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Nakamura, N., J. Tanaka e K. Sobue. "Rous sarcoma virus-transformed cells develop peculiar adhesive structures along the cell periphery". Journal of Cell Science 106, n. 4 (1 dicembre 1993): 1057–69. http://dx.doi.org/10.1242/jcs.106.4.1057.
Alteration of the cell/substratum adhesive structures of rat fibroblasts (3Y1 cells) upon transformation by Rous sarcoma virus (RSV) was investigated by immunofluorescence microscopy. In serum-containing culture medium, 3Y1 cells developed focal adhesions as their main adhesive structures, while BY1 cells expressed peculiar close contacts along the cell periphery with the vitronectin receptor integrin, in addition to podosomes. These peripheral close contacts are referred to as the peripheral adhesions. The peripheral adhesions were observed as a darker region than podosomes by interference reflection microscopy. They were more easily destroyed by incubating the cells with RGD-containing peptide than were the focal adhesions. In contrast to focal adhesions and podosomes, actin bundles were not detected within the peripheral adhesions, where pp60v-src and tyrosine-phosphorylated proteins accumulated. Expression of the integrin was determined by the substratum composition when BY1 cells were cultured in serum-free culture medium. Under such conditions, BY1 cells expressed the peripheral adhesions within 3 hours on adhesion molecule-coated glass. On the other hand, in serum-containing medium, they first developed focal adhesions transiently at their early stage of adhesion, and then the peripheral adhesions were predominantly expressed within 12 hours. Podosomes were formed in a time course similar to that of the peripheral adhesions. These findings suggest that the peripheral adhesion is a class of stable adhesive structure distinct from the focal adhesion or podosome of BY1 cells. Similar close contact-type peripheral adhesions with the integrin were also observed in a variety of cultured cells such as normal fibroblasts at their logarithmic growth phase, phorbol ester-treated fibroblasts, and several malignant tumor cells, with poorly organized focal adhesions and stress fibers. These findings further suggest that the peripheral adhesions may be widely involved in the adhesion of cells that inadequately develop stress fibers and focal adhesions.
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Lipke, Peter N., Jason M. Rauceo e Albertus Viljoen. "Cell–Cell Mating Interactions: Overview and Potential of Single-Cell Force Spectroscopy". International Journal of Molecular Sciences 23, n. 3 (20 gennaio 2022): 1110. http://dx.doi.org/10.3390/ijms23031110.
It is an understatement that mating and DNA transfer are key events for living organisms. Among the traits needed to facilitate mating, cell adhesion between gametes is a universal requirement. Thus, there should be specific properties for the adhesion proteins involved in mating. Biochemical and biophysical studies have revealed structural information about mating adhesins, as well as their specificities and affinities, leading to some ideas about these specialized adhesion proteins. Recently, single-cell force spectroscopy (SCFS) has added important findings. In SCFS, mating cells are brought into contact in an atomic force microscope (AFM), and the adhesive forces are monitored through the course of mating. The results have shown some remarkable characteristics of mating adhesins and add knowledge about the design and evolution of mating adhesins.
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Katoh, Kazuo. "FAK-Dependent Cell Motility and Cell Elongation". Cells 9, n. 1 (12 gennaio 2020): 192. http://dx.doi.org/10.3390/cells9010192.
Fibroblastic cells show specific substrate selectivity for typical cell–substrate adhesion. However, focal adhesion kinase (FAK) contributes to controlling the regulation of orientation and polarity. When fibroblasts attach to micropatterns, tyrosine-phosphorylated proteins and FAK are both detected along the inner border between the adhesive micropatterns and the nonadhesive glass surface. FAK likely plays important roles in regulation of cell adhesion to the substrate, as FAK is a tyrosine-phosphorylated protein that acts as a signal transduction molecule at sites of cell–substrate attachment, called focal adhesions. FAK has been suggested to play a role in the attachment of cells at adhesive micropatterns by affecting cell polarity. Therefore, the localization of FAK might play a key role in recognition of the border of the cell with the adhesive micropattern, thus regulating cell polarity and the cell axis. This review discusses the regulation and molecular mechanism of cell proliferation and cell elongation by FAK and its associated signal transduction proteins.
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Ventre, Maurizio, Carlo Fortunato Natale, Carmela Rianna e Paolo Antonio Netti. "Topographic cell instructive patterns to control cell adhesion, polarization and migration". Journal of The Royal Society Interface 11, n. 100 (6 novembre 2014): 20140687. http://dx.doi.org/10.1098/rsif.2014.0687.
Topographic patterns are known to affect cellular processes such as adhesion, migration and differentiation. However, the optimal way to deliver topographic signals to provide cells with precise instructions has not been defined yet. In this work, we hypothesize that topographic patterns may be able to control the sensing and adhesion machinery of cells when their interval features are tuned on the characteristic lengths of filopodial probing and focal adhesions (FAs). Features separated by distance beyond the length of filopodia cannot be readily perceived; therefore, the formation of new adhesions is discouraged. If, however, topographic features are separated by a distance within the reach of filopodia extension, cells can establish contact between adjacent topographic islands. In the latter case, cell adhesion and polarization rely upon the growth of FAs occurring on a specific length scale that depends on the chemical properties of the surface. Topographic patterns and chemical properties may interfere with the growth of FAs, thus making adhesions unstable. To test this hypothesis, we fabricated different micropatterned surfaces displaying feature dimensions and adhesive properties able to interfere with the filopodial sensing and the adhesion maturation, selectively. Our data demonstrate that it is possible to exert a potent control on cell adhesion, elongation and migration by tuning topographic features’ dimensions and surface chemistry.
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Young, Katherine A., Laura Biggins e Hayley J. Sharpe. "Protein tyrosine phosphatases in cell adhesion". Biochemical Journal 478, n. 5 (10 marzo 2021): 1061–83. http://dx.doi.org/10.1042/bcj20200511.
Adhesive structures between cells and with the surrounding matrix are essential for the development of multicellular organisms. In addition to providing mechanical integrity, they are key signalling centres providing feedback on the extracellular environment to the cell interior, and vice versa. During development, mitosis and repair, cell adhesions must undergo extensive remodelling. Post-translational modifications of proteins within these complexes serve as switches for activity. Tyrosine phosphorylation is an important modification in cell adhesion that is dynamically regulated by the protein tyrosine phosphatases (PTPs) and protein tyrosine kinases. Several PTPs are implicated in the assembly and maintenance of cell adhesions, however, their signalling functions remain poorly defined. The PTPs can act by directly dephosphorylating adhesive complex components or function as scaffolds. In this review, we will focus on human PTPs and discuss their individual roles in major adhesion complexes, as well as Hippo signalling. We have collated PTP interactome and cell adhesome datasets, which reveal extensive connections between PTPs and cell adhesions that are relatively unexplored. Finally, we reflect on the dysregulation of PTPs and cell adhesions in disease.
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Simmons, David L. "Dissecting the modes of interactions amongst cell adhesion molecules". Development 119, Supplement (1 dicembre 1993): 193–203. http://dx.doi.org/10.1242/dev.119.supplement.193.
The process of cell adhesion can be mediated by more than SO molecules. Fortunately, most of these can be grouped into a small number of super families. For example, more than half of all leukocyte adhesion molecules are members of the immunoglobulin super-family. The principles of cell-cell adhesion are reviewed including: kinetics and equilibria; on/off rates; affinities/avidities; homotypic/heterotypic interactions; mapping and delineation of binding sites. These principles are illustrated with two CAMs: firstly the interaction of the homotypic epithelial/myeloid adhesins CD66, and the endothelial adhesin, CD31, and secondly the heterotypic adhesins ICAM-1, 2 and 3, which interact with the leukocyte integrin LFA-1.
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Lotz, M. M., C. A. Burdsal, H. P. Erickson e D. R. McClay. "Cell adhesion to fibronectin and tenascin: quantitative measurements of initial binding and subsequent strengthening response." Journal of Cell Biology 109, n. 4 (1 ottobre 1989): 1795–805. http://dx.doi.org/10.1083/jcb.109.4.1795.
Cell-substratum adhesion strengths have been quantified using fibroblasts and glioma cells binding to two extracellular matrix proteins, fibronectin and tenascin. A centrifugal force-based adhesion assay was used for the adhesive strength measurements, and the corresponding morphology of the adhesions was visualized by interference reflection microscopy. The initial adhesions as measured at 4 degrees C were on the order of 10(-5)dynes/cell and did not involve the cytoskeleton. Adhesion to fibronectin after 15 min at 37 degrees C were more than an order of magnitude stronger; the strengthening response required cytoskeletal involvement. By contrast to the marked strengthening of adhesion to FN, adhesion to TN was unchanged or weakened after 15 min at 37 degrees C. The absolute strength of adhesion achieved varied according to protein and cell type. When a mixed substratum of fibronectin and tenascin was tested, the presence of tenascin was found to reduce the level of the strengthening of cell adhesion normally observed at 37 degrees C on a substratum of fibronectin alone. Parallel analysis of corresponding interference reflection micrographs showed that differences in the area of cell surface within 10-15 nm of the substratum correlated closely with each of the changes in adhesion observed: after incubation for 15 min on fibronectin at 37 degrees C, glioma cells increased their surface area within close contact to the substrate by integral to 125-fold. Cells on tenascin did not increase their surface area of contact. The increased surface area of contact and the inhibitory activity of cytochalasin b suggest that the adhesive "strengthening" in the 15 min after initial binding brings additional adhesion molecules into the adhesive site and couples the actin cytoskeleton to the adhesion complex.
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Mentzer, S. J., D. V. Faller e S. J. Burakoff. "Interferon-gamma induction of LFA-1-mediated homotypic adhesion of human monocytes." Journal of Immunology 137, n. 1 (1 luglio 1986): 108–13. http://dx.doi.org/10.4049/jimmunol.137.1.108.
Abstract Cell-cell adhesion plays an important role in monocyte function. To investigate the molecular basis for monocyte adhesion, we used recombinant interferon-gamma to induce the formation of homotypic monocyte adhesions. The induction of homotypic adhesions correlated with the increased expression of the LFA-1 membrane molecule. LFA-1 surface expression was increased twofold, whereas expression levels of other monocyte surface molecules including CR3 and p150,95 were unchanged. The direct involvement of LFA-1 in monocyte adhesion was addressed by anti-LFA-1 monoclonal antibody inhibition of homotypic adhesions. Two monoclonal antibodies to distinct epitopes on the LFA-1 alpha-chain completely inhibited homotypic adhesions. Antibodies to a variety of other monocyte surface molecules, often present at higher cell surface density than LFA-1, did not inhibit homotypic adhesion. A panel of monoclonal antibodies that recognized different functional epitopes on the LFA-1 alpha-chain inhibited homotypic monocyte in a hierarchy identical to that observed in previous studies of cell-mediated cytotoxicity. These findings suggest that LFA-1 serves an adhesive function for human mononuclear phagocytes. In addition to providing a molecular basis for homotypic monocyte adhesions, the results suggest a more general role for LFA-1 in monocyte adhesion reactions.
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Willaert, Ronnie G., Yeseren Kayacan e Bart Devreese. "The Flo Adhesin Family". Pathogens 10, n. 11 (28 ottobre 2021): 1397. http://dx.doi.org/10.3390/pathogens10111397.
The first step in the infection of fungal pathogens in humans is the adhesion of the pathogen to host tissue cells or abiotic surfaces such as catheters and implants. One of the main players involved in this are the expressed cell wall adhesins. Here, we review the Flo adhesin family and their involvement in the adhesion of these yeasts during human infections. Firstly, we redefined the Flo adhesin family based on the domain architectures that are present in the Flo adhesins and their functions, and set up a new classification of Flo adhesins. Next, the structure, function, and adhesion mechanisms of the Flo adhesins whose structure has been solved are discussed in detail. Finally, we identified from Pfam database datamining yeasts that could express Flo adhesins and are encountered in human infections and their adhesin architectures. These yeasts are discussed in relation to their adhesion characteristics and involvement in infections.
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Murphy-Ullrich, J. E., e M. Höök. "Thrombospondin modulates focal adhesions in endothelial cells." Journal of Cell Biology 109, n. 3 (1 settembre 1989): 1309–19. http://dx.doi.org/10.1083/jcb.109.3.1309.
We examined the effects of thrombospondin (TSP) in the substrate adhesion of bovine aortic endothelial cells. The protein was tested both as a substrate for cell adhesion and as a modulator of the later stages of the cell adhesive process. TSP substrates supported the attachment of some BAE cells, but not cell spreading or the formation of focal adhesion plaques. In contrast, cells seeded on fibrinogen or fibronectin substrates were able to complete the adhesive process, as indicated by the formation of focal adhesion plaques. Incubation of cells in suspension with soluble TSP before or at the time of seeding onto fibronectin substrates resulted in an inhibition of focal adhesion formation. Furthermore, the addition of TSP to fully adherent cells in situ or prespread on fibronectin substrates caused a reduction in the number of cells, which were positive for focal adhesions, although there was no significant effect on cell spreading. In a dose-dependent manner, TSP reduced the number of cells with adhesion plaques to approximately 60% of control levels. The distribution of remaining adhesion plaques in TSP-treated cells was also altered: plaques were primarily limited to the periphery of cells and were not present in the central cell body, as in control cells treated with BSA. The observed effects were specific for TSP and were not observed with platelet factor 4, beta-thromboglobulin, or fibronectin. The TSP-mediated loss of adhesion plaques was neutralized by the addition of heparin, fucoidan, other heparin-binding proteins, and by a monoclonal antibody to the heparin binding domain of TSP, but not by antibodies to the core or carboxy-terminal regions of TSP. The interaction of the heparin-binding domain of TSP with cell-associated heparan sulfate appears to be an important mechanistic component for this activity of TSP. These data indicate that TSP may have a role in destabilizing cell adhesion through prevention of focal adhesion formation and by loss of preformed focal adhesions.
Stewart, Alasdair Gwilym. "Studies of focal adhesion kinase in epithelial cells : involvement in cell-cell adhesion". Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1446839/.
Epithelial cell-cell adhesion is mediated by tight junctions, adherens junctions and desmosomes. Epithelial cell-matrix adhesion is mediated by hemidesmosomes and focal contacts. These complexes exhibit great plasticity, and each contains molecular components which are able to participate in one or more of the other adhesive complexes. Focal adhesion kinase (FAK/pl25FAK) is a non-receptor tyrosine kinase which transduces signals from integrins at sites of focal contact to promote adhesion, spreading and migration. FAK possesses a central kinase domain which is flanked by large, non-catalytic, amino- and carboxy-terminal domains. Whereas the functions of the carboxy-terminal and kinase domains of FAK are well understood, the role of the amino-terminal domain remains unclear. FAK expression was examined in the human epithelial cell line, HEK 293. Amino-terminal FAK immunoreactivity was noted at sites of cell-cell contacts and in the nucleus, in contrast to carboxy-terminal immunoreactivity, which was largely cytoplasmic and perinuclear. Western blot analysis of endogenous FAK revealed expression of a presumptive proteolytic cleavage fragment corresponding to the amino- terminal domain. A series of FAK constructs was generated to test the hypothesis that the observed amino-terminal FAK localisation was due to this proteolytic fragment. Epitope- tagged Amino-Terminal FAK (ATF) constructs localised primarily at areas of cell-cell contact and in the nucleus in HEK 293 cells. This localisation was independent of Tyrosine 397, the major FAK autophosphorylation site. This sub-cellular distribution was confirmed in another epithelial cell line, MDCK, in which transiently transfected ATF constructs also localised primarily to the nucleus and at cell-cell contacts. HEK 293 cells were characterised with respect to expression of adhesive proteins, and ATF was found to co- localise with the tight junction protein occludin, with cortical actin and with junctional ?1 integrin. Immunoprecipitation data suggests that none of these proteins forms a precipitable complex with ATF. These findings indicate that the amino-terminal domain of FAK is capable of localising at epithelial cell-cell contacts and suggest a novel role for FAK in mediating cross-talk between focal contacts and cell-cell contacts through endogenously expressed amino-terminal FAK fragments.
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Armstrong, Nicola J. "Continuum modelling of cell-cell adhesion". Thesis, Heriot-Watt University, 2008. http://hdl.handle.net/10399/2167.
Cells adhere to each other through the binding of cell adhesion molecules at the cell surface. This process, known as cell-cell adhesion, is fundamental in many areas of biology, including early embryo development, tissue homeostasis and tumour growth. Here \~e present a new continuum mathematical model of this phenomenon by considering · the movement of cells in response to the adhesive forces generated through binding. We demonstrate that the model predicts aggregative behaviour, characteristic of an adhesive cell population. Further, when extended to two cell populations, the model predicts cell sorting behaviour dependent on the strengths of adhesive bonds between cells. While cell sorting has been demonstrated previously with discrete approaches, we believe that this is the first continuous model to capture this behaviour. In the latter part of this work we apply the model of cell-cell adhesion to somitogenesis and tumour growth. In applying the model to somitogenesis we demonstrate that the model predicts somite formation under particular parameter constraints. We suggest that these parameter constraints may provide a means by which to test competing theories of the mechanisms responsible for somitogenesis. In applying the model to tumour growth and invasion we demonstrate that the model predicts that mutations which alter cells adhesive properties have a significant influence on tumour dynamics. In particular, the model predicts that irregular invasion patterns are the consequence of increased cell-matrix adhesion and an inhomogeneous host environment.
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Muniz, Maisonet Maritza. "Topographical Enhancement of Cell Adhesion on Poorly Adhesive Materials". Scholar Commons, 2015. https://scholarcommons.usf.edu/etd/5748.
The overall thrust of this dissertation is to gain a fundamental understanding of the synergistic effects between surface topography and chemical functionality of poorly adhesive materials on enhancing the adhesion of mouse embryonic fibroblasts. Cellular response to surface topography and chemical functionality have been extensively studied on their own providing valuable information that helps in the design of new and improved biomaterials for tissue engineering applications. However, there is a lack of understanding of the synergistic effect of microscale and nanoscale topography with chemical functionality and the relative impact and contribution of each in modulating cellular behavior. By understanding the relationship between these cues, in particular using materials that are poorly adhesive, this study will provide new clues as to how cells adapt to their environment and also suggest new dimensions of biomaterial design for fine-tuning cellular control.
A microstructure that combined non adhesive materials with defined surface topography and surface chemistry is presented, to assess and correlate the enhancement of mouse embryonic fibroblasts cell adhesion and spreading. Poly (N-isopropylacrylamide) or PNIPAAm electrospun fibers were overlaid on PNIPAAm thin films (100 nm) at various time points to investigate the role of topography on such coatings by keeping the chemical functionality the same. After doing this, several topographical patterns were developed, spanning from sparse to dense fiber mats, and cell adhesion strongly depended on the relative available areas for attachment on either the fibers or the supporting surface. To gain a better understanding of this finding, two surface chemistries, non-adhesive (self-assembled monolayer of polyethylene glycol (PEGSAM) alkanethiol on gold) or an adhesive coating (3-aminopropyltriethoxysilane (APTES) on glass) with well characterized adhesive properties were included in this study to assess the effect of topographical cues provided by the PNIPAAm electrospun fibers on cellular responses. With the deposition of the PNIPAAm fibers onto a PEGSAM surface, cell adhesion increased to almost 100%, and unlike the PNIPAAm surface, cell spreading was significantly enhanced. With the deposition of PNIPAAm fibers onto APTES, both cell adhesion and spreading were unaffected up to 60% fiber coverage. For both surfaces, PNIPAAm fiber densities above 60% coverage lead to adhesion and spreading independent of the underlying surface. These findings indicate the presence of a sparse topographical feature can stimulate cell adhesion on a typically non-adhesive material, and that a chemical dissimilarity between the topographic features and the background enhances this effect through greater cell-surface interaction.
In addition to the aforementioned studies, cell response was also assessed on PNIPAAm thin films coatings with thicknesses ranging from 100 nm to 7 nm. Cell adhesion and spreading was enhanced as the thickness of the thin film decreased. This change was more noticeable below 30 nm, wherein 7 nm shows the highest cell adhesion and spreading enhancement. The results reported are preliminary results and further experiments will be conducted, to support the data. It is believed that cellular response was enhanced due to a change in surface topography at the nanoscale level.
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Maghzal, Nadim. "The epithelial cell adhesion molecule (EpCAM) regulates cell motility and cell-cell adhesion by inhibiting PKC signaling". Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114215.
Tissue cohesion is achieved in part by a large family of plasma membrane-bound cell adhesion molecules (CAMs). During morphogenesis, CAM-mediated interactions provide adhesive forces required for cells to aggregate and form tissues. CAM-mediated adhesions in developing cells are highly dynamic, which provides the fluidity required for cellular movements that drive morphogenesis. Xenopus laevis gastrulation is an established model to study morphogenetic movements. During this phase of development, the mesoderm moves inside the embryo through involution, and migrates along the inner surface of the ectoderm while remaining separated from this tissue. Members of the Fagotto lab have identified the Xenopus orthologue of the Epithelial Cell Adhesion Molecule (EpCAM) in a gain-of-function screen to find gene products that cause aberrant ectoderm/mesoderm tissue mixing in the gastrula. EpCAM is a well known tumor-associated antigen that is specifically expressed in epithelial tissues, where its overexpression often correlates with malignancy. The initial aim of this thesis was to understand the molecular mechanism through which EpCAM promotes ectoderm/mesoderm tissue mixing. Overexpression of EpCAM in cells at the boundary increases their "invasive" behavior via a signaling property of its cytoplasmic domain (EpTAIL) that inhibits PKC signaling to promote cell motility. The most important findings of this thesis are that 1) EpTAIL inhibits PKC activity to promote cell motility and cell-cell adhesion by acting as a PKC pseudosubstrate domain that binds the enzyme on its catalytic site, and 2) this previously unknown mode of PKC inhibition is not specific to EpCAM as other PKC pseudosubstrate-mimicking plasma membrane proteins were identified and could potentially play important roles in the regulation of PKC activity. The data presented in this thesis further our understanding of EpCAM biology and unravel a new mode of PKC regulation that is valuable as PKCs are one of the major families of cytoplasmic kinases in cells. Les mécanismes de liaison cellulaire sont établis en partie par une vaste famille de protéines d'adhésion cellulaire ou CAMs. Lors de la morphogenèse, les interactions induites par les CAMs créent des forces d'adhésion nécessaires afin que les cellules puissent s'agréger et former des tissues. Les adhésions induites par les CAMs dans les cellules en développement sont très dynamiques et offrent ainsi la fluidité nécessaire aux mouvements cellulaires qui régissent la morphogenèse. La gastrulation chez la grenouille Xenopus laevis sert de modèle d'étude des mouvements morphogéniques. Durant ce stade de développement, le mésoderme se déplace vers l'intérieur de l'embryon via un mouvement d'involution et migre le long de la paroi interne de l'ectoderme tout en maintenant une séparation des deux tissues. Des membres du laboratoire de Dr. Fagotto ont réussi à identifier un orthologue de la protéine «Epithelial Cell Adhesion Molecule (EpCAM) » chez Xenopus dans un tri de gain de fonction permettent d'identifier des protéines pouvant être à l'origine d'aberrations au niveau du maintien de la séparation de l'ectoderme et du mésoderme durant la gastrulation. EpCAM est un antigène associé aux tumeurs exprimé dans les cellules épithéliales et dont la surexpression corrèle avec des tumeurs malignes. L'objectif initial de cette thèse était de découvrir les mécanismes moléculaires pouvant expliquer l'effet de EpCAM sur les aberrations entre la séparation des tissues de l'ectoderme et du mésoderme. Une surexpression de EpCAM dans les cellules à la bordure de l'ectoderme et du mésoderme cause une augmentation du comportement « invasif » entre les deux tissues, via la fonction de transduction du signal de son domaine cytoplasmique (EpTAIL), qui inhibe le signal de la protéine PKC afin de promouvoir le mouvement cellulaire. Les principales contributions de cette thèse ont été 1) EpTAIL inhibe l'activité de PKC en jouant le rôle d'un pseudosubstrat de PKC en interagissant avec le site catalytique de l'enzyme, et 2) ce mécanisme d'inhibition jusqu'à présent inconnu pour PKC n'est pas seulement spécifique à EpCAM, car d'autres protéines membranaires possède également cette capacité à imiter le pseudosubstrat de PKC et pourraient potentiellement avoir un rôle important à jouer au niveau de la régulation de l'activité de PKC. Les donnée présentées dans cette thèse contribuent à approfondir davantage notre connaissance d'EpCAM et dévoilent un nouveau mécanisme de régulation de PKC qui pourrait être important puisque les molécules PKC forment l'une des plus importantes familles de kinases cytoplasmiques dans les cellules.
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Théard, Delphine Francine. "P27Kip1 in cell-cell adhesion and cell polarity". [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2006. http://irs.ub.rug.nl/ppn/291442056.
Dix, Christina Lyn. "Adhesion-dependent cell division". Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10044469/.
Animal cells undergo a dramatic series of cell shape changes as they pass through mitosis and divide which depend both on remodelling of the contrac- tile actomyosin cortex and on the release of cell-substrate adhesions. Here, I use the adherent, non-transformed, human RPE1 cell line as a model system in which to explore the dynamics of these shape changes, and the function of mitotic adhesion remodelling. Although these cells are highly motile, and therefore polarised in interphase, many pause migration and elongate to be- come bipolar prior to mitosis. Interestingly, and in contrast to most reported cell types, these cells do not round fully, and many leave long adhesive tails con- nected to the underlying substrate. These are typically bipolar, persist through- out mitosis, and guide cell respreading following mitotic exit. Further analysis shows that while many proteins are lost from focal adhesion complexes during mitotic rounding, integrin-rich contacts remain in place along these tails as well as defining the tips of retraction fibres. These adhesions are functionally impor- tant in RPE1 cells, since these cells fail to divide when removed from the sub- strate prior to entry into mitosis. The restoration of cell-substrate adhesions at anaphase are sufficient to rescue division in control cells. However, adhesions must persist into mitotic exit for division in cells compromised in their ability to construct an actomyosin ring. Division in these cells depends on respreading, since Ect2 RNAi cells fail to divide on small adhesive islands, but successfully divide on larger patterns with the cytoplasmic bridge connecting daughter cells narrowing as they migrate away from one another. Together these results re- veal the importance of coupling adhesion remodeling to mitotic progression.
Betson, Martha Elizabeth. "Regulation of cell-cell adhesion in keratinocyes". Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274930.
Zhao, Lee Cheng. "Cell adhesion characterization of adhesive forces and effect of topography /". [Gainesville, Fla.] : University of Florida, 2000. http://etd.fcla.edu/etd/uf/2000/ana7043/LCZhao%5FThesis.pdf.
Thesis (M.S.)--University of Florida, 2000. Title from first page of PDF file. Document formatted into pages; contains ix, 79 p.; also contains graphics. Vita. Includes bibliographical references (p. 69-77).
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Elineni, Kranthi Kumar. "Regulation of Cell Adhesion Strength by Spatial Organization of Focal Adhesions". Scholar Commons, 2011. http://scholarcommons.usf.edu/etd/3088.
Cell adhesion to extracellular matrix (ECM) is critical to various cellular processes like cell spreading, migration, growth and apoptosis. At the tissue level, cell adhesion is important in the pathological and physiological processes that regulate the tissue morphogenesis. Cell adhesion to the ECM is primarily mediated by the integrin family of receptors. The receptors that are recruited to the surface are reinforced by structural and signaling proteins at the adhesive sites forming focal adhesions that connect the cytoskeleton to further stabilize the adhesions. The functional roles of these focal adhesions extend beyond stabilizing adhesions and transduce mechanical signals at the cell-ECM interface in various signaling events. The objective of this research is to analyze the role of the spatial distribution of the focal adhesions in stabilizing the cell adhesion to the ECM in relation to cell's internal force balance. The central hypothesis was that peripheral focal adhesions stabilize cell adhesion to ECM by providing for maximum mechanical advantage for resisting detachment as explained by the membrane peeling mechanism. Micropatterning techniques combined with robust hydrodynamic shear assay were employed to test our hypothesis. However, technical difficulties in microcontact printing stamps with small and sparse features made it challenging to analyze the role of peripheral focal adhesions in stabilizing cell adhesion. To overcome this limitation, the roof collapse phenomenon in stamps with small and sparse features (low fill factor stamps) that was detrimental to the reproduction of the adhesive geometries required to test the hypothesis was analyzed. This analysis lead to the valuable insight that the non-uniform pressure distribution during initial contact caused by parallelism error during manual microcontact printing prevented accurate replication of features on the substrate. To this end, the template of the stamp was modified so that it included an annular column around the pattern zone that acted as a collapse barrier and prevented roof collapse propagation into the pattern zone. Employing this modified stamp, the required geometries for the cell adhesion analysis were successfully reproduced on the substrates with high throughput. Adhesive areas were engineered with circular and annular patterns to discern the contribution of peripheral focal adhesions towards cell adhesion strength. The patterns were engineered such that two distinct geometries with either constant adhesive area or constant spreading area were obtained. The significance of annular patterns is that for the same total adhesive area as the circular pattern, the annular pattern provided for greater cell spreading thereby increasing the distance of the focal adhesions from the cell's center. The adhesion strength analysis was accomplished by utilizing hydrodynamic shear flow in a spinning disk device that was previously developed. The results indicate that for a constant total adhesive area, the annular patterns provide for greater adhesion strength by enhancing cell spreading area and providing for greater moment arm in resisting detachment due to shear. The next examination was the effect of the cell's internal force balance in stabilizing the cell adhesion. The working hypothesis was that microtubules provide the necessary forces to resist the tensile forces expressed by the cell contractile machinery, thereby stabilizing cell adhesion. Since microtubule disruption is known to enhance cell contractility, its effect on the cell adhesion strength was examined. Moreover, the force balance in cells was altered by engineering adhesive areas so that the cells were either spherical or completely spread and then disrupted microtubules to understand the significance of the force balance in modulating the cell adhesion strength. The results indicated that disruption of microtubules in cells on adhesive islands resulted in a 10 fold decrease in adhesion strength compared to untreated controls whereas no significant change was observed in completely spread cells between treated and untreated controls. This is in surprising contrast to the previous contractility inhibition studies which indicate a less pronounced regulation of adhesion strength for both micropatterned and spread cells. Taken together, these findings suggest that the internal force balance regulated by cell shape strongly modulates the adhesion strength though the microtubule network. In summary, this project elucidates the role of peripheral focal adhesions in regulating the cell adhesion strength. Furthermore, this study also establishes the importance of the internal force balance towards stabilizing the cell adhesion to the ECM through the microtubule network.
Behrens, Jürgen, e W. James Nelson, a cura di. Cell Adhesion. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-540-68170-0.
Bongrand, Pierre, Per M. Claesson e Adam S. G. Curtis, a cura di. Studying Cell Adhesion. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-662-03008-0.
Berezin, Vladimir, e Peter S. Walmod, a cura di. Cell Adhesion Molecules. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8090-7.
De Bartolo, Loredana. "Cell Adhesion". In Encyclopedia of Membranes, 333–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-44324-8_120.
Peroulis, Dimitrios, Prashant R. Waghmare, Sushanta K. Mitra, Supone Manakasettharn, J. Ashley Taylor, Tom N. Krupenkin, Wenguang Zhu et al. "Cell Adhesion". In Encyclopedia of Nanotechnology, 403. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-90-481-9751-4_100115.
De Bartolo, Loredana. "Cell Adhesion". In Encyclopedia of Membranes, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-40872-4_120-6.
Humphries, Martin J. "Cell Adhesion Assays". In Methods in Molecular Biology, 203–10. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-413-1_14.
Sedlacek, H. Harald, e Tarik Möröy. "Cell-Adhesion Molecules". In Immune Reactions, 55–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79558-9_2.
Tong, Xiajing, e Yan Zou. "Cell Adhesion Molecules". In Advances in Membrane Proteins, 67–83. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-9077-7_4.
Gallant, Nathan D., e Kranthi Kumar Elineni. "Regulation of Adhesion Strength by Focal Adhesion Position and Cell Shape". In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80832.
Cell adhesion to extracellular matrices is critical to numerous cellular functions and is primarily mediated by integrin receptors. Binding and aggregation of integrins leads to the formation of focal adhesions (FA) which connect the cytoskeleton to the extracellular matrix in order to reinforce adhesion and transmit signals [1]. Preliminary observations indicated preferential recruitment of FAs to the periphery of the cell spreading area on both uniformly coated and micropatterned fibronectin surfaces (Fig. 1). The current study investigates the biophysical regulation of cell adhesion strength based on the size and position of FA with the central hypothesis that peripheral FAs stabilize adhesion strength. The hypothesis was tested by delineating the cell spreading area from the total cell adhesive area by employing microcontact printing to pattern substrates with a series of circular and annular adhesive islands which control cell shape (Fig. 2). A well characterized hydrodynamic shear assay known as the spinning disk device was used to quantify the adhesion strength of cells adhered to the micropatterns [2].
2
Tuszynski, George P., Vicki L. Rothman, Andrew Murphy, Katherine Siegler, Linda Smith, Sena Smith, Jerzy Karczewski e Karen A. Knudsen. "Thranbospondin Promotes Cell-and Platelet-Substratum Adhesion". In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643820.
Thrombospondin (TSP), isolated from human platelets, promotes the in vitro, calcium-specific adhesion of a variety of cells, including platelets, melanoma cells, muscle cells, endothelial cells, fibroblasts, and epithelial cells. The cell adhesion-promoting activity of TSP is species independent since human, bovine, pig, rat and mouse cells all adhered to TSP. Furthermore, the cell adhesion-promoting activity of TSP is specific and not due to a nonspecific protein effect or to contamination by fibronectin, vitronectin, or laminin. That is, neither bovine serum albumin nor TSP preparations treated with a monospecific anti-TSP antibody support cell adhesion. As analyzed by polyacrylamide-gel electrophoresis and specific antibody binding assays, the TSP preparations used in these studies contained no detectable fibronectin or laminin and less than 0.04% vitronectin. The cell surface receptor for TSP appears distinct frcm that of fibronectin since an antiserum that blocks cell adhesion to fibronectin has no effect on adhesion to TSP. In addition, The platelet cell surface receptor for TSP appears distinct, frcm that of fibrinogen since thrcmbasthenic platelets adhere to TSP as well as control platelets. Antibodies to the GPIIb-GPIIIa complex block platelet adhesion to fibrinogen but have no effect on adhesion to TSP. Initial characterization of the cell surface receptor for TSP shows it to be protein in nature since cells treated with trypsin fail to adhere to TSP. In summary, our results provide the first clear evidence that TSP specifically promotes cell-substratum adhesion of a variety of cell types independent of the animal species. Our preliminary evidence suggests that the cell-surface receptor(s) for TSP is protein and that it is distinct for the receptor for fibronectin and fibrinogen. Our data suggest that TSP may play a central role in normal adhesive events mediated by platelets and other cells, such as those involved in hemostasis and wound healing. In addition, TSP may be involved in pathological adhesive events mediated by platelets and tumor cells, such as those involved in cardiovascular disease and tumor cell metastasis.
3
Chirasatitsin, Somyot, Priyalakshmi Viswanathan, Giuseppe Battaglia e Adam J. Engler. "Directing Stem Cell Fate in 3D Through Cell Inert and Adhesive Diblock Copolymer Domains". In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14442.
Adhesions are important cell structures required to transduce a variety of chemical and mechanics signals from outside-in and vice versa, all of which regulate cell behaviors, including stem cell differentiation (1). Though most biomaterials are coated with an adhesive ligand to promote adhesion, they do not often have a uniform distribution that does not match the heterogeneously adhesive extracellular matrix (ECM) in vivo (2). We have previously shown that diblock copolymer (DBC) mixtures undergo interface-confined de-mixing to form nanodomins of one copolymer in another (3). Here we demonstrate how diblock copolymer mixtures can be made into foams with nanodomains to better recapitulate native ECM adhesion regions and influence cell adhesion.
4
Lei, Xiaoxiao, Michael B. Lawrence e Cheng Dong. "Mechanics of Cell Rolling Adhesion in Shear Flow". In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0284.
Abstract Leukocyte rolling along endothelial cells is a critical step of leukocyte-endothelium interaction, which plays important roles in tissue inflammation and wound healing [1]. The occurrence of rolling results from the dynamic balance of hemodynamic shearing force acting on the cell and adhesive bond force between cell and endothelium, while the balance strongly depends on the leukocyte deformability [2]. The objective of this study is to elucidate the effects of (1) hydrodynamic shear stress, (2) cell deformation, and (3) surface adhesion strength on the rolling adhesion event through in vitro experiment and theoretical simulation.
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Hu, Jia, e Yaling Liu. "Cell Adhesion on a Wavy Surface". In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14059.
The ability to control the position of cells in an organized pattern on a substrate has become increasingly important for biosensing and tissue engineering applications [1–3]. With the advent of nanofabrication techniques, a number of researchers have studied the effects of nano-scale grooves on cell spreading, migration, morphology, signaling and orientation [4–6]. Recent studies have shown that cell adhesion/spreading can be influenced by a nanostructured surface [7]. In most current studies, the pattern dimensions are much smaller than the size of a cell. In this paper, we focus on studying cell response to micro scale patterns instead of nano-scale patterns.
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Slater, John H., Jordan S. Miller, Shann S. Yu e Jennifer L. West. "Multifaceted Nano- and Micropatterned Surfaces for Cell Adhesion Manipulation". In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13177.
Surfaces displaying nano- and micropatterned cell adhesive ligands have led to numerous discoveries in cell biology. Soft lithography techniques such as microcontact printing are well suited for creating surfaces displaying micropatterns of one ligand type in a single arrangement but are difficult to implement for the creation of multifaceted surfaces that present multiple ligand types with each ligand confined to their own pattern. To better understand the influence of extracellular matrix (ECM) composition on adhesion site formation and gross cell behavior (motility, proliferation, differentiation, etc.) it would be advantageous to posses the ability to create surfaces displaying multiple patterned ligands with length scales ranging from < 0.25 μm2, the typical size of a focal complex to > 1 μm2, the size of focal adhesions. Higher spatial resolution than what is easily achieved with microcontact printing is also desired. Such surfaces would allow for the simultaneous investigations of adhesion site maturation and composition and how changes in these properties can be implemented to engineer cell behavior via cell-surface interactions.
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Dong, Chen. "In Vitro Imaging Technique of Cell Adhesion". In ASME 2002 Pressure Vessels and Piping Conference. ASMEDC, 2002. http://dx.doi.org/10.1115/pvp2002-1630.
It is the first object of this article to contribute a side-view imaging technique to investigate adhesion to a surface-immobilized ICAM-1 in shear flow, wherein T-leukemic Jurket cells have been used. A side view image has revealed that the cell adhesion on ICAM-1 under flow conditions in vitro is quasistratic. Changes in flow shear stress, cell deformability, or substrate ligand strength resulted in a significant change in the characteristic adhesion binding time and contact length. The elongation of cells in shear flow tempers hydrodynamic shear forces on the cell, which affects the transients in cell-surface adhesion. It is the second object to calculate a 3-D flow field with shear stress acting on an adherent cell based on the shape of the cell obtained from the image. The application of the side-view imaging technique and the image analysis may provide a practical assay to reveal fundamental behavior of a cell.
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Zhao, Yihua, Richard Skalak e Shu Chien. "Hydrodynamics in Cell Rolling and Adhesion". In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0237.
Abstract Formulas for the slow viscous motion of a sphere in the presence of a solid wall have been used in analyzing the phenomena of cell rolling and adhesion. The established theories, such as the ones by Brenner and his colleagues [1,2,3], address the ideal situation in which both the sphere and the wall are smooth. However, biological cells such as leukocytes have numerous surface protrusions (microvilli). Therefore, the applicability of the theories of smooth spheres to the problem of cell rolling and adhesion needs to be examined. Also, to facilitate the design and analysis of experiments, it is desirable to have a simple solution that can provides some physical insights into the process.
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Christ, Kevin V., e Kevin T. Turner. "Hydrodynamically-Confined Microflows for Cell Adhesion Strength Measurement". In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13007.
Cell adhesion plays a fundamental role in numerous physiological and pathological processes, and measurements of the adhesion strength are important in fields ranging from basic cell biology research to the development of implantable biomaterials. Our group and others have recently demonstrated that microfluidic devices offer advantages for characterizing the adhesion of cells to protein-coated surfaces [1,2]. Microfluidic devices offer many advantages over conventional assays, including the ability to apply high shear stresses in the laminar regime and the opportunity to directly observe cell behavior during testing. However, a key disadvantage is that such assays require cells to be cultured inside closed microchannels. Assays based on closed channels restrict the types of surfaces that can be examined and are not compatible with many standard techniques in cell biology research. Furthermore, while techniques for cell culture in microchannels have become common, maintaining the viability of certain types of cells in channels remains a challenge.
10
Han, Sangyoon J., e Nathan J. Sniadecki. "Traction Forces During Cell Migration Predicted by the Multiphysics Model". In ASME 2011 International Mechanical Engineering Congress and Exposition. ASMEDC, 2011. http://dx.doi.org/10.1115/imece2011-63843.
Cells rely on traction forces in order to crawl across a substrate. These traction forces come from dynamic changes in focal adhesions, cytoskeletal structures, and chemical and mechanical signals from the extracellular matrix. Several computational models have been developed that help explain the trajectory or accumulation of cells during migration, but little attention has been placed on traction forces during this process. Here, we investigated the spatial and temporal dynamics of traction forces by using a multiphysics model that describes the cycle of steps for a migrating cell on an array of posts. The migration cycle includes extension of the leading edge, formation of new adhesions at the front, contraction of the cytoskeleton, and the release of adhesions at the rear. In the model, an activation signal triggers the assembly of actin and myosin into a stress fiber, which generates a cytoskeletal tension in a manner similar to Hill’s muscle model. In addition, the role that adhesion dynamics has in regulating cytoskeletal tension has been added to the model. The multiphysics model was simulated in Matlab for 1-D simulations, and in Comsol for 2-D simulations. The model was able to predict the spatial distribution of traction forces observed with previous experiments in which large forces were seen at the leading and trailing edges. The large traction force at the trailing edge during the extension phase likely contributes to detachment of the focal adhesion by overcoming its adhesion strength with the post. Moreover, the model found that the mechanical work of a migrating cell underwent a cyclic relationship that rose with the formation of a new adhesion and fell with the release of an adhesion at its rear. We applied a third activation signal at the time of release and found it helped to maintain a more consistent level of work during migration. Therefore, the results from both our 1-D and 2-D migration simulations strongly suggest that cells use biochemical activation to supplement the loss in cytoskeletal tension upon adhesion release.
Rapporti di organizzazioni sul tema "Cell adhesion":
1
Byers, Stephen W. Cell-Cell Adhesion and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, gennaio 2000. http://dx.doi.org/10.21236/ada395237.
Byers, Stephen W. Cell-Cell Adhesion and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, gennaio 1999. http://dx.doi.org/10.21236/ada371168.
Byers, Stephen W. Cell-Cell Adhesion and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, gennaio 1998. http://dx.doi.org/10.21236/ada345188.
Surmacz, Eva. IGF-IR, Cell Adhesion and Metastasis. Fort Belvoir, VA: Defense Technical Information Center, settembre 2001. http://dx.doi.org/10.21236/ada400067.
Surmacz, Eva. IGF-IR, Cell Adhesion and Metastasis. Fort Belvoir, VA: Defense Technical Information Center, settembre 2003. http://dx.doi.org/10.21236/ada420246.
Surmacz, Ewa. IGF-IR, Cell Adhesion and Metastasis. Fort Belvoir, VA: Defense Technical Information Center, settembre 2000. http://dx.doi.org/10.21236/ada392765.
Park, Electa R., Alexis L. Bergsma e Amanda L. Erwin. CD82 and Cell-Cell Adhesion in Metastatic Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, luglio 2013. http://dx.doi.org/10.21236/ada588246.
Bertozzi, Carolyn R. Metabolic Engineering of Reactive Cell Surfaces for Controlled Cell Adhesion. Fort Belvoir, VA: Defense Technical Information Center, settembre 2001. http://dx.doi.org/10.21236/ada421093.
DaCosta, Stacey. IGF Regulation of Cell Adhesion in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, luglio 2000. http://dx.doi.org/10.21236/ada396051.
DaCosta, Stacey. IGF Regulation of Cell Adhesion in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, luglio 2001. http://dx.doi.org/10.21236/ada396635.
