Monkey claudin 14,CLDN14 ELISA kit
- Known as:
- Monkey claudin 14,CLDN14 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- e09c0969
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Blue gene shanghai
- Gene target:
- Monkey claudin 14 CLDN14 ELISA kit
Related genes to: Monkey claudin 14,CLDN14 ELISA kit
- Gene:
- CLDN14 NIH gene
- Name:
- claudin 14
- Previous symbol:
- DFNB29
- Synonyms:
- -
- Chromosome:
- 21q22.13
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-26
- Date modifiied:
- 2016-10-05
Related products to: Monkey claudin 14,CLDN14 ELISA 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(1-3)-beta-D-glucan Sandwich ELISA, Double Antibody(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 Related articles to: Monkey claudin 14,CLDN14 ELISA kit
- Source: PubMed
- This review aims to investigate and establish potential and models for evaluating the anti-urolithiatic activity of therapeutic agents, exploring experimental approaches that can reliably simulate human stone formation and effectively assess the efficacy of anti-urolithiatic compounds. - Source: PubMed
Publication date: 2025/01/21
Kumar Ranjith RJanadri SureshMudagal Manjunatha PSharma Uday RVada SurendraBabu Hari TPrakash Gangireddy Archana Bandapalli - Colorectal cancer (CRC) progression involves complex mechanisms of invasion and metastasis. Claudin-2 (), a tight junction protein, has emerged as a key regulator paracellular permeability and its dysregulation is implicated in chronic inflammatory diseases and cancer. The present study aimed to determine the mechanisms by which deletion affects genes associated with motility and invasion of colon cancer cells. CRISPR/Cas9 was used to knock out in HCT116 cells. Subsequently, gene expression was analyzed using reverse transcription-quantitative PCR and migratory capacity was assessed using wound healing assays. deletion led to the downregulation of genes associated with motility and metastasis, including zonula occludens-1-associated nucleic acid binding protein, N-Myc downstream-regulated gene 1, and , suggesting that supports pro-migratory gene networks. These findings demonstrated that regulates metastatic gene expression in CRC. Although further mechanistic studies are warranted, the present study provided notable genetic and phenotypic evidence of the role of in promoting cancer cell migration and invasion, offering a potential foundation for future studies into its signaling interactions and therapeutic potential. - Source: PubMed
Publication date: 2025/11/27
Alghamdi Rana AAl-Zahrani Maryam H - MicroRNAs (miRNAs) are involved in the pathogenesis of various diseases. Although the role of miR-490-5p in bone-related disorders has been reported, its regulatory mechanism in osteoporotic fractures remains unclear. Therefore, this study aims to investigate the functional mechanism of miR-490-5p in osteoporotic fractures. - Source: PubMed
Dong ZhouZhang ZhidongCheng YonghongLin ChengQi JialongHu Yong - Tight junctions seal the paracellular space between epithelial cells, with their claudin (CLDN) composition dictating epithelial permeability properties. In kidney thick ascending limbs, calcium is reabsorbed paracellularly through a meshwork of CLDN16 and CLDN19 polymers. CLDN14 is strongly upregulated by high blood calcium, restricts this paracellular calcium flux, and is linked to kidney stone disease. How CLDN14 controls paracellular calcium flux and structurally incorporates into this complex junction is unknown. Using confocal and super-resolution microscopy, we show that CLDN14 preferentially associates with CLDN19, thereby gradually replacing CLDN16 in the CLDN19 copolymer in vitro and in mice in vivo. The claudin switch depends on CLDN14 polymerization and occurs on a timescale of days via a pathway independent of dynamin-mediated endocytosis. Our findings reveal a mechanism of tight junction regulation, demonstrating how dynamic claudin remodeling within this complex structure controls renal calcium excretion and contributes to kidney stone pathogenesis. - Source: PubMed
Publication date: 2025/12/01
van der Veen Rozemarijn EBieck MarieMezouar NacéraHaucke VolkerDimke HenrikLehmann Martin