Development of innovative, effective therapies against recurrent/chemotherapy-resistant ovarian cancer remains a high priority. Using high-throughput technologies to analyze genetic fingerprints of ovarian cancer, we have discovered extremely high expression of the genes encoding the proteins claudin-3 and claudin-4. Because claudin-3 and -4 are the epithelial receptors for Clostridium perfringens enterotoxin (CPE), and are sufficient to mediate CPE binding, in this study we evaluated the in vitro and in vivo bioactivity of the carboxy-terminal fragment of CPE (i.e., CPE290-319 binding peptide) as a carrier for tumor imaging agents and intracellular delivery of therapeutic drugs. Claudin-3 and -4 expression was examined with rt-PCR and flow cytometry in multiple primary ovarian carcinoma cell lines. Cell binding assays were used to assess the accuracy and specificity of the CPE peptide in vitro against primary chemotherapy-resistant ovarian carcinoma cell lines. Confocal microscopy and biodistribution

The entire human body and its many compartments are shielded from their external environments by the barrier function of epithelial cell sheets. The paracellular barrier function of tight junctions (TJs) is critical for maintaining homeostasis in any multicellular organism, especially in the skin and internal organs and at the blood-brain barrier. One of the major components of TJs is a family of adhesive membrane proteins known as claudins. Several members of the claudin family are receptors for the bacterial toxin Clostridium perfringens enterotoxin. This toxin often causes food-borne illness both in humans and animals. Saitoh et al. crystallized a complex between the toxin and a claudin that reveals just how the toxin damages epithelial barriers (see the Perspective by Artursson and Knight).. Science, this issue p. 775; see also p. 716 ...

We investigated some immunogenic properties of Clostridium perfringens enterotoxin (CPE) in vitro using murine J774A macrophages (MPhi) and in vivo using Swiss Webster (SW) mice. CPE was a potent mitogen in vitro, where cell proliferation increased with CPE concentration. CPE was nonmitogenic when M …

As mentioned in our introduction, the availability of CPE-directed therapeutics could be helpful for ameliorating several CPE-associated medical conditions. A previous study had suggested that the drug mepacrine might be a candidate CPE therapeutic because the presence of this drug interferes with CPE-induced electrophysiologic activity in artificial lipid bilayers (24). However, that study did not distinguish whether mepacrine inactivates the CPE protein or instead interferes with some step in CPE action, i.e., whether this drug affects CPE binding, CPE pore formation, or CPE pore activity. Furthermore, it was specifically important to determine whether mepacrine is not only protective against CPE electrophysiologic activity in artificial membranes but also inhibits CPE-induced cytotoxicity in mammalian cells, where receptors are present and complex phenomena like membrane vesicle release occur (30).. Therefore, a first major contribution of the current study entailed demonstrating that ...

Open peer review is a system where authors know who the reviewers are, and the reviewers know who the authors are. If the manuscript is accepted, the named reviewer reports are published alongside the article. Pre-publication versions of the article and author comments to reviewers are available by contacting [email protected]. All previous versions of the manuscript and all author responses to the reviewers are also available.. You can find further information about the peer review system here.. ...

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 ...

Shop a large selection of Proteins A-Z products and learn more about Novus Biologicals Claudin-2 Recombinant Protein Antigen Quantity: 100µL:Life Quantity: 100µL.

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 ...

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.

Sigma-Aldrich offers abstracts and full-text articles by [S K Tiwari-Woodruff, A G Buznikov, T Q Vu, P E Micevych, K Chen, H I Kornblum, J M Bronstein].

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

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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 ...

The protein encoded by this intronless gene belongs to the claudin family. Claudins are integral membrane proteins that are components of the epithelial cell tight junctions, which regulate movement of solutes and ions through the paracellular space. This protein is a high-affinity receptor for Clostridium perfringens enterotoxin (CPE) and may play a role in internal organ development and function during pre- and postnatal life. This gene is deleted in Williams-Beuren syndrome, a neurodevelopmental disorder affecting multiple systems. [provided by RefSeq, Sep 2013 ...

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 ...

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

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 ...

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 ...

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 ...

Shop a large selection of products and learn more about Claudin-9 Rabbit anti-Human, Polyclonal, Novus Biologicals 100µL; 100µL; Unlabeled.

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

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 ...

Epithelioid mesothelioma is a cancer caused by asbestos. It is the most common cell type and is most responsive to treatment. Discover more about the disease.

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...

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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 ...

Crohns disease; infective colitis is often a cause of one episode of colitis which is mislabelled as ulcerative colitis e.g. transverse colon the portion Causes and symptoms. Biocare Probiotics 30 Billion Which Uk Are Best benefits of Digestive Enzymes for Cats. John McDougall in his book The McDougall Plan summarizes the multiple benefits of fiber (some info Ive taken from other sources too): Fiber has no calories since Probiotic dosages are listed Introduction Giardia Clostridium perfringens enterotoxin and Cryptosporidium are important causes of diarrhea in dogs and cats. Find and study online flashcards from Pathophysiology 3400. Colorectal cancer commonly known as colon cancer or bowel cancer is a melanoma from uncontrolled cell growth in the Probiotics can also play Biocare Probiotics 30 Billion Which Uk Are Best a role in maintaining oral health (bad eath). I know there have been some posts dealing with probiotics and many have questions about wh Stage IIB: Cancer has C colon ...

& 2004 USCAP, Inc All rights reserved /04 $ immunostaining in distinguishing epithelial mesothelioma and lung adenocarcinoma Karine Llinares 1,2, Fabienne Escande

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,...

Complete information for CLDN18 gene (Protein Coding), Claudin 18, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium

CPE 439 Final Projects: A collection of Zybo-based real-time embedded systems from my Cal Poly CPE439 Real Time Operating Systems course.

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

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 ...

Facts and data of a family history are often able to help in distinguishing between adenocarcinoma and epithelioid mesothelioma. When a patient possesses a family history of carcinoma, it is more likely that he or she suffers from a variant of the disease. When a patient has a history of asbestos exposure, it is more likely that he or she suffers from epithelioid mesothelioma. Or, if you or a loved one got asbestos exposure and received a diagnosis of adenocarcinoma, it may be worthwhile to look for a second diagnostic assessment, either by the same oncology specialist or a physician who has adequate experience in mesothelioma cases ...

Facts and data of a family history are often able to help in distinguishing between adenocarcinoma and epithelioid mesothelioma. When a patient possesses a family history of carcinoma, it is more likely that he or she suffers from a variant of the disease. When a patient has a history of asbestos exposure, it is more likely that he or she suffers from epithelioid mesothelioma. Or, if you or a loved one got asbestos exposure and received a diagnosis of adenocarcinoma, it may be worthwhile to look for a second diagnostic assessment, either by the same oncology specialist or a physician who has adequate experience in mesothelioma cases ...

1. Glomerular charge selectivity was assessed using the ratio of the clearance of pancreatic isoamylase to the clearance of the more anionic salivary isoamylase (CPAm/CSAm) in 30 normal subjects, 14 patients with minimal proteinuria and 23 patients with heavy proteinuria due to primary glomerulopathies. Seven patients with minimal change nephropathy were studied in relapse and remission.. 2. CPAm/CSAm exceeded 2.0 (range 2.1-6.1) in all normal subjects, indicating that the normal glomerular capillary wall possesses charge selectivity at the molecular size of amylase (molecular mass 56 kDa). 3. CPAm/CSAm was significantly lower in patients with heavy proteinuria than in normal subjects or patients with minimal proteinuria. CPAm/CSAm was low in patients with minimal change nephropathy in relapse and rose into the normal range with steroid-induced remission.. 4. These data suggest that heavy proteinuria in primary glomerulopathies is accompanied by loss of glomerular charge selectivity. Remission ...

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 ...

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 ...

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 ...

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

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 ...

The differentiation between adenocarcinoma and mesothelioma can be difficult at histology. In this case, the initial histological diagnosis of metastatic adenocarcinoma was revised following review of clinical and radiologal features, and the cor...

CLDN5_ENST00000618236 Gene, Drug Resistance, Tissue Distribution, Mutation Distribution, Variants, CLDN5_ENST00000618236 Genome Browser, CLDN5_ENST00000618236 References

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 ...

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 ...

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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 ...

Matrix Metalloproteinase-9 Leads to Claudin-5 Degradation via the NF-κB Pathway in BALB-c Mice with Eosinophilic Meningoencephalitis Caused by Angiostrongylus cantonensis. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.

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 ...

PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

Although experimental autologous patch or tubular conduit vascular grafts made from the internal rectus fascia sheath (IRFS) have been reported in the literature, thorough morphological evaluation and verification of the histological arterialisation of such grafts are lacking. Four purpose-bred Beagle dogs were utilised to create eight arterial internal rectus fascia sheath (ARFS) grafts implanted between bisected ends of the external iliac arteries. Four out of the eight ARFS grafts were patent after three months. Haematoxylin-eosin and Azan staining verified that the grafts gained a vessel-like layered structure with the presence of large amounts of collagen fibres. Although the inner surface of the intact IRFS was originally covered with claudin-5-negative and pancytokeratin-positive mesothelial cells in control samples, the internal cells of the ARFS grafts became claudin-5 positive and pancytokeratin negative like in intact arteries. Spindle-shaped cells of the wall of ARFS grafts were ...

Purified Recombinant Mouse Cldn4 Protein, MYC/DDK-tagged from Creative Biomart. Recombinant Mouse Cldn4 Protein, MYC/DDK-tagged can be used for research.

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Expression of CLDN4 (CPE-R, CPETR, CPETR1, hCPE-R, WBSCR8) in rectum tissue. Antibody staining with CAB002610 in immunohistochemistry.

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