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The tight junction protein claudin-1 (CLDN1) has been shown to be essential for hepatitis C virus (HCV) entry-the first step of viral infection. Due to the lack of neutralizing anti-CLDN1 antibodies, the role of CLDN1 in the viral entry process is poorly understood. In this study, we produced antibodies directed against the human CLDN1 extracellular loops by genetic immunization and used these antibodies to investigate the mechanistic role of CLDN1 for HCV entry in an infectious HCV cell culture system and human hepatocytes. Antibodies specific for cell surface-expressed CLDN1 specifically inhibit HCV infection in a dose-dependent manner. Antibodies specific for CLDN1, scavenger receptor B1, and CD81 show an additive neutralizing capacity compared with either agent used alone. Kinetic studies with anti-CLDN1 and anti-CD81 antibodies demonstrate that HCV interactions with both entry factors occur at a similar time in the internalization process. Anti-CLDN1 antibodies inhibit the binding of ...

HCV is a leading cause of hepatocellular carcinoma and cirrhosis all over the world. Claudins belong to family of tight junctions proteins that are responsible for establishing barriers for controlling the flow of molecules around cells. For therapeutic strategies, regulation of viral entry into the host cells holds a lot of promise. During HCV infection claudin-1 is highly expressed in liver and believed to be associated with HCV virus entry after HCV binding with or without co-receptor CD81. The claudin-1 assembly with tight junctions is regulated by post translational modifications. During claudins assembly and disassembly with tight junctions, phosphorylation is required at C-terminal tail. In cellular proteins, interplay between phosphorylation and O-β-GlcNAc modification is believed to be functional switch, but it is very difficult to monitor these functional and vibrant changes in vivo. Netphos 2.0 and Disphos 1.3 programs were used for potential phosphorylation; NetPhosK 1.0 and KinasePhos for

The ability to invade host tissues and metastasize is the major cause of cancer-related death. During tumor invasion, metastasizing cells disrupt normal cell-matrix adhesion and acquire an invasive phenotype. Claudins are adhesion proteins localized at tight junctions (TJs). Claudin-7 is a unique TJ membrane protein in that it has a stronger basolateral membrane distribution than that of apical TJs in epithelial cells. To study the basolateral function of claudin-7, claudin-7 gene silencing experiments were carried out in a lung cancer cell line using the lentivirus shRNA approach. We found that claudin-7 knockdown (KD) cells showed disrupted cell-matrix interactions. Consequently, when claudin-7 KD cells were plated on the uncoated glass surface, they were unable to attach to the glass and died the day after plating. In contrast, control cells adhered well and grew normally. Using immunofluorescent microscopy and biochemistry methods, we found that claudin-7 co-localized and ...

The results of this study show that the amount of mobile receptor and the speed at which it diffuses varies according to its location within the cell. CD81 and claudin-1 are expressed equally in the filopodia and plasma membrane, whereas SR-BI is expressed at lower levels in the filopodia compared to the plasma membrane. We show that addition of both sE2 and sE1E2 has varying affects on both the speed and mobility of CD81 and claudin-1 and that the majority of significant effects observed for claudin-1 are observed at areas of potential cell contact. Finally, we demonstrate that addition of ITX5061 affects the diffusion coefficient of CD81 and CLDN-1 and the amount of mobile SR-BI. Furthermore, the effects on SR-BI are limited to areas of cell contact or exploratory regions. In summary, we present data which we hope will further current knowledge of the activity of these receptors in relation to their role in HCV infection ...

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Blood-brain barrier (BBB) leakage plays a key role in cerebral ischemia-reperfusion injury. It is quite necessary to further explore the characteristic and mechanism of BBB leakage during stroke. We induced a focal cerebral ischemia model by transient middle cerebral artery occlusion in male rats for defining the time course of BBB permeability within 120 h following reperfusion and evaluate the specific role of tight junction (TJ) associated proteins claudin-5, occludin, and ZO-1 as well as protein kinase C delta (PKCδ) pathway in BBB leakage induced by reperfusion injury. We verified a bimodal increase in the permeability of the BBB following focal ischemia by Evans blue assay. Two peaks of BBB permeability appeared at 3 h and 72 h of reperfusion after 2 h focal ischemia, respectively. The leak at the endothelial cell was represented at the level of transmission electron microscopy. TTC staining results showed increased infarct size with time after cerebral ischemia reperfusion. The mRNA and ...

The expression of claudin-11 in benign and malignant bladder tissue and the effect of forced expression of claudin-11 on tight junction function and invasiveness of bladder cancer cells were studied. Claudin-11 expression was tested in bladder cancer cell lines (T24/83, RT 112/84 and EJ138) using reverse transcription-polymerase chain reaction (RT-PCR) and in benign and malignant bladder tissue by quantitative RT-PCR and immunohistochemistry. T24/83 cells were transfected with the pcDNA.1/NT-GFP-TOPO vector containing full-length human claudin-11 sequence. Stable-transfected cells overexpressing claudin-11 (T24Cl-11Ex), wild-type cells (T24WT) and the empty plasmid control clone (T24GFP) were compared using transurothelial resistance (TUR), in vitro adhesion, invasion and growth assays. Claudin-11 was strongly expressed in the non-invasive RT112/84 cell line compared to the invasive T24/83 and EJ138 TCC cell lines. Benign bladder tissue demonstrated equal expression of claudin-11 mRNA as ...

DESCRIPTION (provided by applicant): Disruption of the cell-cell junction with concomitant changes in the expression of junctional proteins is a hallmark of cancer metastasis and invasion. Role of adherent junction proteins have been studied extensively in cancer, however the role of tight junction proteins is less understood. Claudins are the recently identified tetraspanins, which are integral to the structure and function of tight junctions (TJs). Recent studies have shown changes in expression/cellular localization for claudins during tumorigenesis, however a cause and effect relationship has not been established. Here, we report a highly increased expression for claudin-1 in human primary colon carcinoma and metastatic tissues and cell lines derived from similar sources with relatively frequent nuclear localization. Furthermore, using genetic manipulations of claudin-1 expression in colon cancer cell lines, we demonstrate a role for claudin-1 in the regulation of epithelial to mesenchymal ...

Claudin-1 is an integral membrane protein component of tight junctions. The Snail family of transcription factors are repressors that play a central role in the epithelial-mesenchymal transition, a process that occurs during cancer progression. Snail and Slug members are direct repressors of E-cadherin and act by binding to the specific E-boxes of its proximal promoter. In the present study, we demonstrate that overexpression of Slug or Snail causes a decrease in transepithelial electrical resistance. Overexpression of Slug and Snail in MDCK (Madin-Darby canine kidney) cells down-regulated Claudin-1 at protein and mRNA levels. In addition, Snail and Slug are able to effectively repress human Claudin-1-driven reporter gene constructs containing the wild-type promoter sequence, but not those with mutations in two proximal E-box elements. We also demonstrate by band-shift assay that Snail and Slug bind to the E-box motifs present in the human Claudin-1 promoter. Moreover, an inverse correlation in ...

TY - JOUR. T1 - Interendothelial claudin-5 expression depends on cerebral endothelial cell-matrix adhesion by Β 1-integrins. AU - Osada, Takashi. AU - Gu, Yu Huan. AU - Kanazawa, Masato. AU - Tsubota, Yoshiaki. AU - Hawkins, Brian T.. AU - Spatz, Maria. AU - Milner, Richard. AU - Del Zoppo, Gregory J.. PY - 2011/10. Y1 - 2011/10. N2 - The hypothesis tested by these studies states that in addition to interendothelial cell tight junction proteins, matrix adhesion by Β 1-integrin receptors expressed by endothelial cells have an important role in maintaining the cerebral microvessel permeability barrier. Primary brain endothelial cells from C57 BL/6 mice were incubated with Β 1-integrin function-blocking antibody (Ha2/5) or isotype control and the impacts on claudin-5 expression and microvessel permeability were quantified. Both flow cytometry and immunofluorescence studies demonstrated that the interendothelial claudin-5 expression by confluent endothelial cells was significantly decreased in a ...

Read Claudin-8 Expression in Renal Epithelial Cells Augments the Paracellular Barrier by Replacing Endogenous Claudin-2, The Journal of Membrane Biology on DeepDyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips.

The aim of this study was to characterize the hCMEC/D3 cell line, an in vitro model of the human Blood Brain Barrier (BBB) for the expression of brain endothelial specific claudins-3 and -12. hCMEC/D3 cells express claudins-3 and -12. Claudin-3 is distinctly localized to the TJ whereas claudin -12 is observed in the perinuclear region and completely absent from TJs. We show that the expression of both proteins is lost in cell passage numbers where the BBB properties are no longer fully conserved. Expression and localization of claudin-3 is not modulated by simvastatin shown to improve barrier function in vitro and also recommended for routine hCMEC/D3 culture. These results support conservation of claudin-3 and -12 expression in the hCMEC/D3 cell line and make claudin-3 a potential marker for BBB characteristics in vitro.

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Claudin-1 (CLDN1) is a structural tight junction (TJ) protein and is expressed in differentiating keratinocytes and Langerhans cells in the epidermis. Our objective was to identify immunoreactive CLDN1 in human epidermal Langerhans cells and to examine the pattern of epidermal Langerhans cells in genetic human CLDN1 deficiency [neonatal ichthyosis, sclerosing cholangitis (NISCH) syndrome]. Epidermal cells from healthy human skin labelled with CLDN1-specific antibodies were analysed by confocal laser immunofluorescence microscopy and flow cytometry. Skin biopsy sections of two patients with NISCH syndrome were stained with an antibody to CD1a expressed on epidermal Langerhans cells. Epidermal Langerhans cells and a subpopulation of keratinocytes from healthy skin were positive for CLDN1. The gross number and distribution of epidermal Langerhans cells of two patients with molecularly confirmed NISCH syndrome, however, was not grossly altered. Therefore, CLDN1 is unlikely to play a critical role in ...

Claudin-4 (Clostridium perfringens enterotoxin receptor) is a tight junction protein encoded by the gene CLDN4. Expression of Claudin-4 has been associated with either poor prognosis or a more favorable diagnosis, depending on the type of cancer. Claudin-4 has been shown to distinguish adenocarcinoma from malignant mesothelioma with 99% specificity in malignant effusions (1). Claudin-4 overexpression was able to independently predict survival in a breast cancer multivariate analysis as it was associated with poor prognosis, high tumor grade and Her2 expression and was inversely correlated with estrogen receptor staining (2). In luminal breast cancer, the increase of Claudin-4 protein was correlated with the increase of tumor grade and with Ki-67, and thus demonstrated an overall shorter life survival (3). Basal-like tumors also demonstrated overexpression of Claudin-4 (4). Counter to the above breast cancer subtypes, the presence of Claudin-4 in triple negative breast cancer was a biomarker that

Objective Helicobacter pylori strains that express the oncoprotein CagA augment risk for gastric cancer. However, the precise mechanisms through which cag+ strains heighten cancer risk have not been fully delineated and model systems that recapitulate the gastric niche are critical for understanding pathogenesis. Gastroids are three-dimensional organ-like structures that provide unique opportunities to study host-H. pylori interactions in a preclinical model. We used gastroids to inform and direct in vitro studies to define mechanisms through which H. pylori modulates expression of the cancer-associated tight junction protein claudin-7.. ...

In this work, we assessed the effects of sinomenine (SN) on intestinal octreotide (OCT) absorption both in Caco-2 cell monolayers and in rats. We also investigated the molecular mechanisms of tight junction (TJ) disruption and recovery by SN-mediated changes in the claudin-1 and protein kinase C (PKC) signaling pathway. The data showed that exposure to SN resulted in a significant decrease in the expression of claudin-1, which represented TJ weakening and paracellular permeability enhancement. Then, the recovery of TJ after SN removal required an increase in claudin-1, which demonstrated the transient and reversible opening for TJ. Meanwhile, the SN-mediated translocation of PKC-α from the cytosol to the membrane was found to prove PKC activation. Finally, SN significantly improved the absolute OCT bioavailability in rats and the transport rate in Caco-2 cell monolayers. We conclude that SN has the ability to enhance intestinal OCT absorption and that these mechanisms are related at least in part to

For every experimental group, brains from at minimum 3 distinct litter had been analyzed and when compared to the in accordance NaCl handle group. qPCR approach improvement exposed that only samples must be when compared to every other which have gone through experimental treatment, mind isolation, storage, purification and evaluation preparing steps with each other. Therefore, for every DEX-treatment the according NaCl handle group was carried out at the exact same time. In addition, owing to the large complete variety of samples, but limited sample variety which could be purified at the same time, only samples from mice at the same age and identical variety of antenatal injections ended up compared to every other by using a two-tailed Student`s t-take a look at. Data are offered as the signifies ± SEM. The major tight junction molecule and mind endothelial mobile marker claudin-five was investigated originally. Triple maternal DEX remedy drastically decreased claudin-5 mRNA expression to .54 ...

Claudin-3 is a major protein of tight junctions (TJs) in the intestinal epithelium and is critical for maintaining cell-cell adhesion, barrier function, and epithelium polarity. Recent studies have shown high claudin-3 levels in several solid tumors, but the regulation mechanism of claudin-3 expression remains poorly understood. In the present study, colorectal cancer (CRC) tissues, HT-29 and DLD-1 CRC cell lines, CRC murine model (C57BL/6 mice) and c-kit loss-of-function mutant mice were used. We demonstrated that elevated claudin-3 levels were positively correlated with highly expressed c-kit in CRC tissues based upon analysis of protein expression. In vitro, claudin-3 expression was clearly increased in CRC cells by overexpressed c-kit or stimulated by exogenous recombinant human stem cell factor (rhSCF), while significantly decreased by the treatment with c-kit or c-Jun N-terminal kinase (JNK) inhibitors. Chromatin immunoprecipitation (ChIP) and luciferase reporter assay showed that SCF/c-kit

immune Uncategorized PA-824, Rabbit Polyclonal to C-RAF (phospho-Thr269). The blood-epididymis barrier (BEB) is formed by epithelial tight junctions mediating selective permeability from the PA-824 epididymal epithelium. the paracellular permeability had been examined by two strategies TER and FITC-Dextran-based tracer diffusion assays. Both assays soon add up to related outcomes indicating a time-dependent disruption from the BEB differentially for the three TGF? isoforms (TGF?3>TGF?1>TGF?2) inside a TGF?-recetor-1 kinase- and Smad-dependent way. The small junction proteins claudin-1 was discovered to be decreased by the procedure with TGF?s whereas occludin had not PA-824 been affected. Epididymal epithelial cells are mainly attentive to TGF?s PA-824 through the basolateral side recommending that TGF? may impact for the epididymal epithelium through the stroma cell tradition versions the knockdown of 1 of the claudins (1 -3 -4 or -7) led to dramatically reduced transepithelial electrical level ...

Epithelial barrier dysfunction is a significant factor in many allergic diseases, including eosinophilic esophagitis (EoE). Infiltrating leukocytes and tissue adaptations increase metabolic demands and decrease oxygen availability at barrier surfaces. Understanding of how these processes impact barrier is limited, particularly in allergy. Here, we identified a regulatory axis whereby the oxygen-sensing transcription factor HIF-1α orchestrated epithelial barrier integrity, selectively controlling tight junction CLDN1 (claudin-1). Prolonged experimental hypoxia or HIF1A knockdown suppressed HIF-1α-dependent claudin-1 expression and epithelial barrier function, as documented in 3D organotypic epithelial cultures. L2-IL5OXA mice with EoE-relevant allergic inflammation displayed localized eosinophil oxygen metabolism, tissue hypoxia, and impaired claudin-1 barrier via repression of HIF-1α/claudin-1 signaling, which was restored by transgenic expression of esophageal epithelial-targeted stabilized ...

The primary reservoir for hepatitis C virus (HCV) replication is believed to be hepatocytes, which are highly polarized with tight junctions (TJ) separating their basolateral and apical domains. HepG2 cells develop polarity over time, resulting in the formation and remodeling of bile canalicular (BC) structures. HepG2 cells expressing CD81 provide a model system to study the effects of hepatic polarity on HCV infection. We found an inverse association between HepG2-CD81 polarization and HCV pseudoparticle entry. As HepG2 cells polarize, discrete pools of claudin-1 (CLDN1) at the TJ and basal/lateral membranes develop, consistent with the pattern of receptor staining observed in liver tissue. The TJ and nonjunctional pools of CLDN1 show an altered association with CD81 and localization in response to the PKA antagonist Rp-8-Br-cyclic AMPs (cAMPs). Rp-8-Br-cAMPs reduced CLDN1 expression at the basal membrane and inhibited HCV infection, supporting a model where the nonjunctional pools of CLDN1 ...

Findings: hCMEC/D3 cells express claudins-3 and -12. Claudin-3 is distinctly localized to the TJ whereas claudin -12 is observed in the perinuclear region and completely absent from TJs. We show that the expression of both proteins is lost in cell passage numbers where the BBB properties are no longer fully conserved. Expression and localization of claudin-3 is not modulated by simvastatin shown to improve barrier function in vitro and also recommended for routine hCMEC/D3 culture ...

Cytoplasmic expression of claudin-1 in metastatic melanoma cells correlates to increased migration, and increased secretion of MMP-2 in a PKC dependent manner, whereas claudin-1 nuclear expressi...

The C\terminal fragment of enterotoxin (C\CPE) modulates the tight junction protein claudin and disturbs the tight junctional barrier. epithelial cells (HPDEs) had been treated with C\CPE 194 and C\CPE meters19. In well\differentiated cells of the pancreatic malignancy cell collection HPAC, C\CPE 194 and C\CPE meters19 interrupted both the hurdle and fencing features without adjustments in manifestation of claudin\1 and \4, collectively with an boost of MAPK phosphorylation. C\CPE 194, but not really C\CPE meters19, improved the cytotoxicity of the anticancer brokers gemcitabine and H\1. In differentiated pancreatic malignancy cell collection PANC\1 badly, C\CPE 194, but not really C\CPE meters19, reduced claudin\4 phrase and improved MAPK activity and the cytotoxicity of the anticancer agencies. In regular HPDEs, C\CPE 194 and C\CPE meters19 reduced claudin\4 phrase and improved the MAPK activity, whereas they do not really influence the cytotoxicity of the anticancer agencies. Our results ...

View mouse Cldn15 Chr5:136966616-136975858 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression

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Familial hypomagnesemia with hypercalciuria and nephrocalcinosis is an autosomal recessive tubular disorder characterized by excessive renal magnesium and calcium excretion and chronic kidney failure. This rare disease is caused by mutations in the CLDN16 and CLDN19 genes. These genes encode the tight junction proteins claudin-16 and claudin-19, respectively, which regulate the paracellular ion reabsortion in the kidney. Patients with mutations in the CLDN19 gene also present severe visual impairment. Our goals in this study were to examine the clinical characteristics of a large cohort of Spanish patients with this disorder and to identify the disease causing mutations. We included a total of 31 patients belonging to 27 unrelated families and studied renal and ocular manifestations. We then analyzed by direct DNA sequencing the coding regions of CLDN16 and CLDN19 genes in these patients. Bioinformatic tools were used to predict the consequences of mutations. Clinical evaluation showed ocular defects in

Background: Claudins are integral membrane proteins that are involved in forming cellular tight junctions. One member of the claudin family, claudin-3, has been shown to be overexpressed in breast, ovarian, and pancreatic cancer. Here we use immunohistochemistry to evaluate its expression in benign prostatic hyperplasia (BPH), prostatic intraepithelial neoplasia (PIN), normal tissue adjacent to prostatic adenocarcinoma (NAC), primary prostatic adenocarcinoma (PCa), and metastatic prostatic adenocarcinoma (Mets).Methods: Tissue microarrays were immunohistochemically stained for claudin-3, with the staining intensities subsequently quantified and statistically analyzed using a one-way ANOVA with subsequent Tukey tests for multiple comparisons or a nonparametric equivalent. Fifty-three cases of NAC, 17 cases of BPH, 35 cases of PIN, 107 cases of PCa, and 55 cases of Mets were analyzed in the microarrays.Results: PCa and Mets had the highest absolute staining for claudin-3. Both had significantly ...

Mammals are able to rapidly produce red blood cells in response to stress. The molecular pathways used in this process are important in understanding responses to anaemia in multiple biological settings. Here we characterise the novel gene Claudin 13 (Cldn13), a member of the Claudin family of tight junction proteins using RNA expression, microarray and phylogenetic analysis. We present evidence that Cldn13 appears to be co-ordinately regulated as part of a stress induced erythropoiesis pathway and is a mouse-specific gene mainly expressed in tissues associated with haematopoietic function. CLDN13 phylogenetically groups with its genomic neighbour CLDN4, a conserved tight junction protein with a putative role in epithelial to mesenchymal transition, suggesting a recent duplication event. Mechanisms of mammalian stress erythropoiesis are of importance in anaemic responses and expression microarray analyses demonstrate that Cldn13 is the most abundant Claudin in spleen from mice infected with ...

Recent investigations revealed that epithelial TJs contain charge- and size-selective pores, which control the paracellular flux of charged and uncharged solutes. The paracellular flux occurs through two distinct pathways: one high-capacity pathway with size-restrictive pores and one low-capacity pathway that is size independent, at least for substances with radii of up to 7 Å (Van Itallie et al., 2008; Watson et al., 2001). The physical basis of the low-capacity pathway is not yet completely understood, whereas the high-capacity pathway is well described. It consists of small pores with radii of ~4 Å, and is responsible for the flux of small charged and uncharged solutes. Expression of claudin-2 affects only the high-capacity pathway, by inducing an increase in pore number and a change in charge selectivity (Van Itallie et al., 2008). In a recent attempt to model the claudin-2-induced channel (Yu et al., 2009), the pore diameter, calculated from permeability to organic cations and from the ...

Congenital tufting enteropathy (CTE) is a severe autosomal recessive human diarrheal disorder with characteristic intestinal epithelial dysplasia. CTE can be caused by mutations in genes encoding EpCAM, a putative adhesion molecule, and HAI-2, a cell surface protease inhibitor. A similar phenotype occurs in mice whose intestinal epithelial cells (IECs) fail to express the tight junction-associated protein claudin-7. EpCAM stabilizes claudin-7 in IECs, and HAI-2 regulates the cell surface serine protease matriptase, a known modifier of intestinal epithelial physiology. Therefore, we hypothesized that HAI-2, matriptase, EpCAM, and claudin-7 were functionally linked. Herein we have demonstrated that active matriptase cleaves EpCAM after Arg80 and that loss of HAI-2 in IECs led to unrestrained matriptase activity and efficient cleavage of EpCAM. Cleavage of EpCAM decreased its ability to associate with claudin-7 and targeted it for internalization and lysosomal degradation in conjunction with ...

Aim of this volume is to clarify the relationship between molecular structure and function of tight junction proteins, as well as their regulation and their role in diseases. Current research may form a basis for future diagnostic and therapeutic approaches to diseases which seem to have not much in common but are characterized by defects of organ barriers, like Crohns disease, renal hypertension, inner ear deafness, and cancerous diseases. Topics include the functions of distinct tight junction proteins as barrier or channel formers for solutes and water, characteristics of the tight junction in inflammatory bowel diseases, posttranslational modifications of tight junction proteins, the relation between renal tight junction proteins and blood pressure control, and the molecular structure of claudin-claudin interactions NOTE: Annals volumes are available for sale as individual books or as a journal. For information on institutional journal subscriptions, please visit www.blackwellpublishing.com/nyas.

Occludin plays a critical role in maintaining the barrier properties of a tight junction. Thus, mutation or absence of occludin increases epithelial leakiness which is an important barrier in preventing metastasis of cancer. Loss of occludin or abnormal expression of occludin has been shown to cause increased invasion, reduced adhesion and significantly reduced tight junction function in breast cancer tissues. Furthermore, patients with metastatic disease displayed significantly lower levels of occludin suggesting that the loss of occludin and thereby loss of tight junction integrity is important in metastatic development of breast cancer.[24]. Occludin also plays an important role in the apoptosis. The C-terminus of occludin is important in receiving and transmitting cell survival signals. In standard cells, loss or disruption of occludin and other tight junction proteins leads to initiation of apoptosis through extrinsic pathways.[25] Studies involving high levels of expression of occludin in ...

GGRNA , 2020-04-07 23:23:15 , RefSeq release 60 (20130726)] RefSeq ID Version Symbol GeneID Definition NM_001101389 NM_001101389.1 CLDN25 644672 Homo sapiens claudin 25 (CLDN25), mRNA. NM_001111319 NM_001111319.1 CLDN22 53842 Homo sapiens claudin 22 (CLDN22), mRNA. NM_020982 NM_020982.3 CLDN9 9080 Homo sapiens claudin 9 (CLDN9), mRNA. NM_001001346 NM_001001346.3 CLDN20 49861 Homo sapiens claudin 20 (CLDN20), mRNA. NM_001306 NM_001306.3 CLDN3 1365 Homo sapiens claudin 3 (CLDN3), mRNA. NM_012131 NM_012131.2 CLDN17 26285 Homo sapiens claudin 17 (CLDN17), mRNA. NM_016369 NM_016369.3 CLDN18 51208 Homo sapiens claudin 18 (CLDN18), transcript variant 1, mRNA. NM_001185056 NM_001185056.1 CLDN11 5010 Homo sapiens claudin 11 (CLDN11), transcript variant 2, mRNA. NM_005602 NM_005602.5 CLDN11 5010 Homo sapiens claudin 11 (CLDN11), transcript variant 1, mRNA. NM_182848 NM_182848.3 CLDN10 9071 Homo sapiens claudin 10 (CLDN10), transcript variant a, mRNA. NM_006984 NM_006984.4 CLDN10 9071 Homo sapiens claudin ...

The tight junction regulates passage of molecules throuth the paracellular spaces. Occludin and claudins are the specific trancmembrance protains present at the tight junction and are believed to regulate the cell barrier functions. To examine the response of the tight junction to hyperosmotic solutions, Ⅰinvestigated the effects of hyperosmotic glycerol on function and protein expression of the tight junction in ECV304 cells. Cell cytotoxicity analysis showed that the high (10%) concentration of glcerol damaged 64.1% of the ECV304 cells (p＜0.001), and this was confirmed morphologically. Treatment with 1%, 2% or 5% glyserol increased the paracellular permeability of fluorescein isothiocyanate (FITC) -labeled dextran by 4.7%, 18.7% and 29.4% (p＜0.05), respectively. In addition, exposure to glycerol at any concentration strongly reduced the expression of occludin, whereas enpression of claudin-1 was affected very slightly. These results suggest that hyperosmotic glycerol would certainly ...

Mouse monoclonal ZO1 tight junction protein antibody [mAbcam 61357] validated for WB, IP, Flow Cyt and tested in Human. Referenced in 2 publications and 5…

Occludin is an integral membrane protein, encoded by the OCLN gene, that is located at tight junctions. Tight junctions act as a physical barrier to prevent solutes and water from passing freely through the paracellular space. Occludin is also known as BLCPMG. It is known to interact with several cytoplasmic proteins via its C terminus, while its extracellular loops are thought to be involved in the regulation of paracellular permeability and cell adhesion. When occludin is expressed in cells that lack tight junctions, it is able to induce cell adhesion. Mutations in the OCLN gene are associated with an autosomal recessive neurologic disorder known as band-like calcification with simplified gyration and polymicrogyria (BLC-PMG).. ...

Occludin is an integral membrane protein, encoded by the OCLN gene, that is located at tight junctions. Tight junctions act as a physical barrier to prevent solutes and water from passing freely through the paracellular space. Occludin is also known as BLCPMG. It is known to interact with several cytoplasmic proteins via its C terminus, while its extracellular loops are thought to be involved in the regulation of paracellular permeability and cell adhesion. When occludin is expressed in cells that lack tight junctions, it is able to induce cell adhesion. Mutations in the OCLN gene are associated with an autosomal recessive neurologic disorder known as band-like calcification with simplified gyration and polymicrogyria (BLC-PMG).. ...

The precise regulation of intestinal epithelial TJs is crucial to maintaining barrier function between the luminal milieu and the internal environment. Recent studies have revealed an important role for Rho GTPases in regulating TJ structure/function (22, 29). In particular, TJ strand organization has been shown to be altered by constitutively active RhoA and Rac1 mutants (22) and inactivation of GTPases by C. difficile toxins is known to cause redistribution of occludin and ZO-1 from membrane microdomains or membrane rafts (32). As a result, we have further explored the mechanisms whereby paracellular permeability is influenced by this family of mediators and investigated whether the inactivation of a single GTPase (RhoA, Rac1, or Cdc42) has an effect on TJ distribution in such membrane rafts and whether TJ proteins involved in strand formation (such as claudin-1 and -2) are altered in this setting.. Using MDCK cell lines that express constitutively active or dominant-negative RhoA, Rac1, or ...

https://doi.org/10.18632/oncotarget.14974 Lianmin Zhang, Yuan Wang, Bin Zhang, Hua Zhang, Meng Zhou, Mei Wei, Qiuping Dong, Yue Xu, Zhaosong Wang, Liuwei Gao, Yanjun Qu, Bowen Shi, Jinfang Zhu,...

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OBJECTIVE To evaluate the possible role of tight junction protein Occludin in nasal polyps. METHODS The expression of Claudin-1, Occludin and ZO-1 in nasal polyps (n = 20) and healthy uncinate mucosa (n = 15) were examined using immunohistochemical staining, real-time quantitative polymerase chain reaction (PCR) and Western blot analysis. The regulatory effects of proinflammatory cytokines (IFN-γ, IL-13, IL-17, TGF-β, TGF-α) on the expression of Occludin in cultured human nasal epithelial cells were investigated. RESULTS The immunohistochemical results showed that Claudin-1, Occludin and ZO-1 were detected both in the nasal polyp group and the control group. The expression sites were the cell membrane and cytoplasm of nasal mucosa epithelial cells. The mean optical density of Claudin-1, Occludin and ZO-1 were 0.187 ± 0.076,0.172 ± 0.109 and 0.098 ± 0.035 respectively in the nasal polyp group and were significantly lower than those in the control group (0.312 ± 0.101, 0.220 ± 0.069 and 0.233

Tight junctions between epithelial and endothelial cells form selective barriers and paracellular channels and regulate paracellular transport of solutes, immune cells, and drugs. More specifically, tight junctions consist of proteins that laterally interconnect neighboring cells of epithelia and endothelia. Certain proteins seal the tight junction, so that a nearly impermeable barrier develops, whereas others form channels that allow for permeation between the cells. Recent investigations have focused on tight junction proteins, belonging to the claudin family (claudins-1 to -27 in humans) and the newly defined group of TAMP (three proteins: occludin, Marvel-D2, and tricellulin). Barriers and Channels Formed by Tight Junction Proteins I showcases work in this area clustered around three major themes: the molecular properties of tight junctions, for example, the role of the claudin family of proteins and the formation of ion and charge-selective channels; the regulation of tight junction

In this study, we demonstrated (I) distinct expression patterns of five genes encoding for proteins involved in the formation of tight junctions in esophageal mucosa. In particular Claudin-1 in ERD and to lesser extent Claudin-2 was expressed at higher levels in patients with GERD. In contrast, ZO-1, ZO-2, and Occludin were not affected by the presence of GERD. (II) In general, altered gene expression of Claudin-1/-2 did not correlate with the degree of histomorphological changes in the esophageal mucosa of patients with GERD.. Tight junctions are composed of transmembrane proteins such as Occludin, 24 Claudins, several junctional adhesion molecules (JAMs) with different isoforms, E-Cadherin as well as cytosolic binding partners [43, 44]. The selection of the five genes studied was based on functional aspects. Occludin is critical for the formation of tight junctions in most tissues [45]. Claudin-1 is one of the numerous Claudins that seals intercellular space leading to higher barrier function ...

ZO-1, ZO-2, and ZO-3, which contain three PDZ domains (PDZ1 to -3), are concentrated at tight junctions (TJs) in epithelial cells. TJ strands are mainly composed of two distinct types of four-transmembrane proteins, occludin, and claudins, between which occludin was reported to directly bind to ZO-1/ZO-2/ZO-3. However, in occludin-deficient intestinal epithelial cells, ZO-1/ZO-2/ZO-3 were still recruited to TJs. We then examined the possible interactions between ZO-1/ZO-2/ZO-3 and claudins. ZO-1, ZO-2, and ZO-3 bound to the COOH-terminal YV sequence of claudin-1 to -8 through their PDZ1 domains in vitro. Then, claudin-1 or -2 was transfected into L fibroblasts, which express ZO-1 but not ZO-2 or ZO-3. Claudin-1 and -2 were concentrated at cell-cell borders in an elaborate network pattern, to which endogenous ZO-1 was recruited. When ZO-2 or ZO-3 were further transfected, both were recruited to the claudin-based networks together with endogenous ZO-1. Detailed analyses showed that ZO-2 and ZO-3 ...

Claudins are a family of proteins that are the most important components of the tight junctions, where they establish the paracellular barrier that controls the flow of molecules in the intercellular space between the cells of an epithelium. They have four transmembrane domains, with the N-terminus and the C-terminus in the cytoplasm. Claudins are small (20-27 kilodalton (kDa)) transmembrane proteins which are found in many organisms, ranging from nematodes to human beings, and are very similar in their structure, although this conservation is not observed on the genetic level. Claudins span the cellular membrane 4 times, with the N-terminal end and the C-terminal end both located in the cytoplasm, and two extracellular loops which show the highest degree of conservation. The first extracellular loop consists on average of 53 amino acids and the second one, being slightly smaller, of 24 amino acids. The N-terminal end is usually very short (4-10 amino acids), the C-terminal end varies in length ...

What happens to the paracellular barrier when the expression of tricellulin is suppressed in epithelial cells? Two independent Eph4 cell clones with suppressed tricellulin expression (KD-1 and KD-2) were established by stably expressing two distinct short interfering RNAs (Brummelkamp et al., 2002). In both clones, tricellulin protein expression was suppressed by ,95% as determined by Western blot analysis (Fig. 5 A), and immunofluorescence microscopy did not detect any tricellulin signals at tricellular contacts (Fig. 5 B). Under confluent conditions, KD-1 and KD-2 cells showed a typical cobblestone-like appearance, and there was no significant difference discerned between parental wild-type Eph4 and KD-1/2 cells with regard to the size/shape of individual cells and the distribution of cadherins (Fig. 5 B). However, when KD-1 and KD-2 cells were stained with anti-occludin mAb (Fig. 5 C) or anti-claudin-3 pAb (not depicted), tTJs as well as bTJs showed remarkable structural changes in that both ...

The tight junctions (TJ), which are located in the apical region between epithelial and endothelial cells, regulate the paracellular diffusion of ions and small molecules and play an important role in maintaining cell polarity, cell-cell integrity, and permeability. In the lung, epithelial cells are attached by TJ structures. They provide a permeable barrier and cell communication. The loss of barrier integrity, which is maintained by the expression of claudins (Cldn), results in cellular permibilization and leads to paracellular diffusion of solutes and harmful molecules. There are 27 known Cldn homologous members in mice and human. Cldn6 is mostly expressed in embryonic stem cells and associated with the programing of epithelial cells during embryo development and lung morphogenesis. In order to test the hypothesis that Cldn6 expression affects lung morphogenesis, we analyzed the expression pattern of Cldn6 during lung ontogenesis to examine cell-specific expression pattern of Cldn6 during each

Epithelial layers are integral for many physiological processes and are maintained by intercellular adhesive structures. During disease, these structures can disassemble, leading to breakdown of epithelia. TJs (tight junctions) are one type of intercellular adhesion. Loss of TJs has been linked to the pathogenesis of many diseases. The present review focuses on the role of vesicle trafficking in regulation of TJs, in particular trafficking of the TJ protein occludin. We examine how endocytosis and endosomal recycling modulate occludin localization under steady-state conditions and during stimulated TJ disassembly. ...

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