles in various physiopathological processes, with several reported to be associated with nonalcoholic fatty liver disease (NAFLD). Herein, we investigated the expression patterns of the cathepsin family in human and mouse livers, cultured hepatocytes, and their roles in NAFLD. Public datasets of NAFLD patients and controls were analyzed to examine hepatic cathepsin expression in human livers. RT-qPCR assessed these genes in mouse livers, HepG2, Hepa1-6, and mouse primary cells. Despite different expression patterns, CTSA, CTSB, CTSD, CTSH, and CTSL were consistently highly expressed across all samples. Notably, steatosis patients and diabetic mice exhibited significantly increased hepatic expression of four cathepsins. Among these, we first observed elevated CTSG and CTSW, with CTSG showing the most pronounced increase. Moreover, hepatic CTSG was increased and positively correlated with disease severity in NASH patients. CTSG was also upregulated in HepG2 cells treated with high glucose or free fatty acids. In vitro, CTSG overexpression promoted, while its knockdown reduced lipid accumulation. In vivo, hepatic CTSG overexpression significantly induced lipid deposition, impaired glucose tolerance, and elevated HOMA-IR. Mechanistically, CTSG upregulated key lipid synthesis genes (ACC, SCD1) and downregulated those involved in lipid oxidation (PPARα, Lcad) and secretion (MTTP) by suppressing Akt. Furthermore, Akt activation alleviated lipid deposition induced by CTSG overexpression, while Akt inhibition abolished the beneficial effect of CTSG knockdown. This study is the first to reveal the expression patterns of the cathepsin family in human and mouse livers, and identifies that hepatic CTSG is elevated in NAFLD and can promote lipid deposition, supporting CTSG as a novel potential therapeutic target for NAFLD. - Source: PubMed
Yang WeiliLin JiaqiPan QiuyueJiang YanShi TingtingCao Xi - Neuroblastoma is a pediatric malignancy characterized by significant clinical heterogeneity. Although MYCN amplification is a well-established marker of high-risk disease, its interplay with the tumor immune microenvironment-particularly tumor-associated macrophages (TAMs)-remains poorly understood. In this study, we developed an integrated gene signature incorporating genes associated with both MYCN amplification status and TAM infiltration, leading to the identification of 16 differentially expressed genes implicated in both biological processes. Six of these genes (CMBL, LY6E, KLRB1, CTSH, CD3D, and PTGDS) were utilized to construct a risk-scoring model that effectively stratified neuroblastoma patients into high- and low-risk groups with significantly distinct clinical outcomes ( < 0.001). Notably, LY6E emerged as the most prognostically significant gene within the signature. More importantly, we revealed that LY6E modulates M2-type macrophage polarization in neuroblastoma for the first time, suggesting a novel mechanism through which it may contribute to shaping an immunosuppressive tumor microenvironment. - Source: PubMed
Publication date: 2026/04/15
Li LijuanZeng YuZhang QinfenZhuang GaojianLiu YuWang XuanWang Yuqi - Overcoming profoundly suppressed programmed cell death and an immunosuppressive tumor microenvironment (TME) remains a formidable challenge in gemcitabine-cisplatin-resistant muscle-invasive bladder cancer (GP-R MIBC). To address this, we developed a glutathione (GSH)-responsive nanosystem for co-delivering the cathepsin H (CTSH) inhibitor prodrug E64d and a cisplatin prodrug Pt(IV), implementing a spatiotemporally coordinated "unlock-and-trigger" strategy. Mechanistically, the activated E64 irreversibly inhibits CTSH, thereby unlocking the TNFα-caspase-8 axis to reinstate GSDMD-mediated pyroptosis. Concurrently, caspase-8 dually activates caspase-3 via both direct cleavage and the Bid-mediated mitochondrial pathway. This primed state ensures that the DNA damage induced by the reduced Pt(IV) robustly triggers caspase-3/GSDME-mediated pyroptosis. This synergistic dual-pyroptosis pathway potently stimulates immunogenic cell death (ICD) and reverses the immunosuppressive TME by promoting dendritic cell maturation and CD8T lymphocyte infiltration. Consequently, when combined with an αPD-L1 antibody, this strategy effectively eradicated GP-R bladder tumors and suppressed recurrence in vivo, demonstrating compelling translational potential. In summary, our work presents a translatable nanotherapeutic strategy that resensitizes GP-R MIBC to chemo-immunotherapy by leveraging a synergistic "unlock-and-trigger" mechanism to reactivate pyroptosis. - Source: PubMed
Publication date: 2026/04/12
Wen JintaoZhou BaotongZhang HanchenTang YongboHu HaiweiXiao HaihuaGe Bo - Dysregulation of the peripheral immune system may increase Alzheimer's disease (AD) risk, but the underlying cell type-specific mechanisms remain unclear. - Source: PubMed
Lindbohm Joni VStražar MartinLee Hang-MaoAshenberg OrrMars NinaSipilä Pyry NRipatti SamuliGraham DanKivimäki MikaXavier Ramnik J - This study identifies diagnostic biomarkers of OA-related synovitis from synovial tissue expression and develops a validated diagnostic nomogram (differentially expressed genes = differentially expressed genes; single-sample gene set enrichment analysis [ssGSEA]). We analyzed GEO synovium datasets (training: GSE55235, GSE55457, GSE82107, OA = 30 vs controls = 27; validation: GSE89408, OA = 22 vs controls = 28; cartilage comparator: GSE129147, OA = 10 vs controls = 9) and applied weighted gene correlation network analysis to identify phenotype-linked modules, followed by 4 machine learning models (random forest [RF], support vector machine [SVM], xtreme gradient boosting (XGB), generalized linear model [GLM]) to rank genes, selection of hub genes from the top SVM features, construction and validation of a multigene nomogram predicting OA-related synovitis vs control, and integrative pathway and immune profiling (gene ontology/kyoto encyclopedia of genes and genomes, ssGSEA), competitive endogenous RNA network analysis, and hypothesis-generating protein-ligand docking. In the training synovium set (GSE55235 + GSE55457 + GSE82107; outcome = OA-related synovitis vs control), model area under the curves (AUCs; 95% confidence intervals) were RF 0.944 (0.882-1.000), SVM 1.000 (0.997-1.000), XGB 0.917 (0.842-0.992), and GLM 0.944 (0.882-1.000). In the external synovium validation dataset GSE89408 (outcome = OA-related synovitis vs control), AUCs (95% confidence intervals) were RF 0.729 (0.585-0.873), SVM 0.792 (0.662-0.922), XGB 0.717 (0.571-0.863), and GLM 0.771 (0.636-0.906), emphasizing external validation as the fairer test of model generalizability. The cartilage comparator GSE129147 (outcome = OA vs control in cartilage) yielded SVM AUC 0.833 (0.333-1.000), supporting tissue-specific yet cross-tissue consistency. Five hub genes - CTSH, ephrin-B2, YIPF2, ZNF671, SLC27A6 - were identified from 462 intersecting genes, selected from the SVM model because it showed the smallest residuals and best internal discrimination among the 4 tested algorithms. The 5-gene nomogram showed good calibration and decision-curve net benefit across 10% to 40% threshold probabilities, confirming its diagnostic utility. ssGSEA analysis revealed enriched immune-related pathways and higher infiltration of B cells, macrophages, mast cells, and T-cell subsets in OA synovium, closely associated with the expression of hub genes such as YIPF2 and ZNF671 linked to adaptive-immune and inflammatory signaling. Molecular docking indicated that dexamethasone and triamcinolone acetonide bind to the protein products of the hub genes (-7.1 to -8.5 kcal/mol). The 5-gene synovium-based SVM model provides a validated diagnostic nomogram for OA-related synovitis; docking findings are hypothesis-generating and not evidence of therapeutic efficacy. - Source: PubMed
Wang PengJiang XingwenXia XiaofengZou KaiZuo BinHe Jingxuan