CTSH Antibody
- Known as:
- CTSH Antibody
- Catalog number:
- XW-7949
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CTSH Antibody
Related genes to: CTSH 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 Antibody
Related articles to: CTSH Antibody
- Peptidyl arginine deiminase 4 (PAD4) is previously known for its role in inflammatory bowel disease (IBD) through its facilitation of neutrophil extracellular traps (NETs) by citrullinating histones. However, the specific citrullinated substrates have not been fully elucidated, especially non-histones. By performing citrullination mapping, we unraveled the involvement of cathepsin H (CTSH), a novel substrate of PAD4, which undergoes citrullination at the R315 site. Then the citrullination of CTSH obviously altered its molecular conformation and subsequently reduced its enzymatic activity, which significantly boosted the formation of NETs. Consistently, CTSH knockout mice demonstrated exacerbated colonic inflammation and higher levels of NETs, which might be achieved by activating the phosphatidylinositol 3-kinase/protein kinase B (PI3K-Akt) signaling pathway. These findings underscore the critical role of CTSH in IBD pathogenesis and position it as a potential therapeutic target, highlighting the complex interplay among PAD4, CTSH, and IBD. - Source: PubMed
Publication date: 2026/07/28
Song Yi-HangHuang Feng-XingGu LunChang XinYang Xin-YuePang Ru-XiWu Hai-CongKang Zheng-ChunLi Zhao-ShenBai YuWang PeiWang Shu-Ling - Mitochondria, as crucial organelles in eukaryotic cells, are deeply involved in cellular energy metabolism and biogenesis. Currently, mitochondria have been found to transfer between cells and regulate a range of cellular functions and research has found that mitochondrial transfer has been shown to play an important role in regulating bone homeostasis. - Source: PubMed
Publication date: 2026/07/14
Diao JiayongHe QixuanLiu QuanzhenLiu YuxuanChen SimiaoZhang YuzheGui HoudaChen JingyiWu DongniPang XinyuZhang QingyueWang Ya-NanZhang Dongjiao - Primary chondrocytes often lose matrix-forming capacity during in vitro expansion, limiting scalable cartilage engineering. Here, we examined aging-independent regulation of chondrogenic function during long-term expansion of primary auricular chondrocytes and sought molecular features associated with late-passage functional decline. - Source: PubMed
Publication date: 2026/06/13
Alemujiang DilinapaTsuji NaokiSakamoto TomoakiChu Yu-YingHoshi KazutoHikita Atsuhiko - 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