Ask about this productRelated genes to: CTSC Blocking Peptide
- Gene:
- CTSC NIH gene
- Name:
- cathepsin C
- Previous symbol:
- PLS, PALS
- Synonyms:
- DPP1
- Chromosome:
- 11q14.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
Related products to: CTSC Blocking Peptide
Related articles to: CTSC Blocking Peptide
- Preeclampsia (PE) is a major pregnancy complication that poses risks to both the mother and the fetus. Oxidative stress (OS) plays a crucial role in its pathogenesis. This study aims to explore the diagnostic value of oxidative stress-related genes for PE. - Source: PubMed
Ye WenhuaYin Haiyan - Radiotherapy is an important therapeutic modality for advanced hepatocellular carcinoma (HCC), but the limited understanding of radioresistance mechanisms in HCC has hindered its further clinical development. This work aimed to clarify the essential role of Cathepsin C (CTSC) in regulating radioresistance in HCC. The expression of CTSC in HCC tissues was analysed using real-time PCR (RT-PCR) and immunohistochemistry. The role of CTSC in radiotherapy resistance of HCC was investigated through in vitro experiments, in vivo studies (subcutaneous and orthotopic liver tumour models) and clinical data analysis. Additionally, in vivo experiments were conducted to evaluate the effect of blocking the CTSC signalling pathway on reversing radiotherapy resistance in HCC. CTSC expression was significantly higher in HCC tissues than in adjacent non-tumour tissues. Correlation analysis showed that positive CTSC expression was positively associated with aggressive clinicopathological features, including increased tumour number, large tumour size, absence of tumour encapsulation, microvascular invasion and advanced TNM stage. Survival analysis further revealed that CTSC overexpression was linked to poorer overall survival (OS) and progression-free survival (PFS) in HCC patients. In vitro experiments demonstrated that CTSC overexpression increased the clonogenic survival rate of Huh7 cells after ionising radiation (IR) and reduced the apoptosis rate. In both subcutaneous and orthotopic liver tumour models, upregulated CTSC expression significantly decreased radiotherapy sensitivity. Clinically, CTSC overexpression was significantly associated with a poor response to radiotherapy. Mechanistically, CTSC promoted the infiltration of myeloid-derived suppressor cells (MDSCs) while reducing CD8 T cell infiltration by upregulating CXCL1 expression. Importantly, the combination of the CTSC inhibitor AZD7986 with radiotherapy significantly improved radiotherapy sensitivity in HCC models. CTSC contributes to radiotherapy resistance in HCC by recruiting MDSCs. The synergistic application of a CTSC inhibitor with radiotherapy represents an effective combinational treatment strategy for CTSC-positive HCC. - Source: PubMed
Xu JiahuanZhang BilinYang ShiruiSong ShaoranWu JieDang Yunzhi - Ewing sarcoma (ES) is the second most common primary bone malignancy in children and adolescents and remains one of the most lethal pediatric cancers. Found in more than 85% of patients with ES, results from the t(11;22)(q24;q12) chromosomal translocation. This fusion encodes an aberrant transcription factor that dysregulates gene expression and drives oncogenic transformation. Although this oncogene was identified over three decades ago, therapeutic progress has been limited, in part due to the lack of robust and permissive animal models. Prior efforts to generate transgenic mouse models have been unsuccessful, and while zebrafish have emerged as a promising system, a tissue context capable of supporting EWSR1::FLI1-driven tumorigenesis has not been defined. Here, we report that tissue-specific expression of in zebrafish induces tumor formation that recapitulates the histologic and molecular hallmarks of human ES, including small round blue cell morphology and characteristic biomarker expression. Tumors were driven by the promoter and resulted in ~70% incidence of notochord tumors within the first 72-96 h. Of the surviving fish, ~5% developed CD99-positive small round blue cell tumors at ~9 months post-fertilization. This work establishes a stable tissue-specific transgenic model of ES, providing a powerful in vivo platform to investigate disease pathogenesis and evaluate novel therapeutic strategies. - Source: PubMed
Publication date: 2026/03/30
Anderson Rebecca AChen XinOyarbide UsuaAlvarez Nicolas JSievers AidanSchwartz Gary KCorey Seth J - Anti-NMDA receptor (NMDAR) encephalitis is an autoimmune disorder of the central nervous system involving both B- and T-cell activation. In this exploratory study, targeted proteomics was used to characterize protein expression profiles in serum and cerebrospinal fluid (CSF) from patients with anti-NMDAR encephalitis. Samples from eight patients and 16 age- and sex-matched symptomatic controls were analyzed in a retrospective case-control design. Protein concentrations in serum and CSF were quantified using Proximity Extension Assay (PEA) technology targeting 182 proteins related to immunity, synaptic regulation, and neuronal maintenance. Linear regression identified seven significantly altered proteins in CSF and three in serum after Bonferroni correction (p < 0.00027). In CSF, six proteins associated with immune signaling and neuronal support (ADA, CCL19, CXCL5, BMP-4, FGF-5, CDH3) were decreased, while the protease CASP-8 was elevated. In serum, proteases CTSC and CASP-8 were increased, whereas ADA, a key regulator of purine metabolism and immune signaling, was decreased. Strong to moderate correlations between CSF and serum levels were observed for ADA (r = 0.606, p = 0.013) and CASP-8 (r = 0.526, p = 0.037). Longitudinal CSF data from two patients revealed dynamic changes in CXCL5, CCL19, and CASP-8 corresponding to disease activity and treatment response. Overall, these findings revealed distinct yet related proteomic signatures in serum and CSF, suggesting compartment-specific immune responses involving both innate and adaptive pathways. The consistent elevation of CASP-8 highlights its potential as a biomarker of disease activity and warrants further investigation. - Source: PubMed
Publication date: 2026/04/03
Kosek SonjaWiberg AnnaPersson BarbroGabrysch KatjaBurman JoachimPunga Anna Rostedt - Congenital tooth agenesis impairs masticatory function and aesthetics and adversely affects craniofacial development. Although largely considered genetic in origin, its exact etiology remains unclear. This study reports three familial cases of nonsyndromic congenital tooth agenesis (NSTA). Whole genome sequencing (WGS) revealed five pathogenic variants: filamins-B (FLNB) (c.5186C>A, p.Ser1729Ter), methylcrotonyl coenzyme a carboxylase 2 (MCCC2) (c.91C>T, p.Gln31Ter; c.484C>T, p.Gln162Ter; c.340C>T, p.Gln114Ter), laminin subunit alpha 2 (LAMA2) (c.1084A>T, p.Arg362Ter), cathepsin C (CTSC) (c.748C>T, p.Arg250Ter), and chromatin remodeling protein microrchidia family CW-type zinc finger 4 (MORC4) (c.1726C>T, p.Arg576Ter). Among these variants, LAMA2 was associated with a severe tooth agenesis phenotype. The findings offer novel clues toward understanding the etiopathogenesis of this condition. - Source: PubMed
Zheng YuemeiWang DanJiang TongyangYang DanquLu Hong