CATD_RAT Ctsd ELISA tesk kit
- Known as:
- CATD_RAT Ctsd Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16454
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- CATD_RAT Ctsd ELISA tesk kit
Related genes to: CATD_RAT Ctsd ELISA tesk kit
- Gene:
- CTSD NIH gene
- Name:
- cathepsin D
- Previous symbol:
- CPSD
- Synonyms:
- CLN10
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2014-11-18
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- To reconnoitre the mechanism of Abietic acid (AA) in diabetes by and experiments. Using GeneCards, diabetes gene targets were obtained. The protein-protein interaction and network topology analysis were performed using the String platform and Cytoscape 3.7.2. The enrichment analysis was done by Shiny GO. The docking was by Autodeck. Diabetes was induced by injecting STZ (55 mg/kg, i.p once) in Sprague-Dawley rats. The parameters included glucose, lipids, blood pressure, ECG, OGTT, kidney and cardiac markers, liver enzymes, AMPK, Nrf2, PPAR-γ, TLR-4, oxidative markers, LVF tests, and histopathology. AA interacts with 15 important targets (PIK3CD, MAPK1, NF-κB, mTOR, STAT3, GRIN1, ITGB3, ACACA, HSP90AB1, SERPINE1, ADRB1, ULK1, TLR4, CTSD, CDK5). The signalling pathways, like insulin, MAPK1, TLR, AMPK, JAK-STAT, are associated with these proteins. In docking, the highest affinity of AA was observed for ITGB3 (- 8.1), TLR4 (- 7.8), and ACACA (- 7.3). In rats, AA(40 and 80 mg/kg) decrease hyperglycaemia and hyperinsulinemia, improves glucose tolerance, normalize blood pressure, combat dyslipidaemia (decrease triglyceride, total cholesterol, LDL, increase HDL), preserves myocytes and ventricular function (decrease troponin-I, LDH, CK-MB, LVEDP, normal ECG), hepatoprotective (decrease AST, ALT), reno-protective (decrease creatinine, urea, uric acid) and combat oxidative stress (decrease MDA, increase SOD, catalase). Nrf2, AMPK, and PPAR γ levels were increased while TLR-4 levels were decreased after AA treatment. The study is supported by the preserved histopathological architecture of pancreatic, renal, hepatic, and cardiac cells. The present study preliminarily clarifies that AA exhibits therapeutic potential in preclinical models through multitargets and multi-pathways (Nrf/TLR4/PPAR γ), which points out a new direction for further research and clinical application. - Source: PubMed
Publication date: 2026/09/24
Mishra AkashShah Hital - Long-term exposure to polystyrene nanoplastics (PS-NPs) causes neurotoxicity, but the underlying mechanisms remain unclear. We combined network toxicology, molecular docking, and in vivo experiments to investigate the role of MTOR-TFEB-regulated autophagy in PS-NP-induced neurotoxicity. Potential targets related to PS-NPs and neurodegenerative diseases were screened from public databases. Enrichment analysis indicated involvement of neurodegenerative and autophagy pathways. Protein-protein interaction and docking simulations prioritized as a candidate target. Sprague-Dawley rats were gavaged with PS-NPs (0.15 or 1.5 mg/kg) for 60 days. Morris water maze tests showed impaired spatial learning and memory. Western blotting of hippocampal tissues revealed increased p-MTOR/MTOR ratios, decreased total cytoplasmic and nuclear TFEB, reduced lysosomal proteins (LAMP2, CTSD, and CTSB), elevated autophagy markers SQSTM1 and MAP1LC3B-II, and altered apoptosis regulators (BAX up and BCL2 down). Collectively, PS-NPs disrupt the MTOR-TFEB axis, impair lysosomal function and autophagic clearance, and promote apoptosis, leading to neurocognitive deficits. These findings provide mechanistic insights into the MTOR-TFEB axis and highlight it as a candidate pathway warranting further evaluation as a potential intervention target. - Source: PubMed
Publication date: 2026/09/09
Tang NaWang ChunZhang MengLi YajieLiang YongkangZhang JingjingNiu Qiang - Macrophages organise the fibrotic niche of liver cirrhosis. The scar-associated macrophage state is well described, but the genes that define it have rarely been ranked in an unbiased, model-based way, and the statistical limits of such re-analyses are seldom reported. Here we set out to re-derive the scar-associated macrophage programme without supervision, to rank its constituent genes by convergent computational evidence, and to state explicitly what a cohort of this size can and cannot support. We re-analysed 58,358 single-cell transcriptomes from five uninjured and five cirrhotic human livers (GEO GSE136103; Edinburgh DataShare DS_10283_3433). After quality control, Harmony batch integration and Leiden clustering, the mononuclear-phagocyte compartment (9869 cells) was re-clustered. We applied donor-level compositional testing stratified within the CD45+/CD45- sorted fractions, donor-level pseudobulk differential expression, three classifiers with SHapley Additive exPlanations (SHAP) under donor-grouped cross-validation, transcription-factor differential expression, diffusion pseudotime, ligand-receptor modelling and CellOracle in silico perturbation. The donor, never the cell, was the unit of analysis for every condition comparison. A discrete macrophage cluster (390 cells; 60.5% cirrhotic; contributed by all 10 donors) carried a coherent lipid/scar programme comprising LGALS3, GPNMB, TREM2, CD9, FABP5, APOE, APOC1 and CTSD, and was recovered in all 22 clustering configurations tested. The integrated prioritisation was robust: seven genes remained in the top 20 in 100% of 1000 Dirichlet re-weightings. MAFB, MITF and TFEC were significantly enriched transcription factors, and pseudotime placed the state downstream of a monocyte root. Three findings temper these results. No lineage showed a significant compositional change after multiple-testing correction, and every test was underpowered for its observed effect. No gene reached significance in donor-level pseudobulk differential expression. Classifier performance of 0.99 reflects the circularity of predicting a cluster defined from the same matrix; the non-circular contrast of cirrhotic versus uninjured cells gave 0.61-0.65. Overall, a documented, fully reproducible framework re-derives and ranks a TREM2/LGALS3/GPNMB scar-associated macrophage programme and nominates galectin-3, GPNMB and the SPP1 axis as prioritised, clinically unproven candidates. The prioritisation is a hypothesis requiring independent, spatial, protein-level and functional validation. - Source: PubMed
Publication date: 2026/09/09
Faisal ShahEjaz Muhammad AdeelKambey Piniel AlphayoMalik AbdulLi Yin-Xiong - Prolonged exposure to 1,2-dichloroethane (1,2-DCE) can lead to cognitive dysfunction, and neuronal loss is a proven key driver. In mice, 1,2-DCE exposure reduced hippocampal ATP levels, triggering AMPK phosphorylation, mTOR suppression, and ULK1 activation, along with increased Beclin 1 and LC3-II/I levels, collectively indicating enhanced autophagy initiation. Meanwhile, p62 accumulation and decreased LAMP1 and CTSD expression indicated impaired autophagic degradation, accompanied by increased neuronal apoptosis. Consistent with these in vivo findings, PC12 cells, a neuron-like cell line, exhibited mitochondrial dysfunction after exposure to 2-chloroethanol (2-CE, a metabolite of 1,2-DCE in vivo), as evidenced by ATP depletion, mitochondrial membrane potential loss, and elevated ROS production. Furthermore, 2-CE activated the AMPK-mTOR-ULK1 signaling pathway to initiate autophagy, while also disrupting lysosomal structure and function, leading to impaired autophagic flux and enhanced apoptosis. In conclusion, prolonged 1,2-DCE exposure induces mitochondrial dysfunction and ATP depletion, activating AMPK-mTOR-ULK1-mediated autophagy initiation. Meanwhile, concomitant lysosomal damage impairs autophagic degradation, and the combined effect promotes neuronal apoptosis. These findings suggest a potential strategy for preventing and treating 1,2-DCE-induced cognitive impairment. - Source: PubMed
Publication date: 2026/09/09
Luo ZhenlinWang ChenWang ChuntingWang GaoyangCui WantingWang ZijiangZhao Fenghong - Sepsis is a life-threatening condition characterized by a dysregulated host response to infection, in which lysosomal acidification and hydrolytic activity are crucial for effective pathogen clearance by macrophages. Transmembrane Protein 175 (TMEM175) is a key regulator of lysosomal pH, and its deficiency is reported to cause lysosomal over-acidification and impaired cathepsin D (CTSD) activity. However, the role of TMEM175 in sepsis remains uncertain. We hypothesize that TMEM175 deficiency exacerbates sepsis by impairing CTSD activity. TMEM175 mRNA expression levels were measured in peripheral blood mononuclear cells (PBMCs) from septic patients and healthy controls (HCs). Using a cecal ligation and puncture (CLP) mouse model, we evaluated the effects of the TMEM175 inhibitor 2-phenylcyclopentylamine (2-PPA) on mortality and bacterial load in target organs. In vitro, TMEM175-knockdown in macrophages was performed to assess its impact on bacterial clearance, phagocytosis, lysosomal acidification, and cathepsin maturation. Results showed that TMEM175 expression was significantly downregulated in PBMCs from septic patients. Pharmacological inhibition of TMEM175 in CLP mice exacerbated bacterial burden and increased mortality. Mechanistically, TMEM175 deficiency impaired macrophage-mediated bacterial clearance, despite having no effect on the initial phagocytic uptake. This dysfunction was attributed to TMEM175, which directly regulates cathepsin transcription. Additionally, TMEM175 deficiency suppressed PI3K-Akt signaling, reducing inflammatory cytokine production. - Source: PubMed
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