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1

Andrea Tews, Birke, and Laurence Cocquerel. "Occludine, une clé de plus pour l’entrée du virus de l’hépatite C." médecine/sciences 25, no. 6-7 (2009): 549–51. http://dx.doi.org/10.1051/medsci/2009256-7549.

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2

Chen, Yan-hua, Christa Merzdorf, David L. Paul, and Daniel A. Goodenough. "COOH Terminus of Occludin Is Required for Tight Junction Barrier Function in Early Xenopus Embryos." Journal of Cell Biology 138, no. 4 (1997): 891–99. http://dx.doi.org/10.1083/jcb.138.4.891.

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Occludin is the only known integral membrane protein localized at the points of membrane– membrane interaction of the tight junction. We have used the Xenopus embryo as an assay system to examine: (a) whether the expression of mutant occludin in embryos will disrupt the barrier function of tight junctions, and (b) whether there are signals within the occludin structure that are required for targeting to the sites of junctional interaction. mRNAs transcribed from a series of COOH-terminally truncated occludin mutants were microinjected into the antero–dorsal blastomere of eight-cell embryos. 8
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3

DeMaio, Lucas, Mahsa Rouhanizadeh, Srinivasa Reddy, Alex Sevanian, Juliana Hwang, and Tzung K. Hsiai. "Oxidized phospholipids mediate occludin expression and phosphorylation in vascular endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 2 (2006): H674—H683. http://dx.doi.org/10.1152/ajpheart.00554.2005.

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Oxidized l-α-1-palmitoyl-2-arachidonoyl- sn-glycero-3-phosphorylcholine (OxPAPC), a component of minimally modified LDL, induces production of proinflammatory cytokines and development of atherosclerotic lesions. We tested the hypothesis that OxPAPC alters expression, phosphorylation, and localization of tight junction (TJ) proteins, particularly occludin, a transmembrane TJ protein. OxPAPC reduced total occludin protein and increased occludin phosphorylation dose dependently (10–50 μg/ml) and time dependently in bovine aortic endothelial cells. OxPAPC decreased occludin mRNA and reduced the i
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4

Basuroy, S., P. Sheth, C. M. Mansbach, and R. K. Rao. "Acetaldehyde disrupts tight junctions and adherens junctions in human colonic mucosa: protection by EGF and l-glutamine." American Journal of Physiology-Gastrointestinal and Liver Physiology 289, no. 2 (2005): G367—G375. http://dx.doi.org/10.1152/ajpgi.00464.2004.

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Acetaldehyde, a toxic metabolite of ethanol oxidation, is suggested to play a role in the increased risk for gastrointestinal cancers in alcoholics. In the present study, the effect of acetaldehyde on tyrosine phosphorylation, immmunofluorescence localization, and detergent-insoluble fractions of the tight junction and the adherens junction proteins was determined in the human colonic mucosa. The role of EGF and l-glutamine in prevention of acetaldehyde-induced effects was also evaluated. Acetaldehyde reduced the protein tyrosine phosphatase activity, thereby increasing the tyrosine phosphoryl
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5

Ando-Akatsuka, Y., M. Saitou, T. Hirase, et al. "Interspecies diversity of the occludin sequence: cDNA cloning of human, mouse, dog, and rat-kangaroo homologues." Journal of Cell Biology 133, no. 1 (1996): 43–47. http://dx.doi.org/10.1083/jcb.133.1.43.

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Occludin has been identified from chick liver as a novel integral membrane protein localizing at tight junctions (Furuse, M., T. Hirase, M. Itoh, A. Nagafuchi, S. Yonemura, Sa. Tsukita, and Sh. Tsukita. 1993. J. Cell Biol. 123:1777-1788). To analyze and modulate the functions of tight junctions, it would be advantageous to know the mammalian homologues of occludin and their genes. Here we describe the nucleotide sequences of full length cDNAs encoding occludin of rat-kangaroo (potoroo), human, mouse, and dog. Rat-kangaroo occludin cDNA was prepared from RNA isolated from PtK2 cell culture, usi
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6

Lapierre, L. A., P. L. Tuma, J. Navarre, J. R. Goldenring, and J. M. Anderson. "VAP-33 localizes to both an intracellular vesicle population and with occludin at the tight junction." Journal of Cell Science 112, no. 21 (1999): 3723–32. http://dx.doi.org/10.1242/jcs.112.21.3723.

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Tight junctions create a regulated intercellular seal between epithelial and endothelial cells and also establish polarity between plasma membrane domains within the cell. Tight junctions have also been implicated in many other cellular functions, including cell signaling and growth regulation, but they have yet to be directly implicated in vesicle movement. Occludin is a transmembrane protein located at tight junctions and is known to interact with other tight junction proteins, including ZO-1. To investigate occludin's role in other cellular functions we performed a yeast two-hybrid screen u
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7

Saitou, Mitinori, Kazushi Fujimoto, Yoshinori Doi, et al. "Occludin-deficient Embryonic Stem Cells Can Differentiate into Polarized Epithelial Cells Bearing Tight Junctions." Journal of Cell Biology 141, no. 2 (1998): 397–408. http://dx.doi.org/10.1083/jcb.141.2.397.

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Occludin is the only known integral membrane protein of tight junctions (TJs), and is now believed to be directly involved in the barrier and fence functions of TJs. Occludin-deficient embryonic stem (ES) cells were generated by targeted disruption of both alleles of the occludin gene. When these cells were subjected to suspension culture, they aggregated to form simple, and then cystic embryoid bodies (EBs) with the same time course as EB formation from wild-type ES cells. Immunofluorescence microscopy and ultrathin section electron microscopy revealed that polarized epithelial (visceral endo
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8

Sheth, Parimal, Geetha Samak, J. Andrew Shull, Ankur Seth, and Radhakrishna Rao. "Protein phosphatase 2A plays a role in hydrogen peroxide-induced disruption of tight junctions in Caco-2 cell monolayers." Biochemical Journal 421, no. 1 (2009): 59–70. http://dx.doi.org/10.1042/bj20081951.

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Evidence indicates that PP2A (protein phosphatase 2A) interacts with epithelial tight junctions and negatively regulates the integrity of the tight junction. In the present study, the role of PP2A in the hydrogen peroxide-induced disruption of the tight junction was examined in Caco-2 cell monolayers. Hydrogen peroxide-induced decrease in electrical resistance and increase in inulin permeability was associated with the dephosphorylation of occludin on threonine residues. The hydrogen peroxide-induced decrease in electrical resistance, increase in inulin permeability and redistribution of occlu
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9

Mao, Tangyou, Junxiang Li, Lijuan Liu, et al. "Qingchang Wenzhong Decoction Attenuates DSS-Induced Colitis in Rats by Reducing Inflammation and Improving Intestinal Barrier Function via Upregulating the MSP/RON Signalling Pathway." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/4846876.

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Ulcerative colitis (UC) is a chronic, nonspecific, inflammatory disease for which an effective treatment is lacking. Our previous study found that Qingchang Wenzhong Decoction (QCWZD) can significantly improve the clinical symptoms of UC and ameliorate dextran sulphate sodium- (DSS-) induced ulcerative colitis in rats by downregulating the IP10/CXCR3 axis–mediated inflammatory response. The purpose of the present study was to further explore the mechanism of QCWZD for UC in rats models, which were established by 7-day administration of 4.5% dextran sulphate sodium solution. QCWZD was administe
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10

Jain, Suneet, Takuya Suzuki, Ankur Seth, Geetha Samak та Radhakrishna Rao. "Protein kinase Cζ phosphorylates occludin and promotes assembly of epithelial tight junctions". Biochemical Journal 437, № 2 (2011): 289–99. http://dx.doi.org/10.1042/bj20110587.

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Protein kinases play an important role in the regulation of epithelial tight junctions. In the present study, we investigated the role of PKCζ (protein kinase Cζ) in tight junction regulation in Caco-2 and MDCK (Madin–Darby canine kidney) cell monolayers. Inhibition of PKCζ by a specific PKCζ pseudosubstrate peptide results in redistribution of occludin and ZO-1 (zona occludens 1) from the intercellular junctions and disruption of barrier function without affecting cell viability. Reduced expression of PKCζ by antisense oligonucleotide or shRNA (short hairpin RNA) also results in compromised t
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11

Li, Danxi, and Randall J. Mrsny. "Oncogenic Raf-1 Disrupts Epithelial Tight Junctions via Downregulation of Occludin." Journal of Cell Biology 148, no. 4 (2000): 791–800. http://dx.doi.org/10.1083/jcb.148.4.791.

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Occludin is an integral membrane protein of the epithelial cell tight junction (TJ). Its potential role in coordinating structural and functional events of TJ formation has been suggested recently. Using a rat salivary gland epithelial cell line (Pa-4) as a model system, we have demonstrated that occludin not only is a critical component of functional TJs but also controls the phenotypic changes associated with epithelium oncogenesis. Transfection of an oncogenic Raf-1 into Pa-4 cells resulted in a complete loss of TJ function and the acquisition of a stratified phenotype that lacked cell–cell
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12

Guo, Xin, Jaladanki N. Rao, Lan Liu, et al. "Polyamines are necessary for synthesis and stability of occludin protein in intestinal epithelial cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 288, no. 6 (2005): G1159—G1169. http://dx.doi.org/10.1152/ajpgi.00407.2004.

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Occludin is an integral membrane protein that forms the sealing element of tight junctions and is critical for epithelial barrier function. Polyamines are implicated in multiple signaling pathways driving different biological functions of intestinal epithelial cells (IEC). The present study determined whether polyamines are involved in expression of occludin and play a role in intestinal epithelial barrier function. Studies were conducted in stable Cdx2-transfected IEC-6 cells (IEC-Cdx2L1) associated with a highly differentiated phenotype. Polyamine depletion by α-difluoromethylornithine (DFMO
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13

Gopalakrishnan, Shobha, Narayan Raman, Simon J. Atkinson, and James A. Marrs. "Rho GTPase signaling regulates tight junction assembly and protects tight junctions during ATP depletion." American Journal of Physiology-Cell Physiology 275, no. 3 (1998): C798—C809. http://dx.doi.org/10.1152/ajpcell.1998.275.3.c798.

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Tight junctions control paracellular permeability and cell polarity. Rho GTPase regulates tight junction assembly, and ATP depletion of Madin-Darby canine kidney (MDCK) cells (an in vitro model of renal ischemia) disrupts tight junctions. The relationship between Rho GTPase signaling and ATP depletion was examined. Rho inhibition resulted in decreased localization of zonula occludens-1 (ZO-1) and occludin at cell junctions; conversely, constitutive Rho signaling caused an accumulation of ZO-1 and occludin at cell junctions. Inhibiting Rho before ATP depletion resulted in more extensive loss of
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14

RAO, Radhakrishna K., Shyamali BASUROY, Vijay U. RAO, Karl J. KARNAKY та Akshay GUPTA. "Tyrosine phosphorylation and dissociation of occludin–ZO-1 and E-cadherin–β-catenin complexes from the cytoskeleton by oxidative stress". Biochemical Journal 368, № 2 (2002): 471–81. http://dx.doi.org/10.1042/bj20011804.

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The oxidative-stress-induced alteration in paracellular junctional complexes was analysed in Caco-2 cell monolayer. Oxidative stress induced a rapid increase in tyrosine phosphorylation of occludin, zonula occludens (ZO)-1, E-cadherin and β-catenin. An oxidative-stress-induced decrease in transepithelial electrical resistance was associated with a redistribution of occludin—ZO-1 and E-cadherin—β-catenin complexes from the intercellular junctions. Genistein, a tyrosine kinase inhibitor, prevented the oxidative-stress-induced decrease in resistance and redistribution of protein complexes. Occlud
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15

Nusrat, Asma, G. Thomas Brown, Jeffrey Tom, et al. "Multiple Protein Interactions Involving Proposed Extracellular Loop Domains of the Tight Junction Protein Occludin." Molecular Biology of the Cell 16, no. 4 (2005): 1725–34. http://dx.doi.org/10.1091/mbc.e04-06-0465.

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Occludin is a tetraspan integral membrane protein in epithelial and endothelial tight junction (TJ) structures that is projected to have two extracellular loops. We have used peptides emulating central regions of human occludin's first and second loops, termed O-A:101–121 and O-B:210–228, respectively, to examine potential molecular interactions between these two regions of occludin and other TJ proteins. A superficial biophysical assessment of A:101–121 and O-B:210–228 showed them to have dissimilar solution conformation characteristics. Although O-A:101–121 failed to strongly interact with p
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16

Mitic, Laura L., Eveline E. Schneeberger, Alan S. Fanning, and James Melvin Anderson. "Connexin-Occludin Chimeras Containing the Zo-Binding Domain of Occludin Localize at Mdck Tight Junctions and Nrk Cell Contacts." Journal of Cell Biology 146, no. 3 (1999): 683–93. http://dx.doi.org/10.1083/jcb.146.3.683.

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Occludin is a transmembrane protein of the tight junction that functions in creating both an intercellular permeability barrier and an intramembrane diffusion barrier. Creation of the barrier requires the precise localization of occludin, and a distinct family of transmembrane proteins called claudins, into continuous linear fibrils visible by freeze-fracture microscopy. Conflicting evidence exists regarding the relative importance of the transmembrane and extracellular versus the cytoplasmic domains in localizing occludin in fibrils. To specifically address whether occludin's COOH-terminal cy
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17

Benedicto, Ignacio, Francisca Molina-Jiménez, Birke Bartosch, et al. "The Tight Junction-Associated Protein Occludin Is Required for a Postbinding Step in Hepatitis C Virus Entry and Infection." Journal of Virology 83, no. 16 (2009): 8012–20. http://dx.doi.org/10.1128/jvi.00038-09.

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ABSTRACT The precise mechanisms regulating hepatitis C virus (HCV) entry into hepatic cells remain unknown. However, several cell surface proteins have been identified as entry factors for this virus. Of these molecules, claudin-1, a tight junction (TJ) component, is considered a coreceptor required for HCV entry. Recently, we have demonstrated that HCV envelope glycoproteins (HCVgp) promote structural and functional TJ alterations. Additionally, we have shown that the intracellular interaction between viral E2 glycoprotein and occludin, another TJ-associated protein, could be the cause of the
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18

Mooradian, A. "Age-related changes in rat cerebral occludin and zonula occludens-1 (ZO-1)." Mechanisms of Ageing and Development 124, no. 2 (2003): 143–46. http://dx.doi.org/10.1016/s0047-6374(02)00041-6.

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19

Németh, Zsuzsanna, Attila Marcell Szász, Áron Somorácz, et al. "Zonula Occludens-1, Occludin, and E-cadherin Protein Expression in Biliary Tract Cancers." Pathology & Oncology Research 15, no. 3 (2009): 533–39. http://dx.doi.org/10.1007/s12253-009-9150-4.

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20

Muthusamy, Arivalagan, Cheng-Mao Lin, Sumathi Shanmugam, Heather M. Lindner, Steven F. Abcouwer, and David A. Antonetti. "Ischemia–Reperfusion Injury Induces Occludin Phosphorylation/Ubiquitination and Retinal Vascular Permeability in a VEGFR-2-Dependent Manner." Journal of Cerebral Blood Flow & Metabolism 34, no. 3 (2014): 522–31. http://dx.doi.org/10.1038/jcbfm.2013.230.

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Retinal ischemia–reperfusion (IR) induces neurodegenaration as well as blood–retinal barrier (BRB) breakdown causing vascular permeability. Whereas the neuronal death has been extensively studied, the molecular mechanisms related to BRB breakdown in IR injury remain poorly understood. In this study, we investigated the early changes in tight junctional (TJ) proteins in response to IR injury. Ischemia–reperfusion injury was induced in male rat retinas by increasing the intraocular pressure for 45 minutes followed by natural reperfusion. The results demonstrate that IR injury induced occludin Se
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21

REN, JINGJING, MINGWEI YANG, PENGYAN WANG, JIANJUN JIANG, and GENQIANG YAN. "Specific role of the tight junction proteins occludin and claudin-5 on the blood–brain barrier during Listeria monocytogenes infection." Medycyna Weterynaryjna 76, no. 06 (2020): 6416–2020. http://dx.doi.org/10.21521/mw.6416.

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To investigate the blood-brain barrier (BBB) permeability of mice after Listeria monocytogenes infection for further study on the mechanism of L. monocytogenes crossing the BBB, a mouse model was established and Evans blue assay was performed to assess the BBB disruption. Using relative quantitative real-time PCR, the RNA expression of Zonula occludens-1 (ZO-1), occludin and claudin-5 were detected. In addition, the protein expression level of ZO-1, occludin and claudin-5 were detected by immunohistochemistry and western blot. The extravasation of Evans blue dye was significantly different bet
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22

McCarthy, K. M., S. A. Francis, J. M. McCormack, et al. "Inducible expression of claudin-1-myc but not occludin-VSV-G results in aberrant tight junction strand formation in MDCK cells." Journal of Cell Science 113, no. 19 (2000): 3387–98. http://dx.doi.org/10.1242/jcs.113.19.3387.

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Occludin and 18 distinct members of the claudin family are tetra-span transmembrane proteins that are localized in cell-specific tight junctions (TJs). A previous study showed that expression of chick occludin in Madin-Darby canine kidney (MDCK) cells raised transepithelial electrical resistance (TER) and, paradoxically, increased mannitol flux. In the present study, we employed epitope tagged canine occludin expression, under the control of the tetracycline repressible transactivator, to determine the extent to which the unexpected parallel increase in TER and mannitol flux was related to a s
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23

Colgan, Olga C., Gail Ferguson, Nora T. Collins, et al. "Regulation of bovine brain microvascular endothelial tight junction assembly and barrier function by laminar shear stress." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 6 (2007): H3190—H3197. http://dx.doi.org/10.1152/ajpheart.01177.2006.

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Blood-brain barrier (BBB) controls paracellular solute diffusion into the brain microenvironment and is maintained primarily by tight junctions between adjacent microvascular endothelial cells. Studies implicate blood flow-associated shear stress as a pathophysiological mediator of BBB function, although detailed biochemical data are scarce. We hypothesize that shear stress upregulates BBB function via direct modulation of expression and properties of pivotal tight-junction proteins occludin and zonula occludens-1 (ZO-1). Bovine brain microvascular endothelial cells (BBMvECs) were exposed to e
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24

Oh, Kyung-Jin, Hyun-Suk Lee, Kyuyoun Ahn, and Kwangsung Park. "Estrogen Modulates Expression of Tight Junction Proteins in Rat Vagina." BioMed Research International 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/4394702.

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Background. The objectives of this study were to investigate the localization of tight junctions and the modulation of zonula occludens- (ZO-) 1, occludin and claudin-1 expression by estrogen in castrated female rat vagina. Female Sprague-Dawley rats (230–240 g,n=45) were divided into three groups and subjected to a sham operation (control group,n=15), bilateral ovariectomy (Ovx group,n=15), or bilateral ovariectomy followed by daily subcutaneous injection of 17β-estradiol (50 μg/kg/day, Ovx + Est group,n=15). The cellular localization and expression of ZO-1, occludin, and claudin-1 were deter
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25

Sheth, P., N. Delos Santos, A. Seth, N. F. LaRusso, and R. K. Rao. "Lipopolysaccharide disrupts tight junctions in cholangiocyte monolayers by a c-Src-, TLR4-, and LBP-dependent mechanism." American Journal of Physiology-Gastrointestinal and Liver Physiology 293, no. 1 (2007): G308—G318. http://dx.doi.org/10.1152/ajpgi.00582.2006.

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Bile duct epithelium forms a barrier to the backflow of bile into the liver parenchyma. However, the structure and regulation of the tight junctions in bile duct epithelium is not well understood. In the present study, we evaluated the effect of lipopolysaccharide on tight junction integrity and barrier function in normal rat cholangiocyte monolayers. Lipopolysaccharide disrupts barrier function and increases paracellular permeability in a time- and dose-dependent manner. Lipopolysaccharide induced a redistribution of tight junction proteins, occludin, claudin-1, claudin-4, and zonula occluden
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26

Siu, Erica R., Elissa W. P. Wong, Dolores D. Mruk, K. L. Sze, Catarina S. Porto, and C. Yan Cheng. "An Occludin-Focal Adhesion Kinase Protein Complex at the Blood-Testis Barrier: A Study Using the Cadmium Model." Endocrinology 150, no. 7 (2009): 3336–44. http://dx.doi.org/10.1210/en.2008-1741.

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Several integral membrane proteins that constitute the blood-testis barrier (BTB) in mammalian testes, in particular rodents, are known to date. These include tight junction (TJ) proteins (e.g. occludin, junctional adhesion molecule-A, claudins), basal ectoplasmic specialization proteins (e.g. N-cadherin), and gap junction proteins (e.g. connexin43). However, the regulators (e.g. protein kinases and phosphatases) that affect these proteins, such as their interaction with the cytoskeletal actin, which in turn confer cell adhesion at the TJ, remain largely unknown. We report herein that focal ad
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27

Ikenouchi, Junichi, Hiroyuki Sasaki, Sachiko Tsukita, Mikio Furuse, and Shoichiro Tsukita. "Loss of Occludin Affects Tricellular Localization of Tricellulin." Molecular Biology of the Cell 19, no. 11 (2008): 4687–93. http://dx.doi.org/10.1091/mbc.e08-05-0530.

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The tricellular tight junction (tTJ) forms at the convergence of bicellular tight junctions (bTJs) where three epithelial cells meet in polarized epithelia, and it is required for the maintenance of the transepithelial barrier. Tricellulin is a four transmembrane domain protein recently identified as the first marker of tTJ, but little is known about how tricellulin is localized at tTJs. As for the molecular mechanism of association of tricellulin with tight junctions (TJs), we found that tricellulin was incorporated into claudin-based TJs independently of binding to zona occludens-1. Unexpect
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Qin, Lan-hui, Wen Huang, Xue-an Mo, Yan-lan Chen, and Xiang-hong Wu. "LPS Induces Occludin Dysregulation in Cerebral Microvascular Endothelial Cells via MAPK Signaling and Augmenting MMP-2 Levels." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/120641.

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Disrupted blood-brain barrier (BBB) integrity contributes to cerebral edema during central nervous system infection. The current study explored the mechanism of lipopolysaccharide- (LPS-) induced dysregulation of tight junction (TJ) proteins. Human cerebral microvascular endothelial cells (hCMEC/D3) were exposed to LPS, SB203580 (p38MAPK inhibitor), or SP600125 (JNK inhibitor), and cell vitality was determined by MTT assay. The proteins expressions of p38MAPK, JNK, and TJs (occludin and zonula occludens- (ZO-) 1) were determined by western blot. The mRNA levels of TJ components and MMP-2 were
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Karczewski, Jurgen, Freddy J. Troost, Irene Konings, et al. "Regulation of human epithelial tight junction proteins by Lactobacillus plantarum in vivo and protective effects on the epithelial barrier." American Journal of Physiology-Gastrointestinal and Liver Physiology 298, no. 6 (2010): G851—G859. http://dx.doi.org/10.1152/ajpgi.00327.2009.

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Lactobacillus plantarum , a commensal bacterium of humans, has been proposed to enhance the intestinal barrier, which is compromised in a number of intestinal disorders. To study the effect of L. plantarum strain WCFS1 on human barrier function, healthy subjects were administered L. plantarum or placebo in the duodenum for 6 h by means of a feeding catheter. The scaffold protein zonula occludens (ZO)-1 and transmembrane protein occludin were found to be significantly increased in the vicinity of the tight-junction (TJ) structures, which form the paracellular seal between cells of the epitheliu
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Yasumatsu, Hatsumi, and Soichi Tanabe. "The casein peptide Asn-Pro-Trp-Asp-Gln enforces the intestinal tight junction partly by increasing occludin expression in Caco-2 cells." British Journal of Nutrition 104, no. 7 (2010): 951–56. http://dx.doi.org/10.1017/s0007114510001698.

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We have demonstrated previously that Asn-Pro-Trp-Asp-Gln (NPWDQ, amino acids 107–111 of αs2-casein) inhibited allergen permeation, such as that demonstrated by ovalbumin, using Caco-2 cells as an in vitro human intestinal epithelial model and in mouse jejunal and ileal loops ex vivo. In the present study, the mechanism underlying this inhibitory activity was examined in Caco-2 cells. Transepithelial resistance value increased in response to the addition of increasing NPWDQ concentrations (10− 6–10− 4 m), which suggests that this peptide enhanced epithelial barrier function. Next, changes in mR
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31

Samak, G., S. Aggarwal, and R. K. Rao. "ERK is involved in EGF-mediated protection of tight junctions, but not adherens junctions, in acetaldehyde-treated Caco-2 cell monolayers." American Journal of Physiology-Gastrointestinal and Liver Physiology 301, no. 1 (2011): G50—G59. http://dx.doi.org/10.1152/ajpgi.00494.2010.

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The role of mitogen-activated protein kinases (MAPK) in the mechanism of EGF-mediated prevention of acetaldehyde-induced tight junction disruption was evaluated in Caco-2 cell monolayers. Pretreatment of cell monolayers with EGF attenuated acetaldehyde-induced decrease in resistance and increase in inulin permeability and redistribution of occludin, zona occludens-1 (ZO-1), E-cadherin, and β-catenin from the intercellular junctions. EGF rapidly increased the levels of phospho-ERK1/2, phospho-p38 MAPK, and phospho-JNK1. Pretreatment of cell monolayers with U-0126 (inhibitor of ERK activation),
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32

Ahn, Changhwan, Da-Hye Shin, Dongoh Lee, et al. "Expression of claudins, occludin, junction adhesion molecule A and zona occludens 1 in canine organs." Molecular Medicine Reports 14, no. 4 (2016): 3697–703. http://dx.doi.org/10.3892/mmr.2016.5725.

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33

Eadon, Michael T., Bradley K. Hack, Chang Xu, Benjamin Ko, F. Gary Toback, and Patrick N. Cunningham. "Endotoxemia alters tight junction gene and protein expression in the kidney." American Journal of Physiology-Renal Physiology 303, no. 6 (2012): F821—F830. http://dx.doi.org/10.1152/ajprenal.00023.2012.

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Intact tight junctional (TJ) proteins are required for tubular ion transport and waste excretion. Disruption of TJs may contribute to a decreased glomerular filtration rate in acute kidney injury (AKI) via tubular backleak. The effect of LPS-mediated AKI on murine TJs has not been studied extensively. We hypothesized LPS endotoxin administration to mice would disrupt tubular TJ proteins including zonula occludens-1 (ZO-1), occludin, and claudins. ZO-1 and occludin immunofluorescence 24 h post-LPS revealed a marked change in localization from the usual circumferential fencework pattern to one w
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Kim, Jason Y., Umadevi S. Sajjan, Graham P. Krasan, and John J. LiPuma. "Disruption of Tight Junctions during Traversal of the Respiratory Epithelium by Burkholderia cenocepacia." Infection and Immunity 73, no. 11 (2005): 7107–12. http://dx.doi.org/10.1128/iai.73.11.7107-7112.2005.

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ABSTRACT Burkholderia cenocepacia is an opportunistic bacterial species capable of causing life-threatening respiratory tract infection in persons with cystic fibrosis (CF). Unlike most other pathogens in CF, which typically remain confined to the endobronchial spaces, B. cenocepacia can traverse airway epithelium to cause bacteremia and sepsis. The mechanisms by which this occurs, however, are unknown. We examined the transmigration of B. cenocepacia through polarized respiratory epithelium. Representatives of three “epidemic” lineages common among CF patients in North America were able to tr
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McCarthy, K. M., I. B. Skare, M. C. Stankewich, et al. "Occludin is a functional component of the tight junction." Journal of Cell Science 109, no. 9 (1996): 2287–98. http://dx.doi.org/10.1242/jcs.109.9.2287.

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Occludin's role in mammalian tight junction activity was examined by ‘labeling’ the occludin pool with immunologically detectable chick occludin. This was accomplished by first transfecting MDCK cell with the Lac repressor gene. HygR clones were then transfected with chick occludin cDNA inserted into a Lac operator construct. The resulting HygR/NeoR clones were plated on porous inserts and allowed to form tight junctions. Once steady state transepithelial electrical resistance was achieved, isopropyl- beta-D-thiogalactoside was added to induce chick occludin expression. Confocal laser scanning
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Yi, Hongbo, Li Wang, Yunxia Xiong, et al. "Lactobacillus reuteri LR1 Improved Expression of Genes of Tight Junction Proteins via the MLCK Pathway in IPEC-1 Cells during Infection with Enterotoxigenic Escherichia coli K88." Mediators of Inflammation 2018 (August 19, 2018): 1–8. http://dx.doi.org/10.1155/2018/6434910.

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Intestinal epithelial barrier damage disrupts immune homeostasis and leads to many intestinal disorders. Lactobacillus reuteri strains have probiotic functions in their modulation of the microbiota and immune system in intestines. In this study, the effects of L. reuteri LR1, a new strain isolated from the feces of weaning piglets, on intestinal epithelial barrier damage in IPEC-1 cells caused by challenge with enterotoxigenic Escherichia coli (ETEC) K88 were examined. It was found that L. reuteri LR1, in large part, offset the ETEC K88-induced increase in permeability of IPEC-1 cell monolayer
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Garby, Karen B., Teresa S. King, and Fong Y. Tsai. "Recurrence of Pseudoaneurysm after Successful Embolization." Journal of Endovascular Therapy 4, no. 4 (1997): 385–88. http://dx.doi.org/10.1177/152660289700400412.

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Purpose: To report the initial successful treatment of a hepatic pseudoaneurysm by a partially formed coil and subsequent recurrence secondary to coil migration and configuration change. Methods and Results: A 22-year-old man suffered a gunshot wound in the abdomen; a grade 4 liver laceration was identified and repaired. Eight days later, abdominal pain developed, and pseudoaneurysms were noted off both the superior and inferior branches of the right hepatic artery. Coil embolization was successful in occluding both defects; however, the inferior branch coil was incompletely formed. Twenty day
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Han, Xiaonan, Mitchell P. Fink, Takashi Uchiyama, Runkuan Yang, and Russell L. Delude. "Increased iNOS activity is essential for hepatic epithelial tight junction dysfunction in endotoxemic mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 286, no. 1 (2004): G126—G136. http://dx.doi.org/10.1152/ajpgi.00231.2003.

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We tested the hypothesis that increased production of nitric oxide (NO·) by inducible NO· synthase (iNOS) is a key factor responsible for alterations in the expression, localization, and function of key tight junction (TJ) proteins in mice challenged with lipopolysaccharide (LPS, endotoxin). Endotoxemia was associated with hepatobiliary epithelial barrier dysfunction, as evidenced by increased plasma-to-bile leakage of FITC-labeled dextran (relative molecular mass 40 kDa) and increased circulating levels of bile acids and conjugated bilirubin. Immunoblotting revealed decreased expression of zo
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Su, Xiaomin, Jianmei Wei, Houbao Qi та ін. "LRRC19 Promotes Permeability of the Gut Epithelial Barrier Through Degrading PKC-ζ and PKCι/λ to Reduce Expression of ZO1, ZO3, and Occludin". Inflammatory Bowel Diseases 27, № 8 (2021): 1302–15. http://dx.doi.org/10.1093/ibd/izaa354.

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Abstract Background A dysfunctional gut epithelial barrier allows the augmented permeation of endotoxins, luminal antigens, and bacteria into the bloodstream, causing disease. The maintenance of gut epithelial barrier integrity may be regulated by multiple factors. Herein we analyze the role of leucine-rich repeat-containing protein 19 (LRRC19) in regulating the permeability of the gut epithelial barrier. Methods We utilized Lrrc19 knockout (KO) mice and clinical samples through transmission electron, intestinal permeability assay, Western blot, and immunofluorescence staining to characterize
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Tsukamoto, Tatsuo, and Sanjay K. Nigam. "Role of tyrosine phosphorylation in the reassembly of occludin and other tight junction proteins." American Journal of Physiology-Renal Physiology 276, no. 5 (1999): F737—F750. http://dx.doi.org/10.1152/ajprenal.1999.276.5.f737.

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After the simulation of anoxia by ATP depletion of MDCK cell monolayers with metabolic inhibitors, the tight junction (TJ) is known to become structurally perturbed, leading to loss of the permeability barrier. Peripheral TJ proteins such as zonula occludens 1 (ZO-1), ZO-2, and cingulin become extremely insoluble and associate into large macromolecular complexes (T. Tsukamoto and S. K. Nigam. J. Biol. Chem. 272: 16133–16139, 1997). For up to 3 h, this process is reversible by ATP repletion. We now show that the reassembly process depends on tyrosine phosphorylation. Recovery of transepithelial
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Mellas, Rachel E., Noel J. Leigh, Joel W. Nelson, Andrew D. McCall, and Olga J. Baker. "Zonula Occludens-1, Occludin and E-cadherin Expression and Organization in Salivary Glands with Sjögren’s Syndrome." Journal of Histochemistry & Cytochemistry 63, no. 1 (2014): 45–56. http://dx.doi.org/10.1369/0022155414555145.

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Fries, Walter, Carmelo Muja, Carmela Crisafulli, Salvatore Cuzzocrea, and Emanuela Mazzon. "Dynamics of enterocyte tight junctions: effect of experimental colitis and two different anti-TNF strategies." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 4 (2008): G938—G947. http://dx.doi.org/10.1152/ajpgi.00469.2007.

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An alteration of the intestinal barrier is considered to represent an early step in pathogenesis of Crohn's disease. The integrity of intestinal barrier function is guaranteed among other factors by enterocyte tight junction (TJ) proteins. Clinical and experimental data indicate the TNF-α to be the major responsible factor for these defects. In the present study we investigated the very early effects of DNBS-ethanol colitis on ileal enterocyte TJ proteins [occludin, zonula occludens-1 (ZO-1), claudin-2] in controls, mice treated with infliximab (IFX) or with etanercept (ETC), and in knockout m
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Xu, Jianliang, Farhana Anuar, Safiah Mohamed Ali, Mei Yong Ng, Dominic C. Y. Phua, and Walter Hunziker. "Zona Occludens-2 Is Critical for Blood–Testis Barrier Integrity and Male Fertility." Molecular Biology of the Cell 20, no. 20 (2009): 4268–77. http://dx.doi.org/10.1091/mbc.e08-12-1236.

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Tight junction integral membrane proteins such as claudins and occludin are tethered to the actin cytoskeleton by adaptor proteins, notably the closely related zonula occludens (ZO) proteins ZO-1, ZO-2, and ZO-3. All three ZO proteins have recently been inactivated in mice. Although ZO-3 knockout mice lack an obvious phenotype, animals deficient in ZO-1 or ZO-2 show early embryonic lethality. Here, we rescue the embryonic lethality of ZO-2 knockout mice by injecting ZO-2(−/−) embryonic stem (ES) cells into wild-type blastocysts to generate viable ZO-2 chimera. ZO-2(−/−) ES cells contribute ext
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Bilal, Sahar, Shirin Jaggi, Danielle Janosevic, et al. "ZO-1 protein is required for hydrogen peroxide to increase MDCK cell paracellular permeability in an ERK 1/2-dependent manner." American Journal of Physiology-Cell Physiology 315, no. 3 (2018): C422—C431. http://dx.doi.org/10.1152/ajpcell.00185.2017.

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Hydrogen peroxide (H2O2) increases paracellular permeability of Madin-Darby canine kidney (MDCK) cells, but the mechanism mediating this effect remains unclear. Treatment of MDCK cells with H2O2 activated ERK 1/2. Inhibition of ERK 1/2 activation blocked the ability of H2O2 to increase paracellular permeability. Knockdown of zonula occludens-1 (ZO-1) protein but not occludin eliminated the ability of H2O2 to increase paracellular permeability. H2O2 treatment did not, however, affect the total cell content or contents of the Triton X-100-soluble and -insoluble fractions for occludin, ZO-1, or Z
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Antonetti, David A., Alistair J. Barber, Leigh Ann Hollinger, Ellen B. Wolpert, and Thomas W. Gardner. "Vascular Endothelial Growth Factor Induces Rapid Phosphorylation of Tight Junction Proteins Occludin and Zonula Occluden 1." Journal of Biological Chemistry 274, no. 33 (1999): 23463–67. http://dx.doi.org/10.1074/jbc.274.33.23463.

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46

Ma, Jun, Yilong Yao, Ping Wang, et al. "MiR-181a Regulates Blood-Tumor Barrier Permeability by Targeting Krüppel-Like Factor 6." Journal of Cerebral Blood Flow & Metabolism 34, no. 11 (2014): 1826–36. http://dx.doi.org/10.1038/jcbfm.2014.152.

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Blood-tumor barrier (BTB) constitutes an efficient organization of tight junctions that impairs the delivery of therapeutic drugs. However, the methods and molecular mechanisms underlying the BTB opening remain elusive. MicroRNAs (miRNAs) have recently emerged as key regulators of various biologic processes and therapeutic targets. In this study, we have identified microRNA-181a (miR-181a) as a critical miRNA in opening BTB. MicroRNA-181a expression was upregulated in glioma endothelial cells (GECs), which were obtained by coculturing endothelial cells (ECs) with glioma cells. Overexpression o
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47

Li, Nan, Patricia Lewis, Don Samuelson, Kellym Liboni, and Josef Neu. "Glutamine regulates Caco-2 cell tight junction proteins." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 3 (2004): G726—G733. http://dx.doi.org/10.1152/ajpgi.00012.2004.

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Intestinal epithelial tight junction (TJ) barrier dysfunction may lead to inflammation and mucosal injury. Glutamine (GLN) plays a role in maintenance of intestinal barrier function in various animal models and critically ill humans. Recent evidence from intestinal cell monolayers indicates that GLN maintains transepithelial resistance and decreases permeability. The mechanisms of these effects remain undefined. We hypothesized that GLN affects proteins involved in the intercellular junctional complex. GLN availability was controlled in Caco-2 monolayers by addition to the medium and treatment
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48

Ruba, Ashley L., and Seth D. Pollak. "Children’s emotion inferences from masked faces: Implications for social interactions during COVID-19." PLOS ONE 15, no. 12 (2020): e0243708. http://dx.doi.org/10.1371/journal.pone.0243708.

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To slow the progression of COVID-19, the Centers for Disease Control (CDC) and the World Health Organization (WHO) have recommended wearing face coverings. However, very little is known about how occluding parts of the face might impact the emotion inferences that children make during social interactions. The current study recruited a racially diverse sample of school-aged (7- to 13-years) children from publicly funded after-school programs. Children made inferences from facial configurations that were not covered, wearing sunglasses to occlude the eyes, or wearing surgical masks to occlude th
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49

Song, Li, Shujun Ge, and Joel S. Pachter. "Caveolin-1 regulates expression of junction-associated proteins in brain microvascular endothelial cells." Blood 109, no. 4 (2006): 1515–23. http://dx.doi.org/10.1182/blood-2006-07-034009.

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Abstract Recent evidence from this laboratory indicated that reduced expression of caveolin-1 accompanied the diminished expression of tight junction (TJ)–associated proteins occludin and zonula occludens-1 (ZO-1) following stimulation of brain microvascular endothelial cells (BMECs) with the chemokine CCL2 (formerly called MCP-1). Because attenuated caveolin-1 levels have also been correlated with heightened permeability of other endothelia, the objective of this study was to test the hypothesis that reduced caveolin-1 expression is causally linked to the action of CCL2 on BMEC junctional pro
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50

Youakim, Adel, та Minoo Ahdieh. "Interferon-γ decreases barrier function in T84 cells by reducing ZO-1 levels and disrupting apical actin". American Journal of Physiology-Gastrointestinal and Liver Physiology 276, № 5 (1999): G1279—G1288. http://dx.doi.org/10.1152/ajpgi.1999.276.5.g1279.

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The effects of interferon-γ (IFN-γ) on tight junctions in T84 human intestinal epithelial cells were investigated. Treatment of T84 cells with IFN-γ caused a dose- and time-dependent increase in monolayer permeability as assessed by transepithelial electrical resistance measurements. Examination of specific proteins associated with tight junctions by immunoblotting and confocal microscopy revealed changes in the expression levels and localization of some of these proteins after exposure of the cells to IFN-γ. Specifically, IFN-γ treatment resulted in an almost total loss of zonula occludens (Z
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