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Dissertations / Theses on the topic 'Tight junction'

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Published: 4 June 2021

Last updated: 10 March 2023

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1

Morgan, Sarah V. "Tight junction protein expression in human astrocytes." Thesis, University of Sheffield, 2016. http://etheses.whiterose.ac.uk/14403/.

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Tight junctions are formed from a complex of different individual proteins. These complexes are expressed by epithelial cells and form an intercellular barrier which restricts and regulates paracellular permeability. Tight junction proteins have also been shown to be expressed in non-epithelial cells which do not form tight junctions, including astrocytes. The function(s) of these proteins within non-epithelial cells, however, remains unclear. This study aims to characterise the expression of tight junction proteins in astrocytes and investigate the function(s) of these proteins in these cells. The expression of the tight junction proteins occludin, claudin-5 and zonula occludens-1 (ZO-1) was characterised in vitro in both human primary astrocytes and the 1321N1 human astrocytoma cell line and in vivo in human autopsy brain samples. The function(s) of occludin was investigated using a pull-down protein binding assay and mass spectrometry analysis to identify putative binding partners for this protein in astrocytes. The current study demonstrates astrocytic and nuclear expression of occludin and ZO-1 in vitro and in vivo. The expression of claudin 5 in astrocytes remains difficult to determine due to contradictory evidence in which the astrocytic expression of this protein in vitro is not supported in vivo. Putative binding partners were also identified for the N- and C-terminal domains of occludin. Many of these proteins have functions in RNA metabolic processes, consequently their identification as putative occludin binding partners implicates occludin in functions beyond the formation of the tight junction complex. Although these interactions have not yet been validated, this study’s findings provide a platform upon which future research can be constructed.

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2

Chan, Wing-lim, and 陳穎廉. "The SARS coronavirus envelope protein E targets the PALS1 tight junction factor and alters formation of tight junctions of epithelialcells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47169242.

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Tight junctions, as zones of close contact between epithelial and endothelial cells, form a physical barrier as one of the first host defense strategies that prevent the intrusion of pathogens across epithelia and endothelia. Recently, an interaction between the Severe Acute Respiratory Syndrome-Coronavirus (SARS-CoV) envelope protein (E) and PALS1, a member of the CRB tight junction complex, was identified in the Virus-Host Interaction group at HKU-Pasteur Research Centre (Teoh et al, 2010). In this report, I present in vitro data which helps to better understand how this protein-protein interaction could interfere with the formation and maintenance of tight junctions at the apical domain of epithelial cells. In previous research, the interaction between E and PALS1 was identified through a yeast two-hybrid screen and confirmed in vitro. A PDZ-binding motif (PBM) was identified at the C-terminal end of E, which interacts with the PDZ domain of PALS1. The objective of my research was to further enhance the knowledge of this interaction by studying the effect of E expression on PALS1 localization and tight junction structure in epithelial cells. I have shown that expression of E is associated with a partial relocalization of PALS1 to the Golgi compartment. Also, I discovered that when wild-type E, E(wt), was expressed in the MDCKII cell model, the time required for tight junction formation was extended to 6-8 hours, while normal cells only required two hours. Interestingly, expression of the E protein with a deletion of the PBM, E(ΔPBM) did not affect the timing of tight junction formation. This finding indicates that the PBM plays a critical role in the process of alteration of tight junctions mediated by E, most likely through its interaction with PALS1. Furthermore, the localization pattern of E was altered when its PBM was deleted. In the MDCKII model, E(wt) located, as expected, at membranes of the Golgi compartment, whereas E(ΔPBM) had a diffused distribution in the cytosol. This observation suggests that the PBM acts as a localization signal for the E protein to the Golgi region, which is the assembly site of the virus. Finally, to examine the role of the PBM in the context of the whole virus, I participated in the production of SARS-CoV recombinant viruses, with mutations in the PBM of E. Though this work is still in progress, the use of these viruses should help to delineate the role of E PBM in SARS-CoV induced pathogenesis in vitro and ultimately in vivo.
published_or_final_version
Pathology
Master
Master of Philosophy

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3

Thomas, Fay Christina. "Tight junction biogenesis in the mouse preimplantation embryo." Thesis, University of Southampton, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270661.

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4

Ackerman, Margaret E. "Targeting the tight junction : immunotherapy of colon cancer." Thesis, Massachusetts Institute of Technology, 2009. http://hdl.handle.net/1721.1/63023.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, February 2010.
"February 2010." Cataloged from PDF version of thesis.
Includes bibliographical references.
A33 is a cell surface glycoprotein of colon epithelium with a long clinical history as a target in antibody-based cancer therapy. Despite being present in normal colon, radio-labeled antibodies against A33 are selectively retained by tumors at long time points. Accordingly, we have studied the trafficking and kinetic properties of the antigen to determine its promise in multi-step, pretargeted immunotherapy. In vitro, the localization, mobility, and persistence of the antigen were investigated, and this work has demonstrated that the antigen is both highly immobile and extremely persistent, properties which may contribute to the prolonged retention of the clinically administered antibodies, and their uncommon ability to penetrate solid tumors. Secondly, because poor tissue penetration is a significant obstacle to the development of successful antibody drugs for immunotherapy of solid tumors, we assess the contribution of antigen density and turnover rate by evaluating the distance to which antibodies penetrate spheroids when these properties are systematically varied. The results agree well with the quantitative modeling predictions, and demonstrate that dosing distal regions of tumors is best achieved by selecting slowly internalized targets that are not expressed above the level necessary for recruiting a toxic dose of therapeutic. Lastly, we describe the in vitro characteristics and report the promising in vivo biodistribution of a multi-step tumor targeting therapy utilizing a novel bispecific antibody which recognizes both the A33 antigen and a small molecule radiometal chelate. Following these studies, several protein engineering techniques are presented. First, a new method of conducting de novo protein engineering utilizing highly avid magnetic beads is described, in which extremely weak interactions can be captured from large library populations. Secondly, an in vitro assay which utilizes these highly avid magnetic beads is used to score the clinical immunogenicity of therapeutic protein drugs is presented. Finally, the use of sortase A as a means to generate fusion proteins posttranslationally is described. Taken together, this additional work demonstrates a productive intersection of basic research and protein engineering methods.
by Margaret E. Ackerman.
Ph.D.

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5

Althubaiti, Suha. "Characterisation of epidermal tight junction proteins in ageing." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/characterisation-of-epidermal-tight-junction-proteins-in-ageing(a3a50284-018e-45f9-bdcf-a5ad004a0084).html.

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The epidermal tight junction (TJ) plays an important role as a barrier which protects the skin against dehydration and infection. Skin barrier function is known to decline with increasing age (Rabe et al., 2006). Human skin is subject to intrinsic (i.e. chronological) ageing and extrinsic (environmentally-induced) ageing. However, the role of TJs in the ageing process is still unknown. Therefore, in this study, using quantitative immunofluorescent staining TJ protein expression was investigated in intrinsically aged compared to young human skin. Since ultraviolet radiation (UVR) from sunlight is considered the major environmental insult to human skin, TJ proteins were also investigated in photoaged compared to photoprotected human skin, and in skin exposed to a single acute dose of UVR.In aged vs young skin, there was no significant difference either in the expression levels or localisation of TJ proteins.However, significant reduction in claudin-1 (cld-1) and increases in cld-7 and -12 expressions were demonstrated in chronically photoaged human skin suggesting differential regulation of clds in response to photoexposure. By contrast in acutely irradiated human skin, only a reduction in cld-1 expression was observed 24h after a single UVB dose. Moreover, in both chronic and acute UVR exposed human skin, cld-1 was most significantly reduced in the basal layer of the epidermis suggesting that the differentiation state of keratinocytes might be important in their response to UVR.To investigate these effects further, a normal human epidermal keratinocyte (NHEK) cell culture model was employed. A reduction in cld-1 expression and an increase in cld-4 were demonstrated in undifferentiated NHEK cells irradiated with sub lethal doses of UVR. Interestingly, no changes were observed in TJ protein expression in irradiated differentiated keratinocytes. However, when TJ function was measured in these cells using transepithelial electrical resistance (TEER) as a marker of TJ function, UVR induced a significant reduction in TEER. This coincided with an alteration in the organisation of cld-1 in irradiated differentiated keratinocytes.These data demonstrate that TJ protein expression is modulated by acute and chronic exposure to UVR. These observations may explain, at least in part, the decline in skin barrier function observed in response to UVR.

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6

Sonoda, Noriyuki. "Clostridium perfringens Enterotoxin Fragment Removes Specific Claudins from Tight Junction Strands : Evidence for Direct Involvement of Claudins in Tight Junction Barrier." Kyoto University, 2002. http://hdl.handle.net/2433/149669.

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7

McCabe, Mark James, and markmccabe02@hotmail com. "Hormonal regulation of the testicular Sertoli cell tight junction." RMIT University. Applied Sciences, 2008. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20081212.100348.

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The Sertoli cell tight junction (TJ) of the seminiferous epithelium is important for the developmental process of spermatogenesis as it separates germ cells in the seminiferous tubules from the general circulation in the testicular interstitium. Absence of the TJ leads to spermatogenic arrest and infertility. TJs form at puberty as circulating gonadotrophins luteinising hormone/testosterone and follicle stimulating hormone increase. Several studies have demonstrated hormonal regulation of the two major TJ proteins, claudin-11 and occludin, and also of TJ function in vitro and in vivo. Men with low levels of circulating gonadotrophins exhibit an immature and dysfunctional TJ phenotype, which is reversed upon the exogenous application of gonadotrophins. This thesis hypothesises that claudin-11 and occludin are the major contributors to TJ function, and that gonadotrophins regulate TJ function and structure via these two proteins in several species including humans. This PhD was divided into four separate studies to address these hypotheses. The first study selectively silenced the genetic expression of claudin-11 and occludin with small interfering RNA (siRNA) in cultured immature rat Sertoli cells to determine their contribution to Sertoli cell TJ function in vitro. siRNA treatment against either protein significantly (p less than 0.01) reduced TJ function by ~50% as assessed by transepithelial electrical resistance. Immunocytochemistry displayed marked reductions in the localisation of these proteins to the TJ after siRNA treatment. It was concluded that both proteins significantly contributed to TJ function in vitro. The second and third studies then aimed to study hormonal regulation of the TJ in vivo. Weekly injections of the gonadotrophin releasing hormone antagonist acyline were used to suppress circulating gonadotrophins and spermatogenesis in adult rats. Acyline treatment disrupted i) the localisation of occludin to the TJ and ii) TJ function as shown by permeability to a biotin tracer, which was impermeable to TJs in controls. Short-term hormone replacement partially restored the effects of gonadotrophin suppression. It was concluded that gonadotrophins regulate the maintenance of the TJ in rats in vivo. The third study used the hypogonadal (hpg) mouse, which is a naturally occurring model of gonadotrophin deficiency with inactive spermatogenesis. Claudin-11 in hpg mice was not localised at the TJs, and these were dysfunctional as shown by permeability to biotin. Following hormone treatment, TJs were structurally and functionally competent, demonstrating that gonadotrophins also regulate the formation of TJs in vivo. The fourth study subsequently analysed TJs in gonadotrophin suppressed men, and it was found that claudin-11 staining was reduced from continuous bands in control men, to punctate staining in gonadotrophin-suppressed men, demonstrating that gonadotrophins also regulate the localisation of claudin-11 to the TJ in men in vivo. In summary, it is concluded that the Sertoli cell TJ is hormonally regulated, and that the major contributors to TJ function in vivo and in vitro are claudin-11 and occludin. It is hypothesised that the reduction of claudin-11 localisation to the TJ in men may also result in a loss of human Sertoli cell TJ function, suggesting that the TJ may be a potential target of hormonal contraception in men.

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8

Klein, Ryan Reaves Thakker Dhiren R. "Regulation of tight junction barrier function by phospholipase C." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2007. http://dc.lib.unc.edu/u?/etd,1380.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2007.
Title from electronic title page (viewed Apr. 25, 2008). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the School of Pharmacy." Discipline: Pharmacy; Department/School: Pharmacy.

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9

Bryant, Christopher. "Modulation of tight junction composition by the ERK pathway." Thesis, University of Bath, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.659138.

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Epithelia are an essential organising feature of multicellular organisms and the selective permeability of these barriers is regulated by the junctional repertoire of tight junction proteins. The regulation of epithelial permeability is essential for the physiological function of various organs and is often pathologically deregulated, for example in inflammatory disease and cancer. Tight junctions are dynamically regulated in response to diverse stimuli through multiple signalling pathways. The RAF/MEK/ERK pathway has been reported to mediate junctional remodelling in response to various growth factors and hormones, although the unique contribution of this pathway and the mechanisms of reorganisation remain unclear. To address this, specific activation of the RAF/MEK/ERK pathway was achieved through the expression of BRAFWT or oncogenic BRAFV600E in Madin-Darby Canine Kidney (MDCK) II cells, a model epithelial cell line used to study tight junctions. Specific activation of the RAF/MEK/ERK pathway generated a transient increase in transepithelial resistance, which occurred concurrently with the differential regulation of tight junction protein expression levels and subcellular distribution. Claudin-2 protein levels were decreased, while junctional levels of claudin-4 were increased. Total levels of claudin-1, occludin and ZO-1 were unchanged and were retained at areas of cell contact although showing varying degrees of cytoplasmic accumulation. Conditionally active CRAF:ER fusion proteins were expressed to provide increased control of RAF/MEK/ERK signal duration and to study the rates of TJ protein synthesis, degradation and localisation. RAF-mediated downregulation of CLDN2 mRNA caused subsequent claudin-2 protein depletion without influencing rates of internalisation or degradation. In contrast, RAF activation caused the redistribution of claudin-1 and -4 from the lateral membrane to the apical junction. This junctional accumulation could not be attributed to changes in claudin protein levels, stability or endocytic trafficking. Taken together, these data reveal surprising diversity in RAF/MEK/ERK-mediated TJ control, where distinct combinations of claudin-specific regulatory mechanisms act in concert to regulate epithelial permeability.

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10

Tavalali, Shida. "Analyse der Genexpression von Tight-junction-Proteinen der Claudin-Genfamilie." [S.l.] : [s.n.], 2005. http://www.diss.fu-berlin.de/2005/23/index.html.

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11

Zhu, Yihong. "Tight junction in ovarian surface epithelium and epithelial ovarian tumors /." Göteborg : Department of Obstetrics and Gynecology, Institute of Clinical Sciences, Sahlgrenska University Hospital, The Sahlgrenska Academy at Göteborg University, 2007. http://hdl.handle.net/2077/3167.

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12

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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13

Staat, Christian [Verfasser]. "Claudin-Peptide zur Modulation der tight junction-Dichtheit / Christian Staat." Berlin : Freie Universität Berlin, 2015. http://d-nb.info/1080171142/34.

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14

XIE, JIANZHEN. "Analysis of Xenopus laevis claudin (Xcla) tight junction genes in development." NCSU, 2005. http://www.lib.ncsu.edu/theses/available/etd-04272005-222011/.

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Eight Xenopus laevis claudin genes, Xcla1, Xcla4B, Xcla5, Xcla6, Xcla12, Xcla16, Xcla18 and Xcla19, were cloned and sequenced. Their normal mRNA expression was determined from cleavage stage to tadpole stage by whole mount in situ hybridization. The protein expression of Xcla5 was detected at the neural stage by whole mount immunostaining. Overexpression of Xcla5 by injection of synthetic mRNA into embryos caused morphological defects similar to those in embryos exposed to Bisphenol A (BPA). Altered patterns of claudin gene expression in the presence of BPA can be correlated with these developmental defects. The results suggest that claudins may play an important role in neural crest cell migration, epithelial-mesenchymal transition and ultimately organogenesis during embryonic development.

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15

Gehne, Nora [Verfasser]. "Untersuchungen zu Endozytose und Interaktionen von Tight Junction Proteinen / Nora Gehne." Berlin : Freie Universität Berlin, 2017. http://d-nb.info/1140761307/34.

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16

Fuller, Emily Jane. "Yeast mediated modulation of epithelial tight junction opening for drug delivery." Thesis, University of Leeds, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434753.

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17

Nowak, Rachael L. "Expression of tight junction protein ZO-2 in mouse preimplantation embryos." Thesis, University of Southampton, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310747.

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18

Krug, Susanne M. [Verfasser]. "Tight Junction-Proteine als regulierbare Kanal- und Barrierebildner / Susanne M. Krug." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2016. http://d-nb.info/1082237841/34.

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19

Pond, Emma. "Characterisation of tight junctions in polymorphic light eruption." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/characterisation-of-tight-junctions-in-polymorphic-light-eruption(8d043c3d-7f97-41e1-9b87-9523c5b639d6).html.

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Polymorphic light eruption (PLE) is the most common photodermatosis, affecting ~17% of the population. PLE is a delayed-type hypersensitivity response to an antigen induced by solar ultra-violet radiation (UVR). Its effects vary between patients, but the main symptom is a non-scarring, red papular rash in areas exposed to UVR. An effective therapy is low dose ultra-violet B (NBUVB) phototherapy. It is thought that NBUVB phototherapy desensitises the skin to further UVR exposure, but the mechanism by which this happens is unknown. Current immune based studies have been unable to clarify a mechanism as to how PLE arises. However, research in other skin diseases, such as psoriasis and atopic dermatitis, has shown that the barrier function of the skin is compromised by these disorders. Furthermore, research in lesional PLE skin showed an increase in barrier permeability of the skin. Recent research has specifically linked claudin proteins of tight junctions to the barrier dysfunction. Therefore, this study used quantitative immunofluorescent staining to measure tight junction (TJ) proteins and other barrier proteins of interest. Barrier function was also measured by transepidermal water loss (TEWL); a tracer dye penetration assay was used to measure TJ barrier function specifically. All measurements were made in non-lesional PLE skin, as compared to skin from healthy human volunteers. In photoprotected PLE skin the TJ protein claudin-1 was significantly reduced compared to healthy skin. The use of a tracer dye highlighted there was a reduction in TJ barrier function in PLE skin compared to healthy individuals. PLE and healthy skin were then exposed to ultra-violet B (UVB) and 24h later TJ proteins and TJ barrier function were measured. There was no change to claudin-1 after UVB exposure in PLE skin, but claudin-7 was reduced and claudin-12 increased. In contrast, in UVB-irradiated skin in normal controls after UVB exposure claudin-7 and claudin-12 were both increased, whilst claudin-1 was reduced. In PLE patients there was no further change to TJ barrier function, however, in normal controls, skin TJ barrier function was reduced post UVB. Both in healthy and PLE skin TEWL was unchanged before and after UVB exposure. Lastly TJ proteins were investigated after NBUVB in PLE patients. There was a further reduction in claudin-1 in PLE patients as well as a reduction in the TJ protein occludin, however the stratum corneum was significantly thickened. It could be suggested that this is a compensatory measure for the reduction seen in TJ barrier proteins, however further studies are needed to understand this. These data show significant differences in the TJ skin barrier in patients with PLE as compared to healthy human volunteers before and after UVB exposure. Furthermore, in PLE skin there is a significant change to the epidermis after NBUVB phototherapy. These data demonstrate that TJ protein expression and function is altered in PLE skin and may contribute to aetiology of the disorder, however the role of TJ barrier in aetiology is yet to be firmly established.

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20

Springmann, Gunja. "Beitrag und Regulation der Tight Junctions zur Schutzfunktion der epidermalen Hautbarriere /." [S.l. : s.n.], 2005. http://www.gbv.de/dms/bs/toc/502252553.pdf.

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21

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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22

Westphal, Julie Katharina [Verfasser]. "Struktur, Funktion und Regulation des Tight Junction-Proteins Tricellulin / Julie Katharina Westphal." Berlin : Freie Universität Berlin, 2012. http://d-nb.info/1026991358/34.

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23

Plain, Reyes Allein [Verfasser]. "Regulation of the tight junction permeabilities in the TAL / Allein Plain Reyes." Kiel : Universitätsbibliothek Kiel, 2016. http://d-nb.info/1081077557/34.

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24

Steed, E. "Functional analysis of MarvelD3, a novel transmembrane protein of the tight junction." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1339144/.

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Tight junctions are an intercellular adhesion complex of epithelial and endothelial cells. They form a paracellular diffusion barrier and interact with a network of intracellular signalling mechanisms that control junction function, gene expression and cell behaviour. Tight junctions are formed by multiprotein complexes containing cytosolic and transmembrane proteins. In this thesis I have identified a novel fourpass transmembrane protein of the tight junction called MarvelD3 and begun to analyse its function in the regulation of intracellular signalling pathways from the junction. There are two isoforms of MarvelD3, both of which show a broad tissue distribution and are expressed in different types of epithelial and endothelial cells. MarvelD3 co-localises with occludin at the tight junction in epithelial cells. I have found that MarvelD3 is not necessary for junction formation, but may have a role in the regulation of ion conductance properties of the tight junction. Functional analyses combining loss- and gain-of-function approaches in epithelial cell lines have further identified a role for MarvelD3 in the regulation of cell proliferation, migration and the cellular response to hyperosmotic shock. MarvelD3 expression regulates levels of active c-Jun N-terminal kinase (JNK) and AP1 signalling, possibly via an interaction between its N-terminus and the MAP kinase kinase kinase MEKK1. I have also shown MarvelD3 to be implicated in regulation of the actin cytoskeleton, affecting leading edge formation in migrating cells and cytoskeletal rearrangements in response to hyperosmotic shock. I will also describe some initial studies conducted in Xenopus laevis embryos in which depletion of Xenopus MarvelD3 by morpholino injection results in curvature of the anterioposterior axis and reduced pigmentation, possibly resulting from a defect in neural crest cell migration.

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25

Conrad, Marcel [Verfasser]. "Charakterisierung der kanalbildenden Eigenschaften des Tight Junction-Proteins Claudin-17 / Marcel Conrad." Berlin : Freie Universität Berlin, 2014. http://d-nb.info/1052222188/34.

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26

Piontek, Jörg [Verfasser]. "Molekulare Organisation Claudin-basierter Tight Junction-Stränge und deren Modulation / Jörg Piontek." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2016. http://d-nb.info/1108271030/34.

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27

Allen, Hilary Kaye. "The Effects of Enteropathogenic and Commensal Escherichia coli on Tight Junction Permeability." Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1341611861.

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28

Wrede, Esther Johanna [Verfasser]. "Tight-Junction-Proteine als Regulatoren der Permeabilität des Perineuriums / Esther Johanna Wrede." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2011. http://d-nb.info/1025355601/34.

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29

Milatz, Susanne. "Funktionelle Charakterisierung des Tight Junction-Proteins Claudin-3 in Epithel- und Endothelzellen." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2011. http://dx.doi.org/10.18452/16293.

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Die Tight Junction (TJ) reguliert den parazellulären Transport von Ionen, Wasser und Soluten an Epithelien und Endothelien und ist von entscheidender Bedeutung für die Aufrechterhaltung der Funktion von Organen und Geweben. Obwohl Claudin-3 zu den zuerst identifizierten und ubiquitär exprimierten Komponenten der TJ gehört, konnte seine spezifische Funktion bislang nicht geklärt werden. Für die funktionelle Charakterisierung des humanen Claudin-3-Proteins wurden stabile Überexpressionsklone der lecken Nierenepithel-Zelllinie MDCK II generiert. Die Überexpression von Claudin-3 führte zu einer deutlichen Änderung des TJ-Strangmusters sowie zu einer starken Zunahme des transepithelialen Widerstandes und einer verminderten Permeabilität für Ionen und Moleküle der Größe 332 Da und 4000 Da. Der parazelluläre Durchtritt von Wasser war unverändert. Claudin-3 konnte eindeutig als abdichtende Komponente der TJ identifiziert werden. Anhand des endothelialen Zellkulturmodells HUVEC wurden Expression und Regulation von Claudin-3 und anderen TJ-Proteinen unter dem Einfluss mechanischer Strömungsverhältnisse und des Sauerstoffpartialdrucks analysiert. Die Behandlung mit fehlender Wandschubspannung führte zur Hochregulation der abdichtenden TJ-Proteine Occludin, Claudin-3, Claudin-5 und Claudin-11, nicht aber Claudin-23. Die Regulation der einzelnen TJ-Komponenten wurde durch unterschiedliche Signalwege vermittelt, wobei der verstärkten Proteinexpression jeweils eine Hochregulation auf mRNA-Ebene zugrunde lag. Die kombinierte Behandlung mit fehlender Wandschubspannung und Hypoxie resultierte in einer sehr stark erhöhten Expression von Claudin-3. Durch die Hochregulation abdichtender TJ-Komponenten unter Bedingungen fehlender Wandschubspannung und Hypoxie, wie sie in verschiedenen physiologischen und pathologischen Situationen auftreten, könnte einem unerwünschten Durchtritt von Substanzen aus dem Blut in das umliegende Gewebe vorgebeugt werden.
The tight junction (TJ) regulates the paracellular transport of ions, water and solutes in epithelia and endothelia and is of particular importance for a correct function of organs and tissues. Although claudin-3 is one of the first identified and ubiquitously expressed TJ components, its specific function was unsolved as yet. For functional characterization, human claudin-3 was stably overexpressed in the leaky epithelial cell line MDCK II. Overexpression of claudin-3 led to a marked alteration of TJ meshwork pattern, a strong increase in transepithelial resistance and a decrease in permeability for ions and paracellular tracers (332 or 4000 Da). Paracellular water transport was not affected. It was proved that claudin-3 acts as a „tightening“ TJ component. The endothelial cell culture model HUVEC was used for analysis of expression and regulation of claudin-3 and several other TJ proteins under different conditions of wall shear stress and oxygen saturation. Treatment with lacking wall shear stress led to an upregulation of the “tightening” TJ proteins occludin, claudin-3, claudin-5, and claudin-11, but not claudin-23. Upregulation of all proteins was due to increased mRNA levels. Apparently, different signaling pathways were involved in regulation of particular TJ components. Combined treatment with lacking shear stress and hypoxia resulted in drastically increased claudin-3 expression. Upregulation of tightening TJ components under lacking shear stress and hypoxic conditions as occuring in different physiological or pathological situations would limit the passage of solutes from the blood into the surrounding tissue.

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Larivière, Nathalie. "Integral Roles for the Tight Junction Protein Claudin-6 in Regulating Epidermal Homeostasis." Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/30650.

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Forming and maintaining an intact epidermal permeability barrier (EPB) is necessary to mammalian health and dysregulation of this process can result in serious complications. Tight junctions (TJs) and their integral proteins the Claudins (Cldns) have both structural and signaling importance to the skin barrier and the latter is most likely mediated via Cldn tail interaction with cytoplasmic proteins. Given that the family member Cldn6 is known to be important to EPB function, we set out to determine the contribution of its cytoplasmic tail domain to TJ-mediated homoeostasis. Using transgenic mouse models, we overexpressed epidermal-targeted tail truncation mutants and assessed EPB formation and maintenance. We then used yeast 2-hybrid and quantitative proteomic approaches to identify proteins that interact with this tail region and to assess the downstream effects of overexpressing these proteins in human keratinocytes in culture. We demonstrate that a 10 amino acid region in the cytoplasmic tail is required for efficient epidermal maturation and injury repair and that our mouse models may be applicable to postnatal epidermal maturation and human skin aging studies. We show that in addition to the known interacting partner ZO1, the C-terminal tail of Cldn6 also binds FIZ1 (Flt3 interacting zinc finger protein-1), which we characterize for the first time as a mitogenic factor for keratinocytes. FIZ1 stimulates autocrine pathways involving secreted heparin-binding factors IGFBP3 and DKK1, sensitization to IGF signaling, MAP/ERK activation and increased G1 progression. Specific transcription factors, protein kinases and signaling scaffolds that we identified as novel FIZ1-binding partners likely mediate this signaling. Our studies on the Cldn6 cytoplasmic tail support the importance of this region for epidermal maturation and for maintenance of skin homeostasis throughout life. They also delineate the potential for tail interactors such as ZO1 and FIZ1 to act in concert with Cldns in TJ-based signaling networks to regulate the balance between proliferation and differentiation in keratinocytes. These findings provide new insight into the role of the Cldn6 cytoplasmic tail and will ultimately aid in the development of new diagnostic tools and therapeutic approaches for the treatment of skin conditions rooted in barrier defects.

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Dithmer, Sophie [Verfasser]. "Untersuchungen zu Tight-Junction-relevanten Claudinen zur gezielten Modulation zellulärer Barrieren / Sophie Dithmer." Halle, 2018. http://d-nb.info/118109738X/34.

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Schwabe, Joachim [Verfasser], H. [Gutachter] Rittner, and R. [Gutachter] Martini. "Tight Junction Proteine in schmerzhaften Neuropathien / Joachim Schwabe ; Gutachter: H. Rittner, R. Martini." Würzburg : Universität Würzburg, 2019. http://d-nb.info/1187661481/34.

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33

Cording, Jimmi David [Verfasser]. "Interaction, Function and Regulation of the Tight Junction Protein Tricellulin / Jimmi David Cording." Berlin : Freie Universität Berlin, 2016. http://d-nb.info/1081367121/34.

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Hu, Jiachen [Verfasser]. "Angulins and the Tricellular Tight Junction: Role in Inflammatory Bowel Diseases / Jiachen Hu." Berlin : Freie Universität Berlin, 2021. http://d-nb.info/1232726494/34.

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35

Masuda, Sayuri. "Angulin/LSR defines cell corners for tricellular tight junction formation in epithelial cells." Kyoto University, 2011. http://hdl.handle.net/2433/142056.

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36

Morita, Kazumasa. "Claudin multigene family encoding four-transmembrane domain protein components of tight junction strands." Kyoto University, 1999. http://hdl.handle.net/2433/181737.

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37

Mahn, Michaela [Verfasser]. "Charakterisierung von Tight-Junction-Proteinen mit Hilfe eukaryontischer und prokaryontischer Expressionssysteme / Michaela Mahn." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2009. http://d-nb.info/102381661X/34.

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38

Lohrberg, Dörte. "Untersuchungen zur affinitäts-basierten Aufreinigung von tight junction-proteinen und deren potentiellen Interaktionspartnern." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2009. http://dx.doi.org/10.18452/15903.

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Die Epithelien vielzelliger Organismen bilden eine funktionelle Grenzschicht, die für die Homöostase innerhalb und für den spezifischen Stoffaustausch zwischen den Kompartimenten verantwortlich ist. Der interzelluläre Spalt zwischen Epithelzellen wird durch tight junctions verschlossen, die eine selektive Permeabilitätsbarriere bilden. Da viele Krankheiten auf eine Dysfunktion der Barriere zurückzuführen sind, ist eine genaue Kenntnis der molekularen Zusammensetzung der tight junctions aus pharmakologischer Sicht von großem Interesse. In dieser Arbeit wurden Anreicherungsstrategien entwickelt, die eine Proteomanalyse der tight junction-Proteine erlauben. Der Fokus wurde dabei auf die Claudine und Tricellulin gelegt, die als transmembranale Proteine das molekulare Rückgrat der tight junctions bilden. Durch Affinitätsreinigung gelang erstmals eine Anreicherung verschiedener Claudine, die durch Massenspektrometrie identifiziert wurden. Die metabolische Markierung der Proteine mit stabilen Isotopen (SILAC) erlaubte die quantitative Diskriminierung von Proteinen, die unspezifisch an das Matrixmaterial banden. Von den potentiellen Interaktionspartnern der Claudine wurden Integrin-a3, SUMO-1 und Sphingosinkinase 2 ausgewählt, um deren Interaktion mit Claudinen weiter zu verifizieren. Es wurden keine Hinweise auf Wechselwirkungen zwischen Claudinen und Integrin-a3 sowie SUMO-1 gefunden, während die Interaktion von Claudinen mit Sphingosinkinase 2 weder bestätigt noch ausgeschlossen werden konnte. Ferner wurde eine Affinitätsreinigung durchgeführt, um Interaktionspartner von Tricellulin anzureichern. Durch die quantitative massenspektrometrische Analyse wurde ausschließlich Claudin-4 nicht aber Claudin-3 und 7 als potentieller, spezifischer Interaktionspartner von Tricellulin identifiziert. Es wurde aber gezeigt, dass die Kombination aus Affinitätsreinigung und quantitativer Massenspektrometrie einen wertvollen Beitrag zur Entschlüsselung von Protein-Komplexen leisten kann.
Epithelia function as specialized barriers that separate different compartments within multicellular organisms and regulate the specific exchange of substances between them. The intercellular space between adjacent epithelial cells is sealed by tight junctions forming a permeability barrier. Dysregulation of the barrier occurs in a variety of diseases. Hence, a deeper knowledge is required of the molecular composition of tight junctions, in particular with respect to pharmacological applications. In the present study, new enrichment strategies have been established that allow the proteomic analysis of tight junction proteins. Special emphasis was placed on claudins and tricellulin as these transmembrane proteins constitute the molecular backbone of the tight junctions. For the first time, using an affinity purification, the enrichment of several claudins was accomplished that were identified by mass spectrometry. The metabolic labeling of proteins with stable isotopes (SILAC) allowed the quantitative discrimination of proteins that bound unspecifically to the matrix. Integrin-a3, SUMO 1 and sphingosin kinase 2 were chosen for further verifications from the proteins considered to potentially interact with claudins. While there was no evidence for an association of claudins with integrin-a3 and SUMO-1, an interaction of claudins with sphingosin kinase 2 could be neither confirmed nor disproved. Furthermore, an affinity purification was performed in order to enrich interaction partners of tricellulin. Claudin-4 was identified as a specific, potential interaction partner of tricellulin by quantitative mass spectrometric analysis whereas claudin 3 and -7 were determined to be enriched unspecifically. The present study demonstrates that a combination of affinity purification and quantitative mass spectrometry can substantially contribute to the elucidation of protein complexes.

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Aurbek, Nadine. "Expression, Regulation und subzelluläre Lokalisation von Tight-junction-Komponenten in Metastasierungsmodellen humaner duktaler Pankreaskarzinomzellen." München Verl. Dr. Hut, 2008. http://d-nb.info/989216802/04.

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40

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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41

Krug, Susanne M. [Verfasser]. "Tricellulin und seine Funktion in der trizellulären Tight Junction von Epithelzellen / Susanne M. Krug." Berlin : Freie Universität Berlin, 2009. http://d-nb.info/1023818078/34.

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42

Kondo, Nobuyuki. "Thrombin induces rapid disassembly of claudin-5 from the tight junction of endothelial cells." Kyoto University, 2010. http://hdl.handle.net/2433/120612.

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43

Beeman, Neal Edward. "Disruption of the tight junction in cultured epithelia stimulates apoptosis concurrent with cellular extrusion /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2008. http://proquest.umi.com/pqdweb?did=1545957671&sid=2&Fmt=6&clientId=18952&RQT=309&VName=PQD.

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Thesis (Ph.D. in Physiology and Biophysics) -- University of Colorado Denver, 2008.
Typescript. Includes bibliographical references (leaves 89-98). Free to UCD Anschutz Medical Campus. Online version available via ProQuest Digital Dissertations;

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44

Aaku-Saraste, E. (Eeva). "A prelude to neurogenesis." Doctoral thesis, University of Oulu, 1999. http://urn.fi/urn:isbn:9514253655.

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Abstract All neurons and macroglial cells of vertebrates derive from the neuroepithelium. Neuroepithelial (NE) cells first proliferate and, after closure of the neural tube, some cells start generating neurons. It is still unclear what triggers differentiation but apparently there is interplay between extrinsic (secreted or transmembrane signals) and intrinsic factors. Diriving from the embryonic ectoderm, the NE cells inherit epithelial characteristics. It has been shown in other developmental systems that epithelial determinants, such as cell-cell contacts and contact to basal laminar components can guide differentiation. The key epithelial features include cell polarity, and tight junctions. We studied these in the NE at two developmental stages, the neural plate, a proliferative stage and the neural tube, a differentiative stage. The polarity of membrane proteins in NE cells was studied with polarly budding viruses. Mouse embryos were infected with Fowl plague- and vesicular stomatitis viruses and cultured in a whole embryo culture system. Viral envelope proteins (HA and G-protein) were localized by indirect immunofluorescence and immunoelectron microscopy. HA was polarized in the plate stage neuroepithelial cells, whereas in the tube it was not polarized anymore. It is also shown by penetrance of apically injected horseradish peroxidase that in the neural plate, NE cells have functional tight junctions. At this stage, they also express occludin, a transmembrane protein of tight junctions, as shown by indirect immunofluorescence. In the neural tube, the paracellular barrier is lost and there is no occludin expression. In contrast, expression of ZO-1, a cytoplasmic protein binding to occiudin, is upregulated. The downregulation of these epithelial features occurs in all NE cells, irrespective of their mode of division and before any neurons are generated in the NE. The change is initiated already at the plate stage and coincides with the switch from E- to N-cadherin. Later, with birth of neurons, the proliferative cell layer also looses contact to basal lamina. This is probably an important step in the regulation of neurogenesis. Furthermore, lack of apico-basolateral polarity of non-anchored membrane proteins may contribute to the mechanism of rapid neuron generation. Until now, it has been impossible to distinguish a neuroepithelial cell preparing for neuron generation from the surrounding cells that give rise to two precursor cells. In this study, the immediate neuron precursors are shown to express the antiproliferative gene TIS2 1. Using this new marker and ISH in serial sections, we show that the switch to differentiation is initiated in single NE cells.

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45

Bello, I. O. (Ibrahim O. ). "Tight junction proteins and cancer-associated fibroblasts in ameloblastoma, ameloblastic carcinoma and mobile tongue cancer." Doctoral thesis, University of Oulu, 2010. http://urn.fi/urn:isbn:9789514260834.

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Abstract Squamous cell carcinoma (SCC) of the mobile tongue is the most common type of cancer of the oral cavity, accounting for 30-40% of oral cancers. It behaves aggressively and almost half of the affected patients still die of the disease despite great advances in its medical and surgical care. Ameloblastomas are the most common clinically significant type of odontogenic tumors, constituting approximately 1% of all cysts and tumors of the jaw. They are benign but locally invasive tumors with a strong tendency to recur after surgery. Ameloblastic carcinoma combines the histological features of ameloblastoma with cytologic atypia irrespective of the presence or absence of metastasis. The effectiveness of tight junction proteins (claudins 1, 4, 5, 7 and occludin) and cancer-associated fibroblasts (CAFs) as prognostic markers in OTSCC and as markers of malignancy in ameloblastomas was studied. Abundance of CAFs and Claudin 7 derangement was found to be associated with poor disease-specific survival in oral (mobile) tongue cancer. Appearance of CAFs within the epithelial islands of ameloblastoma was found to be a marker of malignancy in the tumor. The prognostic predictability of CAF density, Ki-67 (cell proliferation marker), maspin (tumor suppressor marker) and tumor DNA content (tumor ploidy using image cytometry) in tongue cancers was also tested. CAF density was the only marker strongly predictive of prognosis. In ameloblastomas, α-SMA (for CAFs), Ki-67, epithelial membrane antigen (EMA) and DNA content (using image and flow cytometry) were assessed as markers of ameloblastic carcinoma. Only α-SMA was able to predict ameloblastic carcinoma when found in the epithelial islands. In conclusion, staining for α-SMA and claudin 7 seems to be beneficial for prognostication in tongue cancer, while α-SMA staining may be beneficial in differentiating ameloblastoma from ameloblastic carcinoma.

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46

Stier, Alexander [Verfasser]. "Messung des Wassertransportes an einer Nierenzelllinie : Rolle des Tight Junction-Proteins Claudin-6 / Alexander Stier." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/1042440972/34.

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47

Haddad, Nicholas. "The role of tight junction proteins claudin-3 and claudin-7 in ureteric bud branching." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66666.

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The claudin family of proteins is required for the formation of tight junctions between epithelial cells. Tight junctions form uninterrupted paracellular barriers on the apical surface linking adjacent epithelial cells. As a result, they promote cell-cell adhesion and regulate the paracellular flow of soluble ions. During kidney development, an epithelial outgrowth of the nephric duct called the ureteric bud (UB) emerges and invades the neighboring metanephric mesenchyme where it undergoes a series of branching events in a process known as branching morphogenesis. It has been shown that claudin-3 (Cldn3) and claudin-7 (Cldn7) transcripts are upregulated in the ureteric bud (UB) versus the metanephric mesenchyme (MM) during kidney development. We hypothesize that if Cldn3 and Cldn7 form tight junctions in the epithelial UB, they will determine the pattern of UB branching. Using transmission electron microscopy, we have established that tight junctions are situated between epithelial cells of the UB that undergo branching. Whole-mount in situ hybridization assays established that Cldn3 and Cldn7 transcripts are expressed in the UB at embryonic day (E)10.5, 13.5 and 16.5. Double immunofluorescence experiments revealed that CLDN3 is localized to tight junctions at the apical domain of UB cells, while CLDN7 is predominately expressed on the basolateral membrane. To determine the functional role of these claudins, we took advantage of the mIMCD-3 cell culture model of tubulogenesis. The mIMCD-3 cell line is derived from the embryonic UB, and when placed in a type-I collagen matrix these cells undergo tubulogenesis and branching in a manner morphologically similar to the UB. Double immunofluorescence and Z-stacking showed that mIMCD-3 cells express both CLDN3 and CLDN7 at the tight junction. Stable cell lines expressing either CLDN3 or CLDN7 fused at the N-terminus to the red fluorescent protein (RFP) mCherry w
La famille de protéines claudine est nécessaire pour la formation des jonctions serrées entre les cellules épithéliales. Les jonctions serrées forment des obstacles paracellulaires ininterrompus sur la surface apicale entre les cellules épithéliales adjacentes. En conséquence, ils favorisent l'adhérence cellule-cellule et régularisent le transport des ions solubles paracellulaire. Au cours du développement du rein, une excroissance épithéliale du canal nephric appelée urétérale bourgeon (UB) se dégage et envahit le mésenchyme métanephrique (MM) voisins où il subit une série de manifestations de branchement dans un processus connu sous le nom de la morphogenèse de ramification. Il a été démontré que claudin-3 et claudin-7 transcriptions sont augmentées dans l'UB par rapport au MM au cours du développement du rein. Nous faisons l'hypothèse que, si Cldn3 et Cldn7 forment les jonctions serrées dans l'épithéliales UB, ils détermineront le type de ramification UB.En utilisant la microscopie électronique en transmission, nous avons établi que des jonctions serrées sont situés entre les cellules épithéliales de l'UB qui subissent ramification. L'hybridation in situ établi que claudin-3 et claudin-7 sont exprimés en UB à jour embryonnaire (E) 10,5, 13,5 et 16,5. Double immunofluorescence a révélée que la protéine Cldn3 est localisée à des jonctions serrées au domaine apical de l'UB, tandis que Cldn7 est surtout exprimé sur la membrane basolatérale. Pour déterminer le rôle fonctionnel de ces claudins, nous avons profité de la mIMCD-3 modèle de la culture cellulaire de la formation de tubules. Le mIMCD-3 lignée cellulaire est issue de l'embryon de UB, et lorsqu'il est placé dans un type-I matrice collagène, ces cellules commence à former des tubules et une ramification d'une manière morphologiquement semblables à l'UB. Double immunofluorescence et des

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48

Lentfer, Janina Stephanie [Verfasser], and Ingrid [Akademischer Betreuer] Moll. "Regulation von Tight Junction Proteinen in der kutanen Wundheilung / Janina Stephanie Lentfer. Betreuer: Ingrid Moll." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2012. http://d-nb.info/1027574319/34.

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49

Bellmann, Christian [Verfasser]. "Struktur und Funktion des tight junction-Proteins Occludin unter normoxischen und hypoxischen Bedingungen / Christian Bellmann." Berlin : Freie Universität Berlin, 2014. http://d-nb.info/1052020844/34.

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50

Lentfer, Janina Stephanie Verfasser], and Ingrid [Akademischer Betreuer] [Moll. "Regulation von Tight Junction Proteinen in der kutanen Wundheilung / Janina Stephanie Lentfer. Betreuer: Ingrid Moll." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2012. http://nbn-resolving.de/urn:nbn:de:gbv:18-59047.

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