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Human Polyclonal CLDN5 Primary Antibody für IHC (p), IHC - ABIN266211
Davis, Sonnet, Lazard, Henslee, Gugala, Salisbury, Strecker, Davis, Forsberg, Davis, Olmsted-Davis: Location-dependent heterotopic ossification in the rat model: The role of activated matrix metalloproteinase 9. in Journal of orthopaedic research : official publication of the Orthopaedic Research Society 2016
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Human Polyclonal CLDN5 Primary Antibody für 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 für 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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Human Polyclonal CLDN5 Primary Antibody für IHC (p), IHC - ABIN266210
Hongo, Watanabe, Arita, Kanome, Kageyama, Shioda, Miyazaki: Leptin modulates ACAT1 expression and cholesterol efflux from human macrophages. in American journal of physiology. Endocrinology and metabolism 2009
Human Polyclonal CLDN5 Primary Antibody für 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
In conclusion, our present study indicated that miR (zeige MYLIP Antikörper)-34c regulated the permeability of BTB via MAZ (zeige MAZ Antikörper)-mediated expression changes of ZO-1 (zeige TJP1 Antikörper), occludin (zeige OCLN Antikörper), 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.
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.
Claudin-5 single-nucleotide polymorphism (SNP) rs885985 has two major alleles, G and A, which encode for glutamine (zeige GFPT1 Antikörper) (Q) or a stop signal, respectively, resulting in distinct overlapping open readings.
Data show that the charge of Lys65 in claudin 1 (Cldn1 (zeige CLDN1 Antikörper)) and Glu158 in claudin 3 (Cldn3 (zeige CLDN3 Antikörper)), 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 (zeige PDK1 Antikörper) and Akt (zeige AKT1 Antikörper) and causes sustained phosphorylation of Akt (zeige AKT1 Antikörper), resulting in the disordered proliferation in lung squamous carcinoma cells
The levels of ESM1 (zeige ESM1 Antikörper), CLDN5, IL-1beta (zeige IL1B Antikörper), IL-6 (zeige IL6 Antikörper), and TNF-alpha (zeige TNF Antikörper) were significantly higher in the migraine attack group than in the control group
analysis of the membrane driven cis (zeige CISH Antikörper) interactions of claudin-5 proteins in the formation of the blood brain barrier tight junctions
the expression of claudin-5 and claudin-9 (zeige CLDN9 Antikörper) was down-regulated while the expression of claudin-8 (zeige CLDN8 Antikörper) 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 (zeige VWF Antikörper) 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 (zeige CLDN1 Antikörper) and CLDN5 genes have potential relevance in relation to the progression of glioblastoma multiforme.
This study demonstrated that the claudin-5(+) leukocytes in the central nervous system during neuroinflammation: a novel role for endothelial-derived (zeige MED28 Antikörper) extracellular vesicles.
claudin-3 (zeige CLDN3 Antikörper) and claudin-5 expression is increased by DHEAS (zeige SULT2A1 Antikörper) 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 (zeige MMP9 Antikörper) 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 (zeige TGFB1 Antikörper) drives changes in tight junction protein (zeige OCLN Antikörper) expression and MMP9 (zeige MMP9 Antikörper) activity following acute liver failure; Mouse brain endothelial cells were treated with recombinant rTGFbeta1 and MMP9 (zeige MMP9 Antikörper) and claudin-5 expression was assessed.
In transgenic mice carrying mutated SOD1 (zeige SOD1 Antikörper) genes, a disrupted blood-spinal cord barrier as well as decreased levels of tight junction proteins ZO-1 (zeige TJP1 Antikörper), occludin (zeige OCLN Antikörper), 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 (zeige F2 Antikörper)
Data show that IL-4 (zeige IL4 Antikörper) induces upregulation of the junction protein claudin-5 in endothelial cells (ECs) through activation of Jak (zeige JAK3 Antikörper)/STAT6 (zeige STAT6 Antikörper) and phosphorylation and translocation of FoxO1 (zeige FOXO1 Antikörper) 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