CTSH purified MaxPab Mouse Polyclonal Antibody
- Known as:
- CTSH enriched MaxPab Mouse Polyclonal Antibody
- Catalog number:
- BIN-001512-B01P
- Product Quantity:
- 0.05mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- CTSH purified MaxPab Mouse Polyclonal Antibody
Related genes to: CTSH purified 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 purified MaxPab Mouse Polyclonal Antibody
Related articles to: CTSH purified MaxPab Mouse Polyclonal Antibody
- Diabetic retinopathy (DR) arises from intertwined inflammatory, metabolic, and hypoxia-driven angiogenic programs, yet upstream regulators coordinating these processes remain incompletely defined. Here, we used an integrative multi-omics and experimental framework to identify cathepsin H (CTSH) as a candidate causal driver of proliferative DR (PDR). By combining GWAS, eQTL, pQTL, and mQTL datasets with Mendelian randomization, summary-data-based Mendelian randomization, and Bayesian colocalization, CTSH emerged as the strongest genetically supported candidate across discovery and validation analyses. In the UK Biobank (UKB), circulating CTSH was elevated in diabetic retinopathy and independently predicted incident disease. Single-cell transcriptomic analyses localized CTSH predominantly to myeloid compartments within fibrovascular membranes and linked CTSH-high states to inflammatory, hypoxic, and angiogenic programs. In high-glucose-stimulated THP-1 monocytes, CTSH promoted reactive oxygen species accumulation, NF-κB activation, and increased IL-6, TNF-α, HIF-1α, and VEGF expression, whereas CTSH silencing reversed these effects. Structure-guided virtual screening identified Eriocitrin as a lead CTSH-binding candidate. In db/db mice, intravitreal Eriocitrin improved inner-retinal function, restored OCTA-derived vascular metrics, and partially rescued retinal structure, with efficacy comparable to anti-VEGF treatment across several endpoints. Molecular analyses further showed coordinated suppression of inflammatory, hypoxic, angiogenic, and NF-κB signaling. Together, these findings identify CTSH as an upstream immunometabolic regulator of DR-related inflammatory and angiogenic biology, with the strongest genetic support observed for PDR, and support CTSH targeting as a potential multi-pathway therapeutic strategy beyond VEGF inhibition. - Source: PubMed
Publication date: 2026/04/23
Cui XuehaoZhao QiuchenHui JingwenZhou YuejunGong YawenZhang WeiMahata BideshYu-Wai-Man PatrickHan Quanhong - 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