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Human Polyclonal CLDN5 Primary Antibody for IF, IHC - ABIN6711709
Jiang, Wang, Li, Liu, Chen, Hao: Progesterone exerts neuroprotective effects by inhibiting inflammatory response after stroke. in Inflammation research : official journal of the European Histamine Research Society ... [et al.] 2009
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Human Polyclonal CLDN5 Primary Antibody for ELISA, WB - ABIN563201
Escudero-Esparza, Jiang, Martin: Claudin-5 participates in the regulation of endothelial cell motility. in Molecular and cellular biochemistry 2012
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Cow (Bovine) Polyclonal CLDN5 Primary Antibody for WB - ABIN2778047
Fontijn, Volger, Fledderus, Reijerkerk, de Vries, Horrevoets: SOX-18 controls endothelial-specific claudin-5 gene expression and barrier function. in American journal of physiology. Heart and circulatory physiology 2008
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Rat (Rattus) Polyclonal CLDN5 Primary Antibody for WB - ABIN3043521
Cen, Liu, Li, He, Wang, Liu, Liu, Ji: Alteration in P-glycoprotein at the blood-brain barrier in the early period of MCAO in rats. in The Journal of pharmacy and pharmacology 2013
Cow (Bovine) Polyclonal CLDN5 Primary Antibody for ELISA, ICC - ABIN6260869
Zhang, Jin, Zhang, Gan, Zou, Wang, Fu, Xu, Xing, Xia, Xu: A novel IL-1RA-PEP fusion protein alleviates blood-brain barrier disruption after ischemia-reperfusion in male rats. in Journal of neuroinflammation 2018
Human Polyclonal CLDN5 Primary Antibody for ELISA, ICC - ABIN6260867
Yang, Han, Zhang, Bai, Chao, Hu, Yao: Engagement of circular RNA HECW2 in the nonautophagic role of ATG5 implicated in the endothelial-mesenchymal transition. in Autophagy 2018
Human Polyclonal CLDN5 Primary Antibody for WB - ABIN6678313
Huang, Han, Sun, Zhao, Liu, Yuan, Mao, Peng, Liu, Yin, He: Kv1.3 channel blocker (ImKTx88) maintains blood-brain barrier in experimental autoimmune encephalomyelitis. in Cell & bioscience 2017
Human Polyclonal CLDN5 Primary Antibody for IF (p), IHC (p) - ABIN731243
Ruan, Hu, Ao, Ma, Gao, Liu, Kong, Bao, Yu: The neurovascular protective effects of huperzine A on D-galactose-induced inflammatory damage in the rat hippocampus. in Gerontology 2014
Data show that claudin 5 (Cldn5) mRNA in vivo is merely one of six other high abundant tetraspanning tight junction (TJ) protein transcripts
Significantly higher level of the tight junction protein claudin-5 in both Crohn's Disease twins and healthy co-twins was observed.
Epithelial barrier dysfunction in lymphocytic colitis occurs through downregulation of claudin-4, -5, and -8, and redistribution of claudin-5 and -8 off the tight junction, which contributes to diarrhea by a leak-flux mechanism.
Results show that Claudin 5 expression is activated by SIRT1 deacetylating and potentiating KLF4.
the present study revealed the distinct expression profiles of claudin5, 7 and 8 in nonneoplastic mucosal tissues and gastric carcinoma tissues. Furthermore, the expression of these claudin proteins was highly associated with metastatic progression and prognosis in patients with gastric carcinoma
High CLND5 expression is associated with brain metastasis.
Claudin-5 regulates blood-brain barrier permeability by modifying brain microvascular endothelial cell proliferation, migration.
miR-30a-5p inhibits proliferation, metastasis, and EMT, and upregulates the expression of tight junction claudin-5 in UTUC cells.
Claudin-5 was shown to be regulated VEGFR2/PI3K-Akt dependently by VEGF and PI3K-Akt independently by histamine. Interleukin-8 was shown to downregulate claudin-5 by histamine.
This study shown the changes in gene expression of CDH5 and CLDN5 due to shear stress within individual differentiations also revealed no trend.
Claudin-5 single-nucleotide polymorphism (SNP) rs885985 has two major alleles, G and A, which encode for glutamine (Q) or a stop signal, respectively, resulting in distinct overlapping open readings.
Data show that the charge of Lys65 in claudin 1 (Cldn1) and Glu158 in claudin 3 (Cldn3), and of Gln57 in claudin 5 (Cldn5) are necessary for tight junction (TJ) strand formation.
suggest that the reduction of CLDN5, 7, and 18 expression loses the suppressive ability of interaction between PDK1 and Akt and causes sustained phosphorylation of Akt, resulting in the disordered proliferation in lung squamous carcinoma cells
The levels of ESM1, CLDN5, IL-1beta, IL-6, and TNF-alpha were significantly higher in the migraine attack group than in the control group
analysis of the membrane driven cis interactions of claudin-5 proteins in the formation of the blood brain barrier tight junctions
the expression of claudin-5 and claudin-9 was down-regulated while the expression of claudin-8 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 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 and CLDN5 genes have potential relevance in relation to the progression of glioblastoma multiforme.
Study demonstrate that submandibular glands (SMGs) endothelial barrier was disrupted, resulting in the dilation of blood vessels and infiltration of lymphocytes, which were involved in the pathogenesis of Sjogren's syndrome (SS). The mislocation and upregulation of claudin-5, probably caused by the inflammatory microenvironment, contributed to the disruption of endothelial barrier.
Nitric oxide promotes caveolin-1-mediated delivery of claudin-5 to the autophagosome for autophagy-lysosome-dependent degradation.
This study demonstrated that the claudin-5(+) leukocytes in the central nervous system during neuroinflammation: a novel role for endothelial-derived extracellular vesicles.
claudin-3 and claudin-5 expression is increased by DHEAS 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 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 drives changes in tight junction protein expression and MMP9 activity following acute liver failure; Mouse brain endothelial cells were treated with recombinant rTGFbeta1 and MMP9 and claudin-5 expression was assessed.
In transgenic mice carrying mutated SOD1 genes, a disrupted blood-spinal cord barrier as well as decreased levels of tight junction proteins ZO-1, occludin, 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
Claudin 5 showed identical mRNA expression levels in the brains of adult and aged mice.
TNFalpha acts through NFkappaB signaling and requires a conserved promoter region for the down-regulation of Cldn5 expression.
In female rats, increasing age and 17beta-estradiol treatment alters the expression of ERalpha and distinct blood-brain barrier tight-junction protein isoforms (occludin and claudin-5) without altering functional paracellular permeability.
These findings suggest that claudin-5 is a main claudin expressed in podocytes and that the formation of tight junctions in the nephrosis may be due to local recruitment of claudin-5 rather than due to total upregulation of the claudin protein levels.
This study sought to determine the cell signaling mechanism controlling endothelial CLDN5 expression during acute lung injury.
envision that substances interfering with Cldn5-mediated paracellular barrier tightening could assist an improved drug delivery into the brain because Cldn5 is essential for blood-brain barrier integrity.
Describe claudin-5 as a novel estrogen target in vascular endothelium and show in vivo (brain endothelium) and in vitro (brain and heart endothelium) effects of estrogen on claudin-5 levels.
Data show that IL-4 induces upregulation of the junction protein claudin-5 in endothelial cells (ECs) through activation of Jak/STAT6 and phosphorylation and translocation of FoxO1 from the nucleus to the cytoplasm.
Downregulation of cldn5a in zebrafish showed a failure in organ laterality that resulted from malformed Kupffer's vesicle
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.
In conclusion, our present study indicated that miR-34c regulated the permeability of BTB via MAZ-mediated expression changes of ZO-1, occludin, 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.
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.
, transmembrane protein deleted in VCFS
, transmembrane protein deleted in velocardiofacial syndrome
, brain endothelial cell clone 1 protein
, lung-specific membrane protein
, claudin 5
, claudin 5 (transmembrane protein deleted in velocardiofacial syndrome)