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
- Lung cancer is frequently diagnosed after curative treatment windows have narrowed, creating a need for minimally invasive biomarkers that report tumor development at earlier stages. Extracellular vesicles (EVs) are promising analytical targets because they carry molecular cargo from their originating cells, but tumor-associated EV signals can be rare in blood and obscured in bulk measurements. Here, we present Cygnus (Cyclic-imaging gateway to nanovesicles underlying signature), an end-to-end workflow that integrates cyclic immunofluorescence imaging with multiscale analysis of individual EVs. Cygnus preserves vesicle-level measurements, quantifies marker co-expression, resolves EV subpopulations, and summarizes single-vesicle phenotypes into sample-level profiles. In a genetically engineered mouse model of lung adenocarcinoma, Cygnus revealed dynamic changes in EV protein composition and identified an EpCAM- and/or CTSH-positive EV subpopulation before tumors were detectable by radiography. In a pilot clinical cohort (n = 35), plasma EV profiling showed lung cancer-associated marker patterns compared with non-cancer controls and nominated a CTSH/PDL1/MET marker combination for future validation. These findings support multiplexed individual-EV profiling as a strategy for defining candidate lung cancer-associated EV signatures and position Cygnus as an integrated workflow for translating vesicle-level heterogeneity into sample-level EV profiles. - Source: PubMed
Publication date: 2026/08/25
Cho Mi HyeonChung YeinChoi YoonjeongCha BaekdongSong JayeonOh NuriJo AlaNg Thomas S CKim HyunhoWoo Hyun-KyungKim Chang HyunCastro Cesar MMiller Miles ALee Hakho - 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