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In conclusion, our present study indicated that miR (show MYLIP Proteins)-34c regulated the permeability of BTB via MAZ (show MAZ Proteins)-mediated expression changes of ZO-1 (show TJP1 Proteins), occludin (show OCLN Proteins), and claudin-5.
The results of light- and electron-microscopic observations suggested that cldn5a and 5b are required for Xenopus heart tube formation through epithelialization of the precardiac mesoderm.
identify Claudin5a as a core component of an early cerebral-ventricular barrier system that is required for ventricular lumen expansion in the zebrafish embryonic brain before the establishment of the embryonic blood-brain barrier.
The levels of ESM1 (show ESM1 Proteins), CLDN5, IL-1beta (show IL1B Proteins), IL-6 (show IL6 Proteins), and TNF-alpha (show TNF Proteins) were significantly higher in the migraine attack group than in the control group
analysis of the membrane driven cis (show CISH Proteins) interactions of claudin-5 proteins in the formation of the blood brain barrier tight junctions
the expression of claudin-5 and claudin-9 (show CLDN9 Proteins) was down-regulated while the expression of claudin-8 (show CLDN8 Proteins) was up-regulated in cervical carcinoma tissues compared with adjacent non-neoplastic tissues.
Plasma CLDN5 levels decreased in patients with stable asthma compared with those in control subjects, suggesting that asthma therapy can decrease plasma CLDN5 levels
These data support that loss of claudin-5 in cardiomyocytes and endothelial cells is prevalent in human heart failure
the relationship between vWF (show VWF Proteins) and claudin-5, which are indicators of endothelial cell dysfunction and tight junction activity, may be a predictor of disease activity in rheumatoid arthritis.
The findings suggest that down regulated CLDN1 (show CLDN1 Proteins) and CLDN5 genes have potential relevance in relation to the progression of glioblastoma multiforme.
miR (show MLXIP Proteins)-18a and RUNX1 (show RUNX1 Proteins) could reversely regulate the permeability of blood-tumor barrier as well as the expressions and distributions of ZO-1 (show TJP1 Proteins), occludin (show OCLN Proteins) and claudin-5.
Claudin-5 overexpression promoted the interactions of claudin-1 (show CLDN7 Proteins) and claudin-2 (show CLDN2 Proteins) and enhanced the barrier function of retinal cells.
Data show that C-terminal domain of Clostridium perfringens enterotoxin (cCPE)-binding to claudin 1 (show CLDN7 Proteins) and claudin 5 is prevented by two residues in extracellular loop 2 of Cld1 (show CLDN1 Proteins) (Asn(150) and Thr (show TRH Proteins)(153)) and Cld5 (Asp (show ASIP Proteins)(149) and Thr (show TRH Proteins)(151)).
claudin-3 (show CLDN3 Proteins) and claudin-5 expression is increased by DHEAS (show SULT2A1 Proteins) and tight junction formation is stimulated via a Gnalpha11-coupled receptor in Sertoli cells
Claudin 5 in a murine model of allergic asthma: Its implication and response to steroid treatment
while MMP-9 (show MMP9 Proteins) is not essential for hypoxic-induced cerebral angiogenesis, it plays an important role in post-hypoxic vascular pruning by degrading laminin and claudin-5
Studied if circulating TGFbeta1 (show TGFB1 Proteins) drives changes in tight junction protein (show OCLN Proteins) expression and MMP9 (show MMP9 Proteins) activity following acute liver failure; Mouse brain endothelial cells were treated with recombinant rTGFbeta1 and MMP9 (show MMP9 Proteins) and claudin-5 expression was assessed.
In transgenic mice carrying mutated SOD1 (show SOD1 Proteins) genes, a disrupted blood-spinal cord barrier as well as decreased levels of tight junction proteins ZO-1 (show TJP1 Proteins), occludin (show OCLN Proteins), and claudin-5 were detected.
The aim of the present study was to further characterize the estrogen-responsive elements of claudin-5 promoter.
Two independent pathways triggered by PI3K mediate early and late loss of paracellular claudin-5 expression.
Comparative modelling of intramolecular interfaces in the transmembrane region of claudins led to a complete Cldn5 model.
silencing of claudin-5 did significantly attenuate simvastatin-mediated endothelial cell barrier protection in response to thrombin (show F2 Proteins)
Claudin 5 showed identical mRNA expression levels in the brains of adult and aged mice.
Data show that IL-4 (show IL4 Proteins) induces upregulation of the junction protein claudin-5 in endothelial cells (ECs) through activation of Jak (show JAK3 Proteins)/STAT6 (show STAT6 Proteins) and phosphorylation and translocation of FoxO1 (show FOXO1 Proteins) from the nucleus to the cytoplasm.
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. Mutations in this gene have been found in patients with velocardiofacial syndrome. Alternatively spliced transcript variants encoding the same protein have been found for this gene.
, claudin 5
, claudin 5 (transmembrane protein deleted in velocardiofacial syndrome)
, transmembrane protein deleted in VCFS
, transmembrane protein deleted in velocardiofacial syndrome
, brain endothelial cell clone 1 protein
, lung-specific membrane protein