CA50 Clia Kit
- Known as:
- CA50 Clia Kit
- Catalog number:
- Ⅱc018
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Glory bioscience
- Gene target:
- CA50 Clia Kit
Related genes to: CA50 Clia Kit
- Gene:
- SNORA50A NIH gene
- Name:
- small nucleolar RNA, H/ACA box 50A
- Previous symbol:
- SNORA50, SNORA76A
- Synonyms:
- ACA50
- Chromosome:
- 16q21
- Locus Type:
- RNA, small nucleolar
- Date approved:
- 2006-04-04
- Date modifiied:
- 2015-11-11
Related products to: CA50 Clia Kit
Human ELC ELISA KIT 96 TEST
OxiSelect In Vitro ROS/RNS Assay Kit (Green Fluorescence), Trial Size
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect TBARS Assay Kit (MDA Quantitation), Trial Size
OxiSelect Total Antioxidant Capacity (TAC) Assay Kit, Trial Size
OxiSelect™ In Vitro ROS RNS Assay Kit (Green Fluorescence), Trial Size(1-Kit )11,12-EET DHET Immunoassay Kit(1-Kit )11,12-EET_DHET Immunoassay Kit(1-Kit) 11,12-DHET Immunoassay Kit(1-Kit) 14,15-DHET Human Urine ELISA Kit(1-Kit) 14,15-DHET Hypertension ELISA Kit(1-Kit) 14,15-DHET sEH activity ELISA Kit(1-Kit) 14,15-EET DHET Hypertension ELISA Kit(1-Kit) 14,15-EET_DHET Hypertension ELISA Kit Related articles to: CA50 Clia Kit
- Hemodynamic shear stress critically influences atherosclerosis progression, yet the molecular mechanisms linking biomechanical stimuli to endothelial activation and vascular pathology remain poorly understood. While circular RNAs (circRNAs) participate in endothelial mechanotransduction, the role of mechanosensitive small nucleolar RNA (snoRNA)-like circRNA-a unique subclass harboring snoRNA sequences-in atherosclerosis is unexplored. We characterized sno-circCNOT1 using high-throughput RNA sequencing, RNA interference, immunofluorescence, and co-immunoprecipitation. Functional studies were performed in endothelial cells and mice to assess its role in pyroptosis and atherogenesis. Mechanistic investigations included RNA pull-down, mass spectrometry, and gain- and loss-of-function assays to identify sno-circCNOT1-interacting proteins and downstream signaling. We identified sno-circCNOT1, a circular RNA derived from exon 17 and intron 17, which incorporates snoRNA SNORA50A. Its expression was upregulated by pro-atherogenic interleukin-1β and pathological oscillatory shear stress, but downregulated by laminar shear stress. Functionally, sno-circCNOT1 mediated shear stress-dependent regulation of endothelial pyroptosis and inflammation. Endothelial-specific overexpression of sno-circCNOT1 aggravated atherosclerotic lesion formation in mice. Mechanistically, its snoRNA-like motif was essential for nuclear localization and function. sno-circCNOT1 bound the IF-ROD domain of lamin A/C (LMNA), stabilizing LMNA and facilitating its interaction with the N-terminal domain of methyltransferase-like 14 (METTL14-N), thereby enhancing METTL14 stability. This axis activated NOD-like receptor protein 3 (NLRP3) and amplified endothelial inflammation. Conversely, overexpression of METTL14-N to disrupt this signaling axis attenuates endothelial dysfunction and atherosclerosis progression. sno-circCNOT1 is a mechanosensitive snoRNA-like circRNA that promotes endothelial pyroptosis and atherogenesis via the LMNA/METTL14/NLRP3 axis. METTL14-N offers a protein-based therapeutic approach, positioning this regulatory pathway as a druggable target for atherosclerosis. - Source: PubMed
Publication date: 2026/01/01
Bi LianruZhu YihaoChen ZiqiYang YiyingLeng YanlongWang HuijiePan JiajieZhang XiaozheZeng ZekaiLiang YunjunWu GuifuFan Wendong - IQGAP2 was recently reported as a tumor suppressor of prostate cancer (PC). Nonetheless, its clinical implications remain unknown. To address this issue, we extracted data related to IQGAP2 mRNA expression and genomic alterations from multiple large datasets within the Oncomine and cBioPortal databases and performed in silico analyses to determine a potential association of IQGAP2 mRNA expression and its genomic alterations with PC progression. In 4 cohorts consisting of 118 normal prostate tissues and 277 PCs, IQGAP2 mRNA expression was significantly elevated particularly in low-grade (primary Gleason score ≤3) PCs; these changes separate PC from normal tissues with area under curve values of 0.7-0.8. Significant reductions in IQGAP2 mRNA levels and gene copy number occurred in more than 70 metastases compared to at least 230 local PCs. This duo-alteration in IQGAP2 expression supports IQGAP2 elevation suppressing and its downregulation facilitating PC progression. Deletion and missense mutations were detected in 23 of 492 primary PCs; these alterations significantly associate with PC recurrence (HR=2.71; 95% CI: 1.35-5.44; P=.005) after adjusting for known risk factors and correlate with reductions in disease-free survival (DFS, P=.002). IQGAP2 (5q13.3) genomic alterations were observed in SPOP-marked PCs and co-occurred with deletion in the RN7SK (16p12.2), SNORA50A (16q21), and SNORA50C (17q23.3) genes; the co-occurrence associated with reductions in DFS (P=4.14e-4). In two independent PC populations, MSKCC (n=130) and TCGA provisional (n=490), reductions in IQGAP2 mRNA expression were significantly associated with DFS. Collectively, this investigation reveals an association of IQGAP2 with PC progression. - Source: PubMed
Publication date: 2018/11/11
Xie YanyunZheng LinfengTao Lijian