Relevant bibliographies by topics / Occludin

Academic literature on the topic 'Occludin'

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Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Occludin"

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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 (August 25, 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 h after injection, the full-length and the five COOH-terminally truncated proteins were all detected at tight junctions as defined by colocalization with both endogenous occludin and zonula occludens-1 demonstrating that exogenous occludin correctly targeted to the tight junction. Importantly, our data show that tight junctions containing four of the COOH-terminally truncated occludin proteins were leaky; the intercellular spaces between the apical cells were penetrated by sulfosuccinimidyl-6-(biotinamido) Hexanoate (NHS-LC-biotin). In contrast, embryos injected with mRNAs coding for the full-length, the least truncated, or the soluble COOH terminus remained impermeable to the NHS-LC-biotin tracer. The leakage induced by the mutant occludins could be rescued by coinjection with full-length occludin mRNA. Immunoprecipitation analysis of detergent-solubilized embryo membranes revealed that the exogenous occludin was bound to endogenous Xenopus occludin in vivo, indicating that occludin oligomerized during tight junction assembly. Our data demonstrate that the COOH terminus of occludin is required for the correct assembly of tight junction barrier function. We also provide evidence for the first time that occludin forms oligomers during the normal process of tight junction assembly. Our data suggest that mutant occludins target to the tight junction by virtue of their ability to oligomerize with full-length endogenous molecules.
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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 (February 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 immunoreactivity of zonula occludens-1 at the cell-cell contacts. Furthermore, OxPAPC increased the diffusive flux of 10-kDa dextran in a dose-dependent manner. O2−· production by bovine aortic endothelial cells increased nearly twofold after exposure to OxPAPC. Also, enzymatic generation of O2−· by xanthine oxidase-lumazine and H2O2 by glucose oxidase-glucose increased occludin phosphorylation, implicating reactive oxygen species as modulators of the OxPAPC effects on occludin phosphorylation. Superoxide dismutase and/or catalase blocked the effects of OxPAPC on occludin protein content and phosphorylation, occludin mRNA, zonula occludens-1 immunoreactivity, and diffusive flux of 10-kDa dextran. These findings suggest that changes in TJ proteins are potential mechanisms by which OxPAPC compromises the barrier properties of the vascular endothelium. OxPAPC-induced disruption of TJs, which likely facilitates transmigration of LDL and inflammatory cells into the subendothelial layers, may be mediated by reactive oxygen species.
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Saitou, Mitinori, Kazushi Fujimoto, Yoshinori Doi, Masahiko Itoh, Toyoshi Fujimoto, Mikio Furuse, Hiroshi Takano, Tetsuo Noda, and Shoichiro Tsukita. "Occludin-deficient Embryonic Stem Cells Can Differentiate into Polarized Epithelial Cells Bearing Tight Junctions." Journal of Cell Biology 141, no. 2 (April 20, 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 endoderm-like) cells were differentiated to delineate EBs not only from wild-type but also from occludin-deficient ES cells. Freeze fracture analyses indicated no significant differences in number or morphology of TJ strands between wild-type and occludin-deficient epithelial cells. Furthermore, zonula occludens (ZO)-1, a TJ-associated peripheral membrane protein, was still exclusively concentrated at TJ in occludin-deficient epithelial cells. In good agreement with these morphological observations, TJ in occludin-deficient epithelial cells functioned as a primary barrier to the diffusion of a low molecular mass tracer through the paracellular pathway. These findings indicate that there are as yet unidentified TJ integral membrane protein(s) which can form strand structures, recruit ZO-1, and function as a barrier without occludin.
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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 (June 12, 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 occludin and ZO (zonula occludens)-1 from the intercellular junctions were significantly attenuated by selective inhibitors of PP2A (okadaic acid and fostriecin) and by knockdown of PP2A-Cα (the catalytic subunit of PP2A). The PP2A-Cα protein and PP2A activity were co-immunoprecipitated with occludin, and this co-immunoprecipitation was rapidly increased by hydrogen peroxide. Hydrogen peroxideinduced increase in co-immunoprecipitation of PP2A-Cα with occludin was prevented by PP2, a Src kinase inhibitor. GST (glutathione transferase)-pull down assays using recombinant GST–Occludin-C (C-terminal tail of occludin) and the purified PP2A showed that PP2A binds to the C-terminal domain of occludin; Src-induced tyrosine phosphorylation of GST–Occludin-C enhanced this binding. The present study shows that hydrogen peroxide increases the association of PP2A with occludin by a Src kinase-dependent mechanism, and that PP2A activity is involved in hydrogen peroxide-induced disruption of tight junctions in Caco-2 cell monolayers.
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Ando-Akatsuka, Y., M. Saitou, T. Hirase, M. Kishi, A. Sakakibara, M. Itoh, S. Yonemura, M. Furuse, and S. Tsukita. "Interspecies diversity of the occludin sequence: cDNA cloning of human, mouse, dog, and rat-kangaroo homologues." Journal of Cell Biology 133, no. 1 (April 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, using a mAb against chicken occludin, whereas the others were amplified by polymerase chain reaction based on the sequence found around the human neuronal apoptosis inhibitory protein gene. The amino acid sequences of the three mammalian (human, murine, and canine) occludins were very closely related to each other (approximately 90% identity), whereas they diverged considerably from those of chicken and rat-kangaroo (approximately 50% identity). Implications of these data and novel experimental options in cell biological research are discussed.
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Guo, Xin, Jaladanki N. Rao, Lan Liu, Tongtong Zou, Kaspar M. Keledjian, Dessy Boneva, Bernard S. Marasa, and Jian-Ying Wang. "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 (June 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) decreased levels of occludin protein but failed to affect expression of its mRNA. Other tight junction proteins, zonula occludens (ZO)-1, ZO-2, claudin-2, and claudin-3, were also decreased in polyamine-deficient cells. Decreased levels of tight junction proteins in DFMO-treated cells were associated with dysfunction of the epithelial barrier, which was overcome by exogenous polyamine spermidine. Decreased levels of occludin in polyamine-deficient cells was not due to the reduction of intracellular-free Ca2+ concentration ([Ca2+]cyt), because either increased or decreased [Ca2+]cyt did not alter levels of occludin in the presence or absence of polyamines. The level of newly synthesized occludin protein was decreased by ∼70% following polyamine depletion, whereas its protein half-life was reduced from ∼120 min in control cells to ∼75 min in polyamine-deficient cells. These findings indicate that polyamines are necessary for the synthesis and stability of occludin protein and that polyamine depletion disrupts the epithelial barrier function, at least partially, by decreasing occludin.
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Jain, Suneet, Takuya Suzuki, Ankur Seth, Geetha Samak, and Radhakrishna Rao. "Protein kinase Cζ phosphorylates occludin and promotes assembly of epithelial tight junctions." Biochemical Journal 437, no. 2 (June 28, 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 tight junction integrity. Inhibition or knockdown of PKCζ delays calcium-induced assembly of tight junctions. Tight junction disruption by PKCζ pseudosubstrate is associated with the dephosphorylation of occludin and ZO-1 on serine and threonine residues. PKCζ directly binds to the C-terminal domain of occludin and phosphorylates it on threonine residues. Thr403, Thr404, Thr424 and Thr438 in the occludin C-terminal domain are the predominant sites of PKCζ-dependent phosphorylation. A T424A or T438A mutation in full-length occludin delays its assembly into the tight junctions. Inhibition of PKCζ also induces redistribution of occludin and ZO-1 from the tight junctions and dissociates these proteins from the detergent-insoluble fractions in mouse ileum. The present study demonstrates that PKCζ phosphorylates occludin on specific threonine residues and promotes assembly of epithelial tight junctions.
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Li, Danxi, and Randall J. Mrsny. "Oncogenic Raf-1 Disrupts Epithelial Tight Junctions via Downregulation of Occludin." Journal of Cell Biology 148, no. 4 (February 21, 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 contact growth control. The expression of occludin and claudin-1 was downregulated, and the distribution patterns of ZO-1 and E-cadherin were altered. Introduction of the human occludin gene into Raf-1–activated Pa-4 cells resulted in reacquisition of a monolayer phenotype and the formation of functionally intact TJs. In addition, the presence of exogenous occludin protein led to a recovery in claudin-1 protein level, relocation of the zonula occludens 1 protein (ZO-1) to the TJ, and redistribution of E-cadherin to the lateral membrane. Furthermore, the expression of occludin inhibited anchorage-independent growth of Raf-1–activated Pa-4 cells in soft agarose. Thus, occludin may act as a pivotal signaling molecule in oncogenic Raf- 1–induced disruption of TJs, and regulates phenotypic changes associated with epithelial cell transformation.
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Benedicto, Ignacio, Francisca Molina-Jiménez, Birke Bartosch, François-Loïc Cosset, Dimitri Lavillette, Jesús Prieto, Ricardo Moreno-Otero, 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 (June 10, 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 mislocalization of TJ proteins. Herein we demonstrated, by using cell culture-derived HCV particles (HCVcc), that interference of occludin expression markedly reduced HCV infection. Furthermore, our results with HCV pseudotyped particles indicated that occludin, but not other TJ-associated proteins, such as junctional adhesion molecule A or zonula occludens protein 1, was required for HCV entry. Using HCVcc, we demonstrated that occludin did not play an essential role in the initial attachment of HCV to target cells. Surface protein labeling experiments showed that both expression levels and cell surface localization of HCV (co)receptors CD81, scavenger receptor class B type I, and claudin-1 were not affected upon occludin knockdown. In addition, immunofluorescence confocal analysis showed that occludin interference did not affect subcellular distribution of the HCV (co)receptors analyzed. However, HCVgp fusion-associated events were altered after occludin silencing. In summary, we propose that occludin plays an essential role in HCV infection and probably affects late entry events. This observation may provide new insights into HCV infection and related pathogenesis.
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Winkler, Lars, Rosel Blasig, Olga Breitkreuz-Korff, Philipp Berndt, Sophie Dithmer, Hans C. Helms, Dmytro Puchkov, et al. "Tight junctions in the blood–brain barrier promote edema formation and infarct size in stroke – Ambivalent effects of sealing proteins." Journal of Cerebral Blood Flow & Metabolism 41, no. 1 (February 13, 2020): 132–45. http://dx.doi.org/10.1177/0271678x20904687.

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The outcome of stroke is greatly influenced by the state of the blood–brain barrier (BBB). The BBB endothelium is sealed paracellularly by tight junction (TJ) proteins, i.e., claudins (Cldns) and the redox regulator occludin. Functions of Cldn3 and occludin at the BBB are largely unknown, particularly after stroke. We address the effects of Cldn3 deficiency and stress factors on the BBB and its TJs. Cldn3 tightened the BBB for small molecules and ions, limited endothelial endocytosis, strengthened the TJ structure and controlled Cldn1 expression. After middle cerebral artery occlusion (MCAO) and 3-h reperfusion or hypoxia of isolated brain capillaries, Cldn1, Cldn3 and occludin were downregulated. In Cldn3 knockout mice (C3KO), the reduction in Cldn1 was even greater and TJ ultrastructure was impaired; 48 h after MCAO of wt mice, infarct volumes were enlarged and edema developed, but endothelial TJs were preserved. In contrast, junctional localization of Cldn5 and occludin, TJ density, swelling and infarction size were reduced in affected brain areas of C3KO. Taken together, Cldn3 and occludin protect TJs in stroke, and this keeps the BBB intact. However, functional Cldn3, Cldn3-regulated TJ proteins and occludin promote edema and infarction, which suggests that TJ modulation could improve the outcome of stroke.
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Dissertations / Theses on the topic "Occludin"

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Walter, Juliane Katharina. "Charakterisierung der Struktur, Funktion und Wechselwirkungen der Tight Junction Proteine Occludin und Zonula Occludens 1." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2009. http://dx.doi.org/10.18452/16012.

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Die tight junction schränken die Diffusion durch den parazellulären Raum in Epithel- und Endothelzellschichten für viele Moleküle stark ein. Dadurch behindern sie die Aufnahme von wasserlöslichen Medikamenten in das dahinterliegende Gewebe. Zwei Proteine, die am tight junction Aufbau mitwirken, sind Zonula Occludens Protein 1 (ZO-1) und Occludin. Eine Öffnung der tight junctions stellt eine Möglichkeit für die Verabreichung von Medikamenten dar. Deshalb wurden die tight junction Proteine ZO-1 und Occludin auf ihre Funktion, Struktur und Regulation untersucht. Für die Interaktion beider Proteine gab es ein Modell, welches eine Oligomerisierung der Bindungspartner als Voraussetzung ihrer Interaktion über helikale Wechselwirkungen vorhersagte. Die Annahmen aus dem Modell der Interaktion von ZO-1 und Occludin konnten experimentell bestätigt werden. Für den C-Terminus von Occludin wurde darüber hinaus eine Interaktion über Disulfidbrücken nachgewiesen. Diese Interaktion könnte in der Zelle von pathologischer Bedeutung bei Schlaganfall und Ischchämie sein. Beide Erkrankungen verursachen eine Öffnung der tight junction im Zusammenhang mit oxidativem Stress. ZO-1 bindet über PDZ Domänen eine Vielzahl von tight junction Proteinen, die an der Abdichtung des parazellulären Raums beteiligt sind. Deshalb wurde die Interaktion und Regulation der PDZ-Domänen aus ZO-1 untersucht. Eine Phosphorylierung der PDZ durch die Proteinkinase C alpha sowie eine Interaktion mit den Phosphatasen 2A und 4 konnte nachgewiesen werden. In vitro konnte gezeigt werden, dass die Phosphorylierung der PDZ-Domänen die Bindung an Membranproteine der tight junction beeinflusst. Diese Arbeit leistet einen Beitrag, die Mechanismen, die zum Verschluss des parazellulären Spaltes führen, aufzuklären. Damit zeigt sie Ansatzpunkte für eine pharmakologische Beeinflussung der Permeabilität der tight junction auf.
Tight junctions restrict diffusion through the paracellular gap in endothelia and epithelia. Thereby they constrain the uptake of water soluble drugs to the tissue. Zonula occludens protein 1 (ZO-1) and occludin are some of proteins involved in tight junction assembly. The opening of tight junctions is a possibility to apply drugs. Therefore the structure, function and regulation of ZO-1 and occludin is characterised. In previous studies, a model predicted the interaction of occludin and ZO-1 through helices. It was proposed that the interaction is mediated by oligomers of ZO-1 and Occludin. This author´s experimental research supports these hypotheses. Furthermore, occludin is shown to self assemble via disulfide bridges. This interaction could be of importance during stroke and ischemia. Both diseases cause the opening of tight junctions in combination with oxidative stress. In addition, this author investigated the interaction and regulation of the PDZ domains of ZO-1. It was shown that the PDZ domains are phosphorylated by protein kinase C alpha and interact with protein phosphatases 2A and 4. Phosphorylation led to a reduction in affinity of PDZ to membrane proteins in vitro. This thesis contributes to the understanding of the mechanisms which are involved in the sealing of the paracellular gap.
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Sundstrom, Jeffrey Antonetti David A. "Identification and functional analysis of occludin phosphorylation." [University Park, Pa.] : Pennsylvania State University, 2008. http://etda.libraries.psu.edu/theses/approved/WorldWideIndex/ETD-2566/index.html.

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Andreeva, Anna. "Protein kinase C isoform antagonism controls occludin phosphorylation and tight junction assembly." [S.l. : s.n.], 2004. http://www.diss.fu-berlin.de/2004/149/index.html.

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Schmidt, Anke. "Identifizierung und Charakterisierung der Bindung zwischen dem Zonula-occludens-Protein 1 und dem Tight-junction-Protein Occludin." [S.l.] : [s.n.], 2002. http://www.diss.fu-berlin.de/2002/251/index.html.

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Ikem, Theresa. "Feedback regulation mechanisms controlling occludin expression and tight junction function." Thesis, University of Bath, 2016. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.690735.

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Cell polarity and tight junctions (TJs) are necessary for intact epithelia. Loss of tight junction integrity is consistent with a display of mesenchymal phenotype which is characteristic of metastatic progression. Occludin, the first identified transmembrane protein identified to localize at tight junctions, has been implicated in regulating tight junction function and cellular polarity. The N-terminal region of occludin has been shown to be an important factor in tight junction maintenance but the mechanism is not yet known. Extensive studies by other researchers have been performed to examine factors that drive EMT, while little is known about their functional reversibility in MET. A model system of EMT ↔ MET was previously established using Pa4 cells, an immortalized epithelial cell line derived from rat parotid gland. Stable introduction of an oncogenic form of the kinase Raf1 into Pa4 was used to derive a mesenchymal phenotype (Pa4Raf1) that demonstrates anchorage-independent growth that coincides with a loss of functional TJs including down-regulation of occludin. The N-terminal region of occludin (66 amino acids) was cloned and used as a bait to pull down protein binding partners in Pa4 and Pa4Raf1 cell lysates. This region of occludin was coupled to a hexa-histidine sequence (His-tag). The resulting protein was expressed in E. coli, purified using magnetic nickel beads, and used as a bait to pull down potential binding partners for this region of occludin present in two cell lines: Pa4 and Pa4-Raf1. Importantly, N-terminal region of occludin has a series of serine and tyrosine residues that are predicted to be phosphorylated by a wide range of kinases. In this regard, Ser8, Ser45, Tyr12, Tyr22, Tyr29 and the poly-proline region (Pro-Leu-Ser-Pro-Pro-Pro-Tyr-Arg-Pro) of the N-terminal bait peptide were mutated in order to further elucidate the functions of these residues. Serine was mutated to aspartic acid, tyrosine to glutamic acid, and proline to alanine. The binding partners were also knocked down to identify their effects on occludin colocalization. Many of the potential binding partners that were identified are involved in apoptosis, metastasis and/or cellular oxidation. This research seeks for ways by which manipulating these identified binding partners will transform a cell from a mesenchymal phenotype to an epithelial phenotype.
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Freitas, Antonio Klingem Leite de. "Efeito da SuplementaÃÃo com Alanil-Glutamina nas AlteraÃÃes da Permeabilidade Intestinal em Ratos Treinados Submetidos a um ExercÃcio Prolongado e Exaustivo de NataÃÃo." Universidade Federal do CearÃ, 2013. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=12375.

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Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico
O exercÃcio prolongado e exaustivo induz uma disfunÃÃo da barreira intestinal. VÃrios estudos mostram que a suplementaÃÃo com alanil-glutamina (A/G) melhora a proliferaÃÃo das cÃlulas intestinais e absorÃÃo de eletrÃlitos. O objetivo deste trabalho foi investigar o efeito da suplementaÃÃo com A/G na permeabilidade intestinal em ratos treinados apÃs um exercÃcio prolongado e exaustivo de nataÃÃo. Utilizamos ratos Wistar, divididos em sete grupos: 1) SedentÃrio (S); 2) SedentÃrio A/G (S-A/G); 3) Treinado (T); 4) Treinado A/G (T-A/G); 5) ExaustÃo (E); 6) ExaustÃo A/G (E-A/G) e 7) Recuperado (R). Os animais dos grupos suplementados receberam o dipeptÃdeo A/G. Os animais foram treinados durante 12 semanas de nataÃÃo. Na metodologia realizamos anÃlises bioquÃmicas de pH, pCO2, pO2, SO2, excesso de bases (BE), pelo mÃtodo de gasometria e lactato e glicose. Analisamos a transcriÃÃo das junÃÃes firmes: ZO-1, Ocludina, Claudina-2 e PEPT-1 atravÃs de RT-PCR. A anÃlise da permeabilidade intestinal foi realizada pelo mÃtodo da ingestÃo de Lactulose/Manitol (L/M). Fizemos tambÃm anÃlise histolÃgica do duodeno, jejuno e Ãleo. O presente estudo foi aprovado pela CEPA-UFC, em protocolo de N 13/13. Nossos resultados mostraram que pCO2 e SO2 foram aumentados nos grupos E e E-A/G, mas houve queda nos parÃmetros de pH e BE para estes mesmos grupos. Encontramos queda dos Ãndices de glicose e aumento das concentraÃÃes de lactato. Houve aumento significativo no percentual de excreÃÃo de lactulose nos grupos E e E-A/G em relaÃÃo ao grupo S. Houve, no entanto, queda da excreÃÃo de lactulose com diferenÃa estatÃstica entre os grupos E e E-A/G, mostrando proteÃÃo da A/G frente ao aumento da permeabilidade intestinal promovida pelo exercÃcio exaustivo. O percentual de excreÃÃo do manitol foi aumentado nos grupos E e E-A/G em relaÃÃo ao grupo S. Entretanto, na anÃlise da relaÃÃo da permeabilidade dos dois carboidratos L/M observamos um aumento significativo no grupo E em relaÃÃo ao grupo S. Contudo, houve diferenÃa significativa entre os grupos E e E-A/G mostrando que a A/G conseguiu reverter os efeitos da atividade exaustiva na permeabilidade intestinal. Observamos aumento da ZO-1 e ocludina nos grupos S-A/G e T em relaÃÃo a S. Houve tambÃm aumento de ZO-1 no grupo E em relaÃÃo ao S. PorÃm, a A/G reverteu à transcriÃÃo destas junÃÃes firmes nos grupos T-A/G e E-A/G. A transcriÃÃo de claudina-2 foi reduzida no grupo S-A/G, mas obtivemos um aumento no grupo E em relaÃÃo ao S e uma diminuiÃÃo de E-A/G em relaÃÃo ao E. Em relaÃÃo ao PEPT-1, observamos aumento da transcriÃÃo nos grupos T e E em relaÃÃo ao S. Contudo, a A/G reverteu à transcriÃÃo deste peptÃdeo no grupo E-A/G em relaÃÃo ao E. Numa anÃlise de 72 horas apÃs o teste de exaustÃo encontramos valores para a permeabilidade intestinal similares aos grupos sedentÃrios. ConcluÃmos que o exercÃcio prolongado e exaustivo alterou a permeabilidade intestinal e a suplementaÃÃo crÃnica com alanil-glutamina teve efeito protetor contra este aumento. O possÃvel mecanismo da A/G no processo estudado refere-se a processos mecÃnicos de interaÃÃo cÃlula-cÃlula (ZO-1 e ocludina) e/ou eletrolÃticos (claudina-2).
The prolonged and exhaustive exercise induces intestinal barrier dysfunction. Several studies show that supplementation with alanyl-glutamine (A/G) improves the cell proliferation intestinal and electrolyte absorption. The aim of our study was to investigate the effect of supplementation with A/G in the intestinal permeability in rats trained after prolonged exercise and exhaustive swimming. We used Wistar rats that were divided into seven groups: 1) Sedentary (S); 2) Sedentary A/G (S-A/G); 3) Trained (T); 4) Trained A/G (T-A/G); 5) Exhaustion (E); 6) Exhaustion A/G (E-A/G); 7) Recovered (R). The animal supplemented groups received the dipeptide A/G. The animals were trained for twelve weeks. In the methodology we performed biochemical analysis of pH, pCO2, pO2, SO2, and bases excess (BE), by the method of gas analysis and lactate and glucose. We analyzed the transcription of tight junctions: ZO-1, Occludin, Claudin-2 and PEPT-1 by RT-PCR. The analysis of intestinal permeability was performed by the method of the ingestion of lactulose/mannitol (L/M). We also performed histological analysis of the duodenum, jejunum and ileum. This study was approved by the CEPA-UFC on Protocol NÂ 13/2013. Our results showed that SO2 and pCO2 were higher in groups E and E-A/G, but decreased the parameters pH and BE for these same groups. We found falling glucose levels and increased concentrations of lactate. A significant increase in the percentage of excretion of lactulose in groups E and E-A/G than in group S. There was, however, fall of excretion of lactulose with statistical difference between groups E and E-A/G, showing protection against the alanyl-glutamine increased intestinal permeability promoted by exhaustive exercise. The percentage of excretion of mannitol was increased in groups E and E-A/G than in group S. However, in the analysis of the excretion of both carbohydrates lactulose/mannitol we observed a significant increase in group E than in group S. However, there was significant difference between groups E and E-A/G showing that Ala/Gln was able to reverse the effects of exhaustive activity in intestinal permeability. We observed an increase in ZO-1 and occludin in groups S-A/G and T with respect to S. There was also an increase of ZO-1 in the E group compared to S. However, Ala/Gln reversed the transcription of these tight junctions in groups T-A/G and E-A/G. Transcription of claudin-2 was reduced in the S-A/G, but we obtained and increase in the E group compared to a decrease of S and E-A/G against E. Regarding the PET-1 we showed increased transcription in groups T and E in relation to S. However, the Ala/Gln reversed the transcript of this dipeptide in group E-A/G with respect to E. An analysis 72 hours after the exhaustion test values found for intestinal permeability similar to sedentary group. The prolonged and exhaustive exercise altered intestinal permeability and chronic supplementation with Ala/Gln was protective against the increase. The possible mechanism of Ala/Gln refers to mechanical processes of cell-to-cell interaction (occludin and ZO-1) and/or electrolytic (claudin-2).
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Dörfel, Max J. [Verfasser]. "Der Einfluss posttranslationaler Modifikationen auf die Funktion des Tight Junction-Proteins Occludin / Max Dörfel." Berlin : Freie Universität Berlin, 2012. http://d-nb.info/1027498493/34.

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Castro, Villela Víctor Manuel [Verfasser]. "The interplay between occludin and ZO-1 is redox sensitive / Víctor Manuel Castro Villela." Berlin : Freie Universität Berlin, 2011. http://d-nb.info/1026358752/34.

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Neophytou, Irene. "Expression and characterisation of peptides based on the predicted extracellular domains of human occludin." Thesis, King's College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406444.

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Saitou, Mitinori. "Occludin-deficient Embryonic Stem Cells Can Differentiate into Polarized Epithelial Cells Bearing Tight Junctions." Kyoto University, 1999. http://hdl.handle.net/2433/181723.

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Books on the topic "Occludin"

1

Ash, Major M. Occlusion. 4th ed. Philadelphia: W.B. Saunders, 1995.

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J, Parkins B., ed. Occlusion. 2nd ed. London: Wright, 1990.

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Neff, Peter A. TMJ occlusion and function. Washington: Neff, 1993.

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Júnior, José dos Santos. Occlusion, principles and concepts. 2nd ed. St. Louis, Mo: Ishiyaku EuroAmerica, 1996.

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Júnior, José dos Santos. Occlusion: Principles and concepts. 2nd ed. St. Louis, Mo: Ishiyaku EuroAmerica, 1996.

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Occlusion: Principles and assessment. Oxford: Wright, 1991.

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Júnior, José dos Santos. Occlusion: Principles and treatment. Chicago: Quintessence Pub. Co., 2007.

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Ash, Major M. Dental anatomy, physiology, and occlusion. 8th ed. Philadelphia: W.B. Saunders, 2003.

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J, Capp Nicholas, and Barrett N. Vincent J, eds. Colour atlas of occlusion & malocclusion. St. Louis: Mosby-Year Book, 1991.

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Bergmann, Martin W., Apostolos Tzikas, and Nina C. Wunderlich. Clinical Cases in LAA Occlusion. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-51431-4.

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Book chapters on the topic "Occludin"

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Nishimura, Noriyuki, and Takuya Sasaki. "Cell-Surface Biotinylation to Study Endocytosis and Recycling of Occludin." In Methods in Molecular Biology, 89–96. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-178-9_7.

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Venkat, Ibrahim, Ahamad Tajudin Khader, K. G. Subramanian, and Philippe De Wilde. "Psychophysically Inspired Bayesian Occlusion Model to Recognize Occluded Faces." In Computer Analysis of Images and Patterns, 420–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-23672-3_51.

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Peters, Shane. "Occlusion." In Encyclopedia of Animal Cognition and Behavior, 1–3. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47829-6_1276-1.

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Weik, Martin H. "occluder." In Computer Science and Communications Dictionary, 1132. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/1-4020-0613-6_12685.

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Lazareva, Olga. "Occlusion." In Encyclopedia of Evolutionary Psychological Science, 1–3. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-16999-6_2759-1.

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Hobkirk, John A., Daljit S. Gill, Steven P. Jones, Kenneth W. Hemmings, G. Steven Bassi, Amanda L. O'Donnell, and Jane R. Goodman. "Occlusion." In Hypodontia, 60–81. West Sussex, UK: John Wiley & Sons Ltd., 2013. http://dx.doi.org/10.1002/9781118784877.ch5.

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Sinha, Sudipta N. "Occlusion." In Computer Vision, 1–4. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-03243-2_806-1.

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Lazareva, Olga. "Occlusion." In Encyclopedia of Evolutionary Psychological Science, 5543–44. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-19650-3_2759.

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Zhang, Peixi, Jianhuang Lai, Quan Zhang, and Xiaohua Xie. "MGD: Mask Guided De-occlusion Framework for Occluded Person Re-identification." In Intelligence Science and Big Data Engineering. Visual Data Engineering, 411–23. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-36189-1_34.

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Zhou, Chunluan, and Junsong Yuan. "Learning to Integrate Occlusion-Specific Detectors for Heavily Occluded Pedestrian Detection." In Computer Vision – ACCV 2016, 305–20. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-54184-6_19.

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Conference papers on the topic "Occludin"

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Caraballo, Juan C., Whitney Westphal, Thomas Moninger, and Alejandro P. Comellas. "Diesel Exhaust Particles Induce Dissociation Of Occludin And Zonula Occludens 1 (ZO-1) In Alveolar Epithelial Cells." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1026.

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Lesniak, Kevin, and Conrad S. Tucker. "Real-Time Occlusion Between Real and Digital Objects in Augmented Reality." In ASME 2018 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/detc2018-86346.

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The method presented in this work reduces the frequency of virtual objects incorrectly occluding real-world objects in Augmented Reality (AR) applications. Current AR rendering methods cannot properly represent occlusion between real and virtual objects because the objects are not represented in a common coordinate system. These occlusion errors can lead users to have an incorrect perception of the environment around them when using an AR application, namely not knowing a real-world object is present due to a virtual object incorrectly occluding it and incorrect perception of depth or distance by the user due to incorrect occlusions. The authors of this paper present a method that brings both real-world and virtual objects into a common coordinate system so that distant virtual objects do not obscure nearby real-world objects in an AR application. This method captures and processes RGB-D data in real-time, allowing the method to be used in a variety of environments and scenarios. A case study shows the effectiveness and usability of the proposed method to correctly occlude real-world and virtual objects and provide a more realistic representation of the combined real and virtual environments in an AR application. The results of the case study show that the proposed method can detect at least 20 real-world objects with potential to be incorrectly occluded while processing and fixing occlusion errors at least 5 times per second.
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Caraballo, Juan C., Jennifer Borcherding, and Alejandro Comellas. "Hypoxia Induces Proteasomal Degradation Of Occludin Via A Protein Kinase C-Zeta Pathway." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6393.

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Su, Kang-Cheng, Yu-Chung Wu, Tun-yun Hsueh, and Wann Cherng Perng. "Bile Acids Increase Alveolar Transepithelial Permeability Through Reduction Of Tight-junction Proteins Occludin And ZO-1." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4962.

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Patwardhan, K. A., G. Sapiro, and M. Bertalmio. "Video inpainting of occluding and occluded objects." In rnational Conference on Image Processing. IEEE, 2005. http://dx.doi.org/10.1109/icip.2005.1529993.

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Keber, I., K. Potisk, D. Keber, M. Stegnar, and N. Vene. "PHYSICAL ACTIVITY RELEASES TISSUE PLASMINOGEN ACTIVATOR FROM EXERCISING PARTS OF BODY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643117.

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To determine the origin of tissue plasminogen activator (t-PA) release during physical activity, we studied the separate and combined effects of venous occlusion and acute physical activity on t-PA release in arm and leg. In 15 healthy volunteers 20 min venous occlusions of arm and leg were performed simultaneously before physical activity ( maximal stress testing on treadmill)(occlusion I), immediately after physical activity and 45 min later (occlusion II). Blood samples were drawn from unoccluded arm before occlusion and after physical activity, and from occluded arm and leg after occlusion. Fibrinolytic activity was measured by euglobulin clot lysis time (ECLT) and t-PA activity assay. The amount of released t-PA during different stimuli (fibrinolytic potential) was calculated as the difference between post- and prestimulation fibrinolytic activity. Before physical activity there was a great increase in fibrinolytic activity due to t-PA in the occluded arm but no increase in the occluded leg. Physical activity itself caused a similar increase of systemic fibrinolytic activity as arm occlusion locally. After physical activity arm occlusion evoked equally good response than before it. Fibrinolytic activity during leg occlusion behaved differently: there was an increase in t-PA activity in the occluded leg which persisted one hour after physical activity, when systemic fibrinolytic activity already fell to initial level.These results demonstrated that walking and running triggered t-PA release from the leg vessels. Since leg occlusion was not a stimulus for t-PA release, it served only as a method to demonstrate the effect of physical activity.
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Guo, Zhixin, Wenzhi Liao, Peter Veelaert, and Wilfried Philips. "Occlusion-robust Detector Trained with Occluded Pedestrians." In 7th International Conference on Pattern Recognition Applications and Methods. SCITEPRESS - Science and Technology Publications, 2018. http://dx.doi.org/10.5220/0006569200860094.

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Zhang, Shuo, Zeqi Shen, and Youfang Lin. "Removing Foreground Occlusions in Light Field using Micro-lens Dynamic Filter." In Thirtieth International Joint Conference on Artificial Intelligence {IJCAI-21}. California: International Joint Conferences on Artificial Intelligence Organization, 2021. http://dx.doi.org/10.24963/ijcai.2021/180.

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Foreground occlusion removal task aims to automatically detect and remove foreground occlusions and recover background objects. Since for Light Fields (LFs), background objects occluded in some views may be seen in other views, the foreground occlusion removal task for LFs is easy to achieve. In this paper, we propose a learning-based method combining ‘seeking’ and ‘generating’ to recover occluded background. Specifically, the micro-lens dynamic filters are proposed to ‘seek’ occluded background points in shifted micro-lens images and remove occlusions using angular information. The shifted images are then combined to further ‘generate’ background regions to supplement more background details using spatial information. By fully exploring the angular and spatial information in LFs, the dense and complex occlusions can be easily removed. Quantitative and qualitative experimental results show that our method outperforms other state-of-the-arts methods by a large margin.
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Wang, Peng, Wanyi Li, Wenjun Zhu, and Hong Qiao. "Object tracking with serious occlusion based on occluder modeling." In 2012 IEEE International Conference on Mechatronics and Automation (ICMA). IEEE, 2012. http://dx.doi.org/10.1109/icma.2012.6285122.

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López Sánchez, Daniel, Juan M. Corchado, and Angelica González Arrieta. "Inhibition of Occluded Facial Regions for Distance-Based Face Recognition." In Twenty-Seventh International Joint Conference on Artificial Intelligence {IJCAI-18}. California: International Joint Conferences on Artificial Intelligence Organization, 2018. http://dx.doi.org/10.24963/ijcai.2018/746.

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This work focuses on the design and validation of a CBR system for efficient face recognition under partial occlusion conditions. The proposed CBR system is based on a classical distance-based classification method, modified to increase its robustness to partial occlusion. This is achieved by using a novel dissimilarity function which discards features coming from occluded facial regions. In addition, we explore the integration of an efficient dimensionality reduction method into the proposed framework to reduce computational cost. We present experimental results showing that the proposed CBR system outperforms classical methods of similar computational requirements in the task of face recognition under partial occlusion.
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Reports on the topic "Occludin"

1

Patwardhan, Kedar A., Guillermo Sapiro, and Marcelo Bertalmio. Video Inpainting of Occluding and Occluded Objects. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada437289.

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Penmatsa, Rajeev, and Chris Wyman. Voxel-Space Ambient Occlusion. Fort Belvoir, VA: Defense Technical Information Center, February 2012. http://dx.doi.org/10.21236/ada586797.

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Denton, Trip, John Novatnack, and Ali Shokoufandeh. Drexel Object Occlusion Repository (DOOR). Fort Belvoir, VA: Defense Technical Information Center, July 2005. http://dx.doi.org/10.21236/ada457294.

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Finkel, Leif H., and Paul Sajda. Object Discrimination Based on Depth-From-Occlusion. Fort Belvoir, VA: Defense Technical Information Center, January 1991. http://dx.doi.org/10.21236/ada248104.

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Smith, David. Parallel approximate string matching applied to occluded object recognition. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.5608.

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Finkel, Leif H. Visual Perception of Depth-from-Occlusion: A Neural Network Model. Fort Belvoir, VA: Defense Technical Information Center, July 1992. http://dx.doi.org/10.21236/ada253343.

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Finkel, Leif H. Visual Perception of Depth-from-Occlusion: A Neural Network Model. Fort Belvoir, VA: Defense Technical Information Center, December 1990. http://dx.doi.org/10.21236/ada249771.

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Findel, Leif H. Visual Perception of Depth from Occlusion: A Neural Network Model. Fort Belvoir, VA: Defense Technical Information Center, January 1992. http://dx.doi.org/10.21236/ada249035.

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Wang, Yusu, Pankaj K. Agarwal, and Sariel Har-Peled. An On-Line Occlusio-Culling Algorithm for Fast Walkthrough in Urban Areas. Fort Belvoir, VA: Defense Technical Information Center, January 2001. http://dx.doi.org/10.21236/ada415443.

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Fowlkes, Jeffrey B. Ultrasonically-Induced Vaporization of Perfluorocarbon Droplets for Occlusion Therapy of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada471775.

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