Polyclonal ECSIT (CT)
- Known as:
- Polyclonal ECSIT (CT)
- Catalog number:
- pc-477
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Polyclonal ECSIT ()
Related genes to: Polyclonal ECSIT (CT)
- Gene:
- ECSIT NIH gene
- Name:
- ECSIT signalling integrator
- Previous symbol:
- -
- Synonyms:
- SITPEC
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2006-08-08
- Date modifiied:
- 2014-11-19
Related products to: Polyclonal ECSIT (CT)
Related articles to: Polyclonal ECSIT (CT)
- Embryonic neural stem and progenitor cells occupy a specialized niche along the lateral ventricles, where receptors on their apical membrane sense extracellular cues essential for preserving progenitor identity. How such surface signals are coupled to mitochondrial metabolism remains unclear. Here, we identify EPHA2 as a receptor enriched in cortical progenitors and show that disruption of its non-canonical, ligand-independent signaling compromises progenitor maintenance in vivo. EPHA2 perturbation reduces mitochondrial respiration, Complex I activity, and mitochondrial NAD regeneration, and is accompanied by lower mitochondrial abundance of the Complex I assembly factor ECSIT. Restoring mitochondrial NAD regeneration with MTS-LbNOX, or restoring mitochondrial ECSIT with ECSIT WT-but not a mitochondrial targeting-deficient mutant-attenuates the progenitor defects caused by EPHA2 perturbation. Maternal supplementation with NAD or its precursor NMN similarly mitigates these developmental defects. We further identify a PP2A-sensitive ECSIT phospho-state, including T179, that is consistent with regulated mitochondrial ECSIT accumulation downstream of EPHA2. Together, these findings support a model in which EPHA2 helps maintain embryonic cortical progenitors by sustaining ECSIT-dependent Complex I-linked mitochondrial redox homeostasis. - Source: PubMed
Publication date: 2026/07/10
Diem Nghi TranMy Nhung Truong ThiKim SeunghyunYun JonghyeokTien Nguyen Tran NamLee AraJung MinkyoJang Eun JinGoo Bon SeongYoo Jin YeongShin Sung RyongMun Ji YoungPark Kyeng MinPhuoc Long NguyenPark CanaPark Sang Ki - causes bacterial hemorrhagic ascites in ayu (), a lethal disease characterized by abdominal distension with hemorrhagic ascites, multifocal organ hemorrhages, and histopathologically evident hepatocellular necrosis and inflammatory infiltration. The lack of effective treatments exacerbates mass mortalities, posing a significant threat to aquaculture. Given the severe pathogenesis of infection-which involves bacterial colonization, tissue necrosis, and host immune dysregulation-effective therapeutic strategies are urgently needed. Through a screen of traditional Chinese medicine monomers, we identified harmine, an indole alkaloid derived from seeds, as a potent agent against this pathogen. In vivo, harmine exhibited direct bactericidal activity by disrupting membrane integrity, as evidenced by increasing membrane permeability, and inhibiting biofilm formation. In an ayu infection model, harmine significantly increased host survival, reduced tissue bacterial load, and enhanced innate immunity by augmenting monocyte/macrophage phagocytosis and bactericidal capacity while suppressing pro-inflammatory cytokine release and apoptosis. Mechanistically, the Drug Affinity Responsive Target Stability assay was used to identify the molecular target of harmine, followed by functional validation through -knockdown experiments. Harmine exhibited direct bactericidal activity by disrupting membrane integrity and inhibiting biofilm formation. In the ayu infection model, harmine significantly increased host survival, reduced tissue bacteria1 load, and enhanced innate immunity by augmenting monocyte/macrophage system and bactericidal capacity while suppressing pro-inflammatory cytokine release and apoptosis, the latter likely through modulation of PRDX6-mediated oxidative stress and downstream caspase signaling. Mechanistically, DARTS revealed that harmine binds to peroxiredoxin 6 (PRDX6), a multifunctional enzyme possessing peroxidase, phospholipase A, and lysophosphatidylcholine acyltransferase activities. This binding liberates TNF receptor-associated factor 6 (TRAF6), facilitating its mitochondrial translocation and association with the ECSIT signaling integrator complex, thereby amplifying mitochondrial reactive oxygen species (mROS) production and potentiating macrophage-mediated bacterial killing. These findings establish harmine as a promising therapeutic candidate for controlling infections and underscore the value of host-directed immunomodulation derived from natural products in aquaculture medicine. - Source: PubMed
Publication date: 2026/04/11
Liu Yan-JunLi XiangJiang Yi-FangWang RanYu JingLiu Zhi-GuoCao Jia-FengYang Guan-JunChen Jiong - Although exercise is well established in alleviating aging-associated skeletal muscle atrophy, the underlying mechanism is not fully understood. Evolutionarily conserved signaling intermediate in Toll pathways (ECSIT) has been shown to be a crucial adaptor for inflammation and mitochondrial function; however, little is known about the action of ECSIT in skeletal muscle atrophy. First, the young and middle-aged mice underwent exercise training, and then skeletal muscle atrophy, mitochondrial quality control, and mitochondrial complex in skeletal muscle were detected. Then, we analyzed the Gene Expression Omnibus (GEO) database and performed in vivo experiments to determine the effect of exercise on ECSIT expression. Furthermore, ECSIT was knockdown in myoblasts to examine its effects on muscle atrophy, mitochondrial quality control, and mitochondrial complex. Compared with young mice, middle-aged mice exhibited significant reductions in relative weights of skeletal muscles, grip strength, hang time, and exhaustion exercise performance, while exercise restored these deficits dramatically. Consistently, exercise promoted protein synthesis and inhibited protein degradation in the gastrocnemius of middle-aged mice. Therefore, exercise significantly mitigated skeletal muscle atrophy in middle-aged mice. Concomitantly, exercise alleviated the impaired mitophagy in the gastrocnemius of middle-aged mice. ECSIT expression was elevated in the gastrocnemius of middle-aged mice but was reversed by exercise intervention. Mechanistically, ECSIT knockdown impaired myoblast differentiation, mitochondrial complex, and mitochondrial quality control in myoblasts. Collectively, this study reveals, for the first time, that ECSIT is important for myogenesis by maintaining mitochondrial quality control, thereby facilitating exercise-induced amelioration of skeletal muscle atrophy during aging. - Source: PubMed
Fan JingchengWen XinDuan XuemeiZhang XueZhang Tan - Non-alcoholic fatty liver disease (NAFLD) has emerged as a significant health issue due to the pathological accumulation of fat in the liver in the absence of excessive alcohol intake, with mitochondrial dysfunction being a critical underlying mechanism. This study aimed to evaluate the therapeutic potential of koumiss extract, along with 2-furanic acid and α, α-trehalose, in modulating mitochondrial function and mitigating fat deposition in NAFLD. Utilizing molecular docking techniques, we assessed the binding affinities of these compounds to mitochondrial complex I assembly (MCIA) proteins, while establishing both in vitro (HepG2 cell line) and in vivo (zebrafish model) NAFLD models to measure lipid accumulation and related biochemical parameters, including triglyceride (TG), total cholesterol (TC), and lactate dehydrogenase (LDH) levels, alongside the expression profiles of MCIA proteins. Our results demonstrated that koumiss extract, 2-furanic acid, and α, α-trehalose significantly decreased TG and LDH levels indicative of steatosis in HepG2 cells, while also reducing the expression of MCIA-related proteins. In vivo experiments using a zebrafish NAFLD model demonstrated pronounced liver steatosis in the model group. Treatment with koumiss extract, 2-furanic acid, and α, α-trehalose significantly alleviated liver steatosis and reduced TG and TC levels. Furthermore, mRNA expression levels of ACAD9, ECSIT, NDUFAF1, and NDUFAF2 were significantly downregulated in the treatment groups. Koumiss extract, 2-furanic acid, and α, α-trehalose exhibit significant effects in reducing MCIA-related proteins and steatosis in NAFLD models. Consequently, these results suggest that koumiss extract and its analogs hold promise as therapeutic agents for NAFLD, potentially enhancing liver lipid homeostasis. - Source: PubMed
Publication date: 2026/02/24
Baoyin SachulaBao QinglanLing XiongWang BiligetuBai XiaohongMeng MengChen YingsongWang Tegexibaiyin - Background Cancers remain a significant global health challenge; identification of cutting-edge diagnostic and prognostic markers plus innovative therapeutic targets is crucial. Tripartite motif molecule 59 (TRIM59) is a potential oncogene. However, its specific role in cancers is lacking. We aimed to investigate the expression of TRIM59 in pan-cancer as well as its implications for tumorigenesis, clinicopathological factors, and immune cell infiltration. Moreover, we aimed to investigate the protein-protein interaction and evaluate its potential as a diagnostic and prognostic biomarker in pan-cancer using bioinformatic analysis. Methods We analyzed TRIM59 across different cancer types using public datasets and bioinformatics tools. To study gene expression patterns, we used gene expression profiling interactive analysis (GEPIA), University of Alabama at Birmingham Cancer Data Analysis Portal (UALCAN), tumor immune estimation resource (TIMER), and University of California, Santa Cruz (UCSC) Xena, and validated our findings using additional datasets from the Gene Expression Omnibus (GEO) datasets. We assessed diagnostic performance with receiver operating characteristic (ROC) curve analysis. We also used Kaplan-Meier plotter (K-M plotter), GEPIA, UALCAN, and TIMER to explore how TRIM59 expression relates to patient prognosis and immune cell infiltration. Genetic changes were examined with cBioPortal, while the search tool for recurring instances of neighboring genes (STRING) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis helped us study protein-protein interaction networks and pathway enrichment. For statistical analysis, we used the Limma (Linear Models for Microarray Analysis) program and standard tests. Results TRIM59 was significantly upregulated in 22 cancers, with the highest level of expression in breast cancer (BRCA), esophageal cancer (ESCA), lung squamous cell carcinoma (LUSC), and stomach adenocarcinoma (STAD). High TRIM59 expression is significantly associated with a worse prognosis in kidney renal papillary cell carcinoma (KIRP), liver hepatocellular carcinoma (LIHC), and lung adenocarcinoma (LUAD), and it was also associated with various clinicopathological factors in BRCA, ESCA, LUSC, STAD, and immune markers across all these cancers. High TRIM59 expression is associated with infiltration of different immune cells in BRCA, ESCA, LUSC, STAD, LIHC, KIRP, and LUAD. Also, TRIM59 is associated with various genetic alterations across different types of tumors, and it interacts with several proteins. Conclusion In this study, we found that TRIM59 contributes to the carcinogenesis and increased malignant behavior of BRCA, ESCA, STAD, LUSC, LUAD, and KIRP. We also found that TRIM59 is a potential diagnostic biomarker for BRCA, ESCA, LUSC and STAD and a prognostic biomarker for KIRP, LIHC, and LUAD. Moreover, it correlates with immune infiltration and may be relevant to immunotherapy in these cancers. Furthermore, its correlation with tumor protein 53 (TP53), alpha/beta hydrolase domain containing 5 (ABHD5), and evolutionarily conserved signaling intermediate in toll pathway (ECSIT) may be used as a potential area of therapeutic intervention. - Source: PubMed
Publication date: 2026/01/17
Attaelmanan Gamila AFateh Alrhman Mohamed YAbdelrahman Dina NMohamed TarteelElkhidir MohanadMohamed Roaa RHamad HowaidaMohamed MarwaSiddig ElafMuzzammil MawadaAlfaki Mohamed