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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Claudin 5

claudin-5, CLDN5
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. [provided by RefSeq, Aug 2008] (from NCBI)
Top mentioned proteins: Occludin, ZO-1, CAN, V1a, claudin-1
Papers using claudin-5 antibodies
Caveolin-1 regulates human immunodeficiency virus-1 Tat-induced alterations of tight junction protein expression via modulation of the Ras signaling
Toborek Michal et al., In Environmental Health Perspectives, 2007
... Primary antibodies for occludin, ZO-1, and claudin-5 were obtained from Invitrogen (Camarillo, CA), and all secondary antibodies were purchased from Santa Cruz Biotechnology (Santa Cruz, CA) ...
Papers on claudin-5
Assessment of estradiol-induced gene regulation and proliferation in an immortalized mouse immature Sertoli cell line.
Roy et al., Roorkee, India. In Life Sci, Feb 2016
The cell cycle parameters were assessed, and the expression and regulation of Sertoli cell-specific secretory genes (ABP; androgen-binding protein) and tight junction genes (claudin-5, occluding, and vimentin) in response to estradiol was studied.
Activation of classical estrogen receptor subtypes reduces tight junction disruption of brain endothelial cells under ischemia/reperfusion injury.
Park et al., Seoul, South Korea. In Free Radic Biol Med, Feb 2016
During the early reperfusion period, activation of extracellular signal-regulated kinase1/2 and hypoxia-inducible factor 1α/vascular endothelial growth factor was associated with decreased expression of occludin and claudin-5, respectively, and these changes in TJ protein levels were differentially regulated by ER subtype-specific agonists.
Development of a cell line from the American eel brain expressing endothelial cell properties.
Bols et al., Waterloo, Canada. In In Vitro Cell Dev Biol Anim, Jan 2016
The cells from late-passage cultures (>45) were polygonal, formed capillary-like structures (CLS) on Matrigel, and stained immunocytochemically for von Willebrand factor (vWF) and for three tight junction proteins, zonula occludens-1 (ZO-1), claudin 3, and claudin 5.
Communication from the periphery to the hypothalamus through the blood-brain barrier: an in vitro platform.
Lamghari et al., Porto, Portugal. In Int J Pharm, Jan 2016
The expression of junctional molecules as claudin-5, ZO-1, occludin and VE-cadherin was observed in the bEnd.3
Enhanced Therapeutic Potential of Nano-Curcumin Against Subarachnoid Hemorrhage-Induced Blood-Brain Barrier Disruption Through Inhibition of Inflammatory Response and Oxidative Stress.
Sun et al., China. In Mol Neurobiol, Jan 2016
Mechanically, Cur-NPs attenuated BBB dysfunction after SAH by preventing the disruption of tight junction protein (ZO-1, occludin, and claudin-5).
Checkpoint Kinase 1 Activation Enhances Intestinal Epithelial Barrier Function via Regulation of Claudin-5 Expression.
Kondoh et al., Suita, Japan. In Plos One, Dec 2015
Daunorubicin and rebeccamycin increased claudin-5 expression and the product was distributed in the actin cytoskeleton fraction, which was enriched with TJ proteins.
Transmembrane proteins of the tight junctions at the blood-brain barrier: structural and functional aspects.
Blasig et al., Berlin, Germany. In Semin Cell Dev Biol, Feb 2015
At the BBB, claudin-5 dominates the TJs by preventing the paracellular permeation of small molecules.
Fingolimod (FTY720-P) Does Not Stabilize the Blood-Brain Barrier under Inflammatory Conditions in an in Vitro Model.
Fluri et al., Würzburg, Germany. In Int J Mol Sci, 2014
However, its role in modulating BBB permeability-in particular, on the tight junction proteins occludin, claudin 5 and ZO-1-has not been well elucidated to date.
Changes in the phosphorylation of claudins during the course of experimental colitis.
Xia et al., Hefei, China. In Int J Clin Exp Pathol, 2014
In the present study, we found that the phosphorylated claudin-4 and claudin-7 contents were increased in experimental colitis at days 6 and 8, and colonic phosphorylated claudin-6 was found to be increased at day 4 and day 8. Colonic phosphorylated claudin-5 was found to be decreased at day 4 but increased at day 6.
The role of claudin-5 in blood-brain barrier (BBB) and brain metastases (review).
Jiang et al., Beijing, China. In Mol Med Report, 2014
Metastatic brain tumours are frequently observed in patients with lung, breast and malignant melanoma and a severe complication of metastatic cancers.
The ubiquitin-proteasome pathway regulates claudin 5 degradation.
Miller et al., Haifa, Israel. In J Cell Biochem, 2012
study demonstrated that claudin 5 is a protein with a short half-life that can undergo polyubiquitinationmainly on lysine 199, which apparently leads to its subsequent degradation
Involvement of claudins in zebrafish brain ventricle morphogenesis.
Abdelilah-Seyfried et al., Berlin, Germany. In Ann N Y Acad Sci, 2012
In mammalia, several claudin family members, including claudin-3 and claudin-5, are expressed within microvessel endothelial cells of the blood-brain barrier.
Blood-brain barrier in acute liver failure.
Nguyen, Jacksonville, United States. In Neurochem Int, 2012
Recent reports have not only shown a role of matrix metalloproteinase-9 in the pathogenesis of brain edema in experimental ALF but have also found significant alterations in the tight junction elements including occludin and claudin-5, suggesting a vasogenic injury in the blood-brain barrier (BBB) integrity.
Guanine nucleotide-binding protein Gαi2: a new partner of claudin-5 that regulates tight junction integrity in human brain endothelial cells.
Couraud et al., Paris, France. In J Cereb Blood Flow Metab, 2012
Galphai2 as a novel claudin-5 partner required for TJ integrity in brain endothelial cells.
Matrix metalloproteinase-2-mediated occludin degradation and caveolin-1-mediated claudin-5 redistribution contribute to blood-brain barrier damage in early ischemic stroke stage.
Liu et al., Hengyang, China. In J Neurosci, 2012
Claudin-5 redistribution, mediated by caveolin-1, was observed in blood brain barrier following ischemic stroke.
ETS-related gene (ERG) controls endothelial cell permeability via transcriptional regulation of the claudin 5 (CLDN5) gene.
Oettgen et al., Boston, United States. In J Biol Chem, 2012
ERG plays a pivotal role in regulating endothelial cell barrier function and that this effect is mediated in part through its regulation of CLDN5 gene expression.
TNF-alpha induced NFκB signaling and p65 (RelA) overexpression repress Cldn5 promoter in mouse brain endothelial cells.
Hemmer et al., München, Germany. In Cytokine, 2012
TNFalpha acts through NFkappaB signaling and requires a conserved promoter region for the down-regulation of Cldn5 expression.
The blood-testis barrier and its implications for male contraception.
Mruk et al., New York City, United States. In Pharmacol Rev, 2012
Studies have demonstrated that some unlikely partners, namely adhesion protein complexes (e.g., occludin-ZO-1, N-cadherin-β-catenin, claudin-5-ZO-1), steroids (e.g., testosterone, estradiol-17β), nonreceptor protein kinases (e.g., focal adhesion kinase, c-Src, c-Yes), polarity proteins (e.g., PAR6, Cdc42, 14-3-3), endocytic vesicle proteins (e.g., clathrin, caveolin, dynamin 2), and actin regulatory proteins (e.g., Eps8, Arp2/3 complex), are working together, apparently under the overall influence of cytokines (e.g., transforming growth factor-β3, tumor necrosis factor-α, interleukin-1α).
RNAi-mediated barrier modulation: synergies of the brain and eye.
Campbell et al., Dublin, Ireland. In Ther Deliv, 2010
Using RNAi-based methods for suppression of claudin-5, a molecular constituent of the tight junctions associated with both the blood-brain and inner blood-retina barriers, it has been shown that these barriers can be rendered transiently and size-selectively permeable to molecules up to approximately I kDa.
Endothelial adherens junctions control tight junctions by VE-cadherin-mediated upregulation of claudin-5.
Dejana et al., Milano, Italy. In Nat Cell Biol, 2008
endothelial VE-cadherin at AJs upregulates the gene encoding the TJ adhesive protein claudin-5
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