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CLDN18 encodes a member of the claudin family. Additionally we are shipping Claudin 18 Antibodies (59) and Claudin 18 Proteins (4) and many more products for this protein.
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Data suggest that claudin-18 suppresses the abnormal proliferation and motility of lung epithelial cells mediated by inhibition of phosphorylation of pyruvate dehydrogenase kinase isoform 1 (PDK1 (show PDK1 ELISA Kits)) and proto-oncogene (show RAB1A ELISA Kits) protein c (show PROC ELISA Kits)-akt (Akt (show AKT1 ELISA Kits)).
Human fetal lungs at 23-24 weeks gestational age, the highest-risk period for developing bronchopulmonary dysplasia, a disease of impaired alveolarization, had significantly lower CLDN18 expression relative to postnatal lungs.
Evaluated expression of claudins in gastric cancer and determined their significance for patient outcome. Claudin-3 (show CLDN3 ELISA Kits) and claudin-7 (show CLDN7 ELISA Kits) were expressed in 25.4% and 29.9% of gastric cancer tissues; 51.5% of gastric cancer tissues had reduced claudin-18.
High levels of CLDN18 are associated with non-small-cell lung cancer.
Downregulation of miR (show MLXIP ELISA Kits)-1303 can inhibit proliferation, migration and invasion of gastric cancer cells by targeting CLDN18.
Claudin-18 positivity is a specific phenotype that is characteristic of intestinal-type Mucinous borderline tumours of the ovary
Down-regulation of claudin-18 is associated with the proliferative and invasive potential of gastric cancer.
Reduced expression of olfactomedin 4 (show OLFM4 ELISA Kits) and ectopic expression of claudin-18 might be useful markers in the differential diagnosis of serrated polyps.
Claudin 10 (show CLDN10 ELISA Kits)/18 are most commonly expressed in lung adenocarcinomas. Female patients and non-smokers express these claudins more commonly suggesting that they may play a part in the carcinogenesis of tobacco unrelated carcinoma.
Claudin 18 (a marker for early carcinogenesis) is commonly expressed in precursor lesions of pancreatic ductal adenocarcinomas. Activation of the protein kinase C (show PKC ELISA Kits) pathway might be involved in claudin 18 expression associated with carcinogenesis.
CLDN18 deficiency results in epithelial barrier dysfunction, injury, and impaired alveolarization in mice.
Identify a role for claudin 18 in alveolar fluid homeostasis beyond its direct contributions to barrier properties.
we conclude that the estrogen effects on osteoclasts may in part be mediated via regulation of Cldn-18 signaling
Claudin-18 is expressed at the variety of epithelial tissues in inner ear including Organ of Corti, stria vascularis, Reissner's membrane, spiral limbus, vestibular sensory epithelia, and dark cell area.
Cldn-18 is a novel negative regulator of bone resorption and osteoclast differentiation
Claudin-18 forms a paracellular barrier against H(+) in the stomach. Deficiency causes paracellular H(+) leak, up-regulation of proinflammatory cytokines, recruitment of neutrophils, and atrophic gastritis.
Increased expression of claudin-18 is associated with ulcerative colitis.
This gene encodes a member of the claudin family. Claudins are integral membrane proteins and components of tight junction strands. Tight junction strands serve as a physical barrier to prevent solutes and water from passing freely through the paracellular space between epithelial or endothelial cell sheets, and also play critical roles in maintaining cell polarity and signal transductions. This gene is upregulated in patients with ulcerative colitis and highly overexpressed in infiltrating ductal adenocarcinomas. PKC/MAPK/AP-1 (protein kinase C/mitogen-activated protein kinase/activator protein-1) dependent pathway regulates the expression of this gene in gastric cells. Alternatively spliced transcript variants encoding different isoforms have been identified.
, surfactant associated 5
, surfactant associated protein J
, surfactant, pulmonary associated protein J
, claudin 18-like