AGRIN_RAT Agrn ELISA tesk kit
- Known as:
- AGRIN_RAT Agrn Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16796
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- AGRIN_RAT Agrn ELISA tesk kit
Related genes to: AGRIN_RAT Agrn ELISA tesk kit
- Gene:
- AGRN NIH gene
- Name:
- agrin
- Previous symbol:
- AGRIN
- Synonyms:
- -
- Chromosome:
- 1p36.33
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-14
- Date modifiied:
- 2019-04-23
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- Congenital myasthenic syndromes (CMS) are a group of rare disorders characterized by fatigable muscle weakness and caused by impaired neuromuscular junction (NMJ) function. CMS symptoms are highly variable, but it can be detrimental and lead to death. There are over 40 different genetic subtypes, including CMS and CMS. encodes for neuralagrin, which is released from the nerve terminal and triggers muscle-specific kinase phosphorylation (pMuSK). pMuSK is essential for NMJ development and maintenance, thus agrin deficiency causes NMJ impairment. encodes for collagenous subunit Q (ColQ), which anchors acetylcholinesterase and stabilizes MuSK. As a result, COLQ deficiency results in NMJ degeneration from prolonged transmission signals and decreased pMuSK. Current treatments for CMS and CMS are limited, highlighting the importance of finding more efficient therapies. Recently, a MuSK agonist antibody (ARGX-119) with high affinity for the Frizzled-like domain showed remarkable rescue of a -CMS mouse model. We hypothesized a derivative antibody of ARGX-119 (3B2) could benefit and CMS mouse models. CMS mice were treated at postnatal day 5 (P5), P15 and P35, and CMS mice were treated weekly from P22 to P57. In CMS mice, 3B2 treatment rescued survival, bodyweight, fibre type switching and pMuSK levels, and improved forelimb grip strength and NMJ morphology. In CMS mice, 3B2 treatment was unable to rescue deficits observed. Our findings suggest that MuSK agonists may benefit patients with -CMS, which should be tested in clinical trials. Our study emphasizes that effective CMS treatment is gene-dependent and relies on an accurate genetic diagnosis. - Source: PubMed
Publication date: 2026/05/14
Ho KellyAdjei-Afriyie OfosuCarmona-Martinez RicardoRay RohanO'Neil DanielZeldin JoshuaOury JulienDe Clercq LieselotBurden Steven JVankerckhoven BernhardtVanhauwaert RoelandSpendiff SallyLochmüller Hanns - Gestational diabetes mellitus (GDM) is a common complication during pregnancy, but the role of the basement membrane (BM) in GDM is not well understood. This study aims to investigate BM-related genes in GDM to provide new insights for diagnosis and treatment. Differentially expressed genes were identified from the GSE203346 dataset in the Gene Expression Omnibus and intersected with BM-related genes to identify BM-related differential genes. Machine learning and gene expression validation were used to identify key genes, which were further validated using an artificial neural network. Additional analyses included gene set enrichment analysis, immunoprecipitation, drug prediction, gene localization, and the construction of lncRNA-miRNA-mRNA and transcription factor-mRNA regulatory networks to explore underlying mechanisms. Among 801 differentially expressed genes, 24 BM-related differential genes were identified. COL5A1, TGFBI, AGRN, TNC, and ITGB6 were identified as candidate genes, with COL5A1 and TGFBI showing consistent low expression across datasets and being designated as key genes. The artificial neural network demonstrated that these key genes effectively distinguished GDM from control samples. Gene set enrichment analysis revealed the involvement of these genes in pathways such as systemic lupus erythematosus and cytokine-cytokine receptor interaction. TGFBI showed a significant positive correlation with CD4+ memory T cells, common lymphoid progenitors, hematopoietic stem cells, and smooth muscle, while COL5A1 was positively correlated with common lymphoid progenitors and smooth muscle. Six drugs were identified as interacting with both key genes. Our study suggests that COL5A1 and TGFBI offer the possibility of personalized treatment strategies for GDM in the future. - Source: PubMed
Weng XiaofangGuo XingdiPan Chunmei - Salivary extracellular vesicles (EVs) have been recognized as one of the most promising noninvasive sources of biomarkers for early cancer detection. However, the lack of efficient isolation and accurate identification methods for salivary EVs limits their clinical utility in early cancer diagnosis. Here, we report the rapid and precise identification of esophageal cancer using the Saliva Extracellular vesicle-based Early Diagnostic system (SEEDx). In this system, salivary EVs were isolated, purified, amplified, and analyzed from human saliva by integrating the ultrafast-isolation platform EXODUS with tandem mass tag (TMT)-based proteomics analysis (EXODUS-TMT proteomics). Using TCGA esophageal cancer (EC) and GTEx healthy population cohorts, we developed a diagnostic model consisting of 9 markers (HIST2H2BE, TP53BP2, TPM4, CALR, HDGF, LMNA, GUSB, NADSYN1, and AGRN), which demonstrated high diagnostic accuracy with AUC values of 0.996 for EC and 0.991 for early-stage EC. We further established a cost-effective model using only two markers (HDGF and CALR) to diagnose both EC and early-stage EC, achieving AUC values of 0.950 and 0.935, respectively. This model was validated in an independent, prospectively collected cohort of EC patients, yielding AUC values of 0.873 and 0.854, respectively. Our streamlined EV isolation and identification workflow facilitates noninvasive biomarker discovery for early-stage esophageal cancer detection. This study extends the EXODUS platform to salivary EVs for EC detection, documents matrix-specific workflow optimizations, and identifies saliva-derived biomarker signatures integrated into a multimarker diagnostic model. - Source: PubMed
Publication date: 2026/03/30
Huang LiuLi MengLiu WenpengLou DoudouZhu QingfuHu Tony YLee Luke PLiu Fei - Ovarian cancer remains a significant global health burden, with high-grade serous ovarian cancer (HGSOC) representing the most lethal subtype. Bulk RNA-seq analysis revealed (Kallikrein-5, a serine protease) upregulation in ovarian cancer, correlating with shortened disease-free survival (DFS) and advanced stage in TCGA cohorts. In vitro functional assays further demonstrated that KLK5 promotes metastatic potential in ovarian cancer cells, indicating its role in disease progression. Single-cell and spatial transcriptomic analysis identified elevated expression specifically in HGSOC epithelial cells. Concurrently, KLK5-high tumors exhibited enrichment of collagen-related genes (COL1A1/2, COL6A2) within the fibroblast compartment, suggesting KLK5-driven epithelial-stromal crosstalk mediated by collagen signaling. The co-expression of with implicated extracellular matrix (ECM) remodeling as a potential progression mechanism. Immune profiling revealed that -high tumor microenvironments (TMEs) harbor increased populations of immunosuppressive myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs). Enhanced CD8 + T cell-macrophage interactions observed in these -high tumors may drive macrophage reprogramming and contribute to immune evasion. In conclusion, promotes HGSOC progression through stromal activation, -mediated ECM alterations, and the reshaping of the TME towards an immunosuppressive state. KLK5’s dual role as both a prognostic biomarker and a potential therapeutic target positions it as a promising candidate for precision oncology in HGSOC. - Source: PubMed
Publication date: 2026/03/22
Wang ZheDing LongkunZhu QingweiOu QingjianWang QiXie YingLi LiLiu XuanNi ChenghaoWang YufengLiu YongheYu LitingCai JiahuiGao Lu - Esophageal squamous cell carcinoma (ESCC) remains a highly aggressive malignancy with dismal clinical outcomes and limited treatment options. NAD(P)H quinone oxidoreductase 1 (NQO1) is classically characterized as a cytosolic oxidoreductase that prevents the formation of reactive oxygen species. Here, we demonstrated that NQO1 promoted ESCC progression and lung colonization via an enzymatic activity-independent mechanism. Integrated transcriptomic and direct RNA-binding analyses revealed that NQO1 acted as an RNA-binding protein to stabilize the mRNA encoding agrin (AGRN), thereby increasing AGRN expression. Upregulation of AGRN enhanced endothelial cytoskeletal organization by interacting with filamin A (FLNA) and stimulated angiogenesis through selective extracellular vesicle-mediated transfer. Structure-based screening identified the clinically approved agent panobinostat as a direct NQO1-binding compound that destabilized NQO1 and suppressed AGRN-dependent angiogenic signaling. Importantly, combined treatment with panobinostat and the anti-angiogenic agent anlotinib resulted in superior inhibition of tumor growth and vascularization compared with either monotherapy in patient-derived organoid xenograft models. Together, these findings uncover an enzymatic activity-independent RNA regulatory function of NQO1 in ESCC and provide a mechanistic rationale for targeting the NQO1/AGRN axis. - Source: PubMed
Publication date: 2026/03/16
Wu JunChen ChenLv XiaoxiaWang QiangWang ZhangdingChen YongHou JiaqiFan QingtingRen QinglinSun ChaoLu ShichunShu YushengWang ShouyuWang Xiaolin