Relevant bibliographies by topics / Cell spreading

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Cell spreading'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 January 2023

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Journal articles on the topic "Cell spreading"

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LeBrasseur, Nicole. "Spreading mitochondria." Journal of Cell Biology 172, no. 4 (February 6, 2006): 482. http://dx.doi.org/10.1083/jcb1724rr4.

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Disatnik, Marie-Hélène, and Thomas A. Rando. "Integrin-mediated Muscle Cell Spreading." Journal of Biological Chemistry 274, no. 45 (November 5, 1999): 32486–92. http://dx.doi.org/10.1074/jbc.274.45.32486.

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Lavine, Marc S. "Cell spreading affects energy consumption." Science 370, no. 6518 (November 12, 2020): 806.2–806. http://dx.doi.org/10.1126/science.370.6518.806-b.

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Stewart, M. G., E. Moy, G. Chang, W. Zingg, and A. W. Neumann. "Thermodynamic model for cell spreading." Colloids and Surfaces 42, no. 2 (January 1989): 215–32. http://dx.doi.org/10.1016/0166-6622(89)80193-3.

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Stewart, M. G., E. Moy, G. Chang, W. Zingg, and A. W. Neumann. "Thermodynamic model for cell spreading." Colloids and Surfaces 42, no. 3-4 (December 1989): 215–32. http://dx.doi.org/10.1016/0166-6622(89)80342-7.

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Tsygankova, Oxana M., Changqing Ma, Waixing Tang, Christopher Korch, Michael D. Feldman, Yu Lv, Marcia S. Brose, and Judy L. Meinkoth. "Downregulation of Rap1GAP in Human Tumor Cells Alters Cell/Matrix and Cell/Cell Adhesion." Molecular and Cellular Biology 30, no. 13 (May 3, 2010): 3262–74. http://dx.doi.org/10.1128/mcb.01345-09.

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ABSTRACT Rap1GAP expression is decreased in human tumors. The significance of its downregulation is unknown. We show that Rap1GAP expression is decreased in primary colorectal carcinomas. To elucidate the advantages conferred on tumor cells by loss of Rap1GAP, Rap1GAP expression was silenced in human colon carcinoma cells. Suppressing Rap1GAP induced profound alterations in cell adhesion. Rap1GAP-depleted cells exhibited defects in cell/cell adhesion that included an aberrant distribution of adherens junction proteins. Depletion of Rap1GAP enhanced adhesion and spreading on collagen. Silencing of Rap expression normalized spreading and restored E-cadherin, β-catenin, and p120-catenin to cell/cell contacts, indicating that unrestrained Rap activity underlies the alterations in cell adhesion. The defects in adherens junction protein distribution required integrin signaling as E-cadherin and p120-catenin were restored at cell/cell contacts when cells were plated on poly-l-lysine. Unexpectedly, Src activity was increased in Rap1GAP-depleted cells. Inhibition of Src impaired spreading and restored E-cadherin at cell/cell contacts. These findings provide the first evidence that Rap1GAP contributes to cell/cell adhesion and highlight a role for Rap1GAP in regulating cell/matrix and cell/cell adhesion. The frequent downregulation of Rap1GAP in epithelial tumors where alterations in cell/cell and cell/matrix adhesion are early steps in tumor dissemination supports a role for Rap1GAP depletion in tumor progression.
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Sadahira, Yoshito, Tadashi Yoshino, and Naoya Kojima. "B16 melanoma cell spreading on activated endothelial cells." In Vitro Cellular & Developmental Biology - Animal 30, no. 10 (October 1994): 648–50. http://dx.doi.org/10.1007/bf02631266.

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McInnes, C., P. Knox, and D. J. Winterbourne. "Cell spreading on serum is not identical to spreading on fibronectin." Journal of Cell Science 88, no. 5 (December 1, 1987): 623–29. http://dx.doi.org/10.1242/jcs.88.5.623.

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Adhesion and spreading of cell lines on dishes coated with serum-derived proteins were studied after removal of cell-surface proteoglycans. A mixture of glycosaminoglycans lyases from heparin-induced Flavobacterium heparinum removed 80% of the [35S]sulphate-labelled glycosaminoglycans from the surface of attached cells within 30 min, but this had little effect on cell morphology. The rate of cell attachment to dishes coated with serum was unaffected by prior treatment of cells with this mixture of glycosaminoglycan lyases. While a heparan sulphate lyase preparation abolished cell spreading in response to fibronectin there was no effect of the enzyme on the spreading mediated by vitronectin. These results suggest that, although heparan sulphate is required for spreading on purified fibronectin, the spreading stimulated by serum under routine culture conditions requires neither cellular heparan sulphate nor serum-derived fibronectin.
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Cramer, L. P., and T. J. Mitchison. "Myosin is involved in postmitotic cell spreading." Journal of Cell Biology 131, no. 1 (October 1, 1995): 179–89. http://dx.doi.org/10.1083/jcb.131.1.179.

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We have investigated a role for myosin in postmitotic Potoroo tridactylis kidney (PtK2) cell spreading by inhibitor studies, time-lapse video microscopy, and immunofluorescence. We have also determined the spatial organization and polarity of actin filaments in postmitotic spreading cells. We show that butanedione monoxime (BDM), a known inhibitor of muscle myosin II, inhibits nonmuscle myosin II and myosin V adenosine triphosphatases. BDM reversibly inhibits PtK2 postmitotic cell spreading. Listeria motility is not affected by this drug. Electron microscopy studies show that some actin filaments in spreading edges are part of actin bundles that are also found in long, thin, structures that are connected to spreading edges and substrate (retraction fibers), and that 90% of this actin is oriented with barbed ends in the direction of spreading. The remaining actin in spreading edges has a more random orientation and spatial arrangement. Myosin II is associated with actin polymer in spreading cell edges, but not retraction fibers. Myosin II is excluded from lamellipodia that protrude from the cell edge at the end of spreading. We suggest that spreading involves myosin, possibly myosin II.
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Wells, William A. "Exclusion is spreading." Journal of Cell Biology 168, no. 1 (December 28, 2004): 11. http://dx.doi.org/10.1083/jcb1681rr3.

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Dissertations / Theses on the topic "Cell spreading"

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Treloar, Katrina K. "Mathematical models for collective cell spreading." Thesis, Queensland University of Technology, 2015. https://eprints.qut.edu.au/86960/1/Katrina_Treloar_Thesis.pdf.

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Collective cell spreading is frequently observed in development, tissue repair and disease progression. Mathematical modelling used in conjunction with experimental investigation can provide key insights into the mechanisms driving the spread of cell populations. In this study, we investigated how experimental and modelling frameworks can be used to identify several key features underlying collective cell spreading. In particular, we were able to independently quantify the roles of cell motility and cell proliferation in a spreading cell population, and investigate how these roles are influenced by factors such as the initial cell density, type of cell population and the assay geometry.
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Promwikorn, Waraporn. "Regulation of gene expression and cell cycle progression by cell shape." Thesis, University of Liverpool, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250316.

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Jin, Hua. "The role of Abl tyrosine kinase in cell spreading." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3274697.

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Thesis (Ph. D.)--University of California, San Diego, 2007.
Title from first page of PDF file (viewed October 5, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
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Streicher, Pia. "Studying integrin-mediated cell spreading using a biomimetic system." Paris 6, 2008. http://www.theses.fr/2008PA066668.

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L'adhésion cellulaire dépendant des intégrines a été étudiée grâce à un système modèle réaliste. Nous avons développé une méthode basée sur celle initialement mise au point pour d'autres protéines dans l'équipe de P. Bassereau. Elle consiste à reconstituer l'intégrine αIIbβ3 dans des protéoliposomes (0. 1 -0. 2 µm de diamètre), puis à électroformer les vésicules géantes à partir des protéoliposomes partiellement séchés. Le succès de la reconstitution a été vérifié en analysant l'incorporation de la protéine et son activité biologique. La dynamique de l'adhésion ces vésicules sur des surfaces couvertes par le fibrinogène a été étudiée en détail. Nous avons identifié trois régimes et nous avons comparé les données expérimentales du régime 1) et 3) avec des prédictions théoriques. Dans les deux régimes, l'adhésion est limitée par la diffusion des ligands jusqu'à la zone adhésive.
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Vo, Brenda. "Novel likelihood-free Bayesian parameter estimation methods for stochastic models of collective cell spreading." Thesis, Queensland University of Technology, 2016. https://eprints.qut.edu.au/99588/1/Brenda_Vo_Thesis.pdf.

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Biological processes underlying skin cancer growth and wound healing are governed by various collective cell spreading mechanisms. This thesis develops new statistical methods to provide key insights into the mechanisms driving the spread of cell populations such as motility, proliferation and cell-to-cell adhesion, using experimental data. The new methods allow us to precisely estimate the parameters of such mechanisms, quantify the associated uncertainty and investigate how these mechanisms are influenced by various factors. The thesis provides a useful tool to measure the efficacy of medical treatments that aim to influence the spread of cell populations.
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Redmann, Anna-Lena. "Kinetics of cell attachment and spreading on hard and soft substrates." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/290385.

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A very important aspect for the functioning of an organism is that cells adapt their behaviour to external stimuli. They continuously interact with their environment, and biochemical and physical cues can activate cellular signalling, which leads to changes in cell behaviour such as proliferation and shape. Understanding cells' interactions with their environment is also important for understanding diseases. For example mechanosensing, which is the sensing of the cell's mechanical environment, has been associated with cancer development. In order for a cell to be able to sense its mechanical environment, it needs to form attachments to the environment. In my thesis, I have worked on three different tasks: the development of a new measurement technique and the study of initial cell adhesion and of cell spreading. When a cell from suspension first comes into contact with a substrate, it forms initial attachment bonds with proteins on the substrate surface. These bonds are mediated through integrins, which are transmembrane heterodimers, binding to the cell's environment on one side and to the cell's cytoskeleton on the other side. I study this initial cell attachment by measuring the force needed to detach cells, called cell adhesion strength. For these experiments I built a detachment device, which allows the detachment of cells from a substrate by vibrating the substrate in liquid. The device combines cell incubation, detachment and imaging. I measured the dependence of initial integrin bond formation on external factors such as incubation temperature and substrate stiffness. Once initial integrin bonds are formed, many different proteins are recruited to the adhesion site in order to form stronger adhesions. Amongst these proteins are signalling proteins, which direct the behaviour of the cell as a whole. One of the first cellular reactions to a substrate after initial integrin binding is cell spreading. This can be seen by the cell changing its shape from spherical to dome-like on the substrate. Because cell spreading is a very early response of a cell to a substrate, the onset time of spreading can be used as a quantitative measure for the time it takes the cell to sense a substrate and signal shape change. In my work, I look at the distribution of the time of initial cell spreading in a population of cells. I measure this distribution under different growth conditions such as pH, change of incubation medium from DMEM to PBS, substrate stiffness and incubation temperature. In my detachment experiments, I observe that vibration accelerates cell spreading in those cells which remain on the substrate. This is a connection between the detachment experiments and the cell spreading experiments and it shows how cells react to external forces. By changing the medium temperature in the cell detachment and cell spreading experiments, I am able to analyse the kinetics of these two processes. I use a signalling network model to analyse the internal cellular signalling path that leads from a spherical to a spread cell.
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Moore, Edward Andrew. "Cell attachment and spreading on physical barriers used in periodontal guided tissue regeneration /." Oklahoma City : [s.n.], 2002. http://library.ouhsc.edu/epub/theses/Moore-William-A.pdf.

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Gill, Amritpal Singh. "Development of a Novel Single-Cell Attachment and Spreading Platform Utilizing Fused-Fiber Nanonets." Thesis, Virginia Tech, 2015. http://hdl.handle.net/10919/73504.

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Initial attachment to the extracellular matrix (ECM) and consequent spreading is a necessary process in the cell cycle of which little is known. Cell spreading has been well-recognized in 2D systems, however, the native fibrous ECM presents cells with 3D biophysical cues. Thus, using suspended fibers as model systems, we present the development of a novel platform (Cell-STEPs) capable of capturing cell attachment dynamics and forces from the moment a cell in suspension contacts the fiber. Cell-STEPs comprises of a custom glass-bottom petri dish with a lid to deliver a constant supply of CO2 to maintain pH. Fibrous scaffolds are attached in the dish to allow cellular investigations over extended periods of time. We find that cell-fiber attachment occurs in three progressive phases: initial attachment of cell to fiber (phase 0), rapid drop in circularity (phase 1), and increase in cell spread area (phase 2). Furthermore, using iterative inverse methods, forces involved in cell spreading through deflection of fibers were estimated. Our findings provide new insights in attachment biomechanics, including initial sensing and latching of cell to fiber with a negligible or protrusive force, followed by rapid loss in circularity through protrusion sensing at nearly constant spread area and minimal force generation, transitioning to a final phase of increased contractile forces until spread area and force saturation is observed. Also, anisotropic spreading of cells on single and two-fibers are closely related, while cells attached to several fibers take longer and spread isotropically. The Cell-STEPs platform allows, for the first time, detailed interrogations in the discrete and orchestrated adhesion steps involved in cell-fibrous matrix recognition and attachment along with simultaneous measurements of forces involved in cell attachment.
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Messmer-Blust, Angela F. "Murine Guanylate-Binding Protein-2: An interferon-induced GTPase that inhibits cell adhesion, cell spreading and MMP-9 expression." University of Toledo / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1263394455.

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Tse, Kathy Wan-Kei. "The role of Pyk2 and FAK in B cell migration, adhesion, and spreading." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/25041.

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The ability of the B cell receptor (BCR) to stimulate integrin-mediated adhesion, and induce cytoskeletal reorganization and cell spreading enhances the ability of B cells to bind and respond to antigens (Ag). The proper localization and trafficking of B cells in the secondary lymphoid organs are also critical for B cells to encounter Ags and to be activated. Proline-rich tyrosine kinase (Pyk2) and focal adhesion kinase (FAK) are related cytoplasmic tyrosine kinases that have been shown to regulate cell adhesion, morphology, and migration. However, their functions in B cells are not clear. The overall hypothesis of this thesis was that Pyk2 and FAK are downstream targets of BCR, integrin, and chemokine receptor signaling, and that they are involved in B cell morphological regulation, migration, and adhesion. I showed that the BCR and integrins collaborate to induce the phosphorylation of Pyk2 and FAK on key tyrosine residues, modifications that increase the kinase activity of Pyk2 and FAK. Activation of the Rap1 GTPase is critical for BCR-induced integrin activation and for BCR-induced reorganization of the actin cytoskeleton and I showed that inhibition of Pyk2 and FAK function by either gene knockdown or the use of chemical inhibitors impaired B cell spreading. Marginal zone (MZ) B cells are innate-like B cells that are responsible for T cell-independent responses to microbial pathogens. The proper localization of MZ B cells is dependent on integrated migration and retention signals provided by the stromal cells in the spleen. Because MZ B cells are not found in Pyk2-/- mice, I hypothesized that Pyk2 and FAK are involved in MZ B cell retention in the spleen. I showed that Pyk2 and FAK are required for MZ B cell migration and that Pyk2 is required for integrin-dependent adhesion in response to chemoattractant stimulation. Moreover, I found that FAK is involved in chemokine-induced Akt phosphorylation in MZ B cells. In summary, Pyk2 and FAK are downstream targets of the Rap GTPases and play a key role in regulating B cell morphology, migration, and adhesion.
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Books on the topic "Cell spreading"

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L, Gauthier Mona. Calmodulin-binding proteins in dictyostelium chemotaxis and breast cancer cell spreading. 2002.

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Al-Anazi, KA, WK Al-Anazi, and AM Al-Jasser. Update on COVID-19 Infections and the Promising Role of Mesenchymal Stem Cell Therapies in their Management. Heighten Science Publications Inc., 2020. http://dx.doi.org/10.29328/ebook1002.

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The pandemic of COVID-19 has adversely affected almost every aspect of our lives but the world health and economic sectors suffer most of the repercussions of this disease. The search for a cure for this rapidly spreading virus which is causing massive life losses around the globe requires clear understanding of the immunopathogenesis of this virus as well as the mechanisms of actions of the various therapeutic modalities that are employed in the treatment of this life-threatening viral infection. Mesenchymal stem cells have antimicrobials effects in addition to their anti-inflammatory and immunomodulatory properties. They have been utilized in the treatment of various infections and their complications both in animal models and in human clinical trials. Mesenchymal stem cells derived from certain sources and their secretory products are particularly effective in the treatment of pneumonia, sepsis, acute lung injury, and acute respiratory distress syndrome which are common complications of COVID-19 infections. The review will discuss the various aspects of COVID-19 and it will highlight the promising role of mesenchymal stem cells in treating the complications of COVID-19 infections.
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Book chapters on the topic "Cell spreading"

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Margolis, Leonid B. "Cell Spreading and Intracellular pH in Mammalian Cells." In Mechanics of Swelling, 443–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84619-9_25.

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Borodich, Feodor M., and Stanislav N. Gorb. "Spreading of Red Caviar Cells: The Knife-Cell and the Cell-Cell Adhesive Interactions." In Biologically-Inspired Systems, 117–37. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-85175-0_7.

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Sheetz, Michael P., Benjamin J. Dubin-Thaler, Gregory Giannone, Guoying Jiang, and Hans-Günther Döbereiner. "Functional Phases in Cell Attachment and Spreading." In Cell Migration in Development and Disease, 1–13. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2005. http://dx.doi.org/10.1002/3527604669.ch1.

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Biber, Stephanie, and Lisa Wiesmüller. "Analysis of Replication Dynamics Using the Single-Molecule DNA Fiber Spreading Assay." In Cell Cycle Checkpoints, 57–71. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1217-0_4.

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MacLeod, Matthew, Rachid Chreyh, and Gabriel Wainer. "Improved Cell-DEVS Models for Fire Spreading Analysis." In Lecture Notes in Computer Science, 472–81. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/11861201_55.

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Shang, Hui, and Gabriel Wainer. "A Model of Virus Spreading Using Cell-DEVS." In Lecture Notes in Computer Science, 373–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/11428848_50.

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Kempski, O., H. Otsuka, T. Seiwert, and A. Heimann. "Spreading Depression Induces Permanent Cell Swelling Under Penumbra Conditions." In Brain Edema XI, 251–55. Vienna: Springer Vienna, 2000. http://dx.doi.org/10.1007/978-3-7091-6346-7_51.

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Timar, J., B. Liu, R. Bazaz, J. D. Taylor, and K. V. Honn. "Fatty Acid Modulation of Cancer Cell Spreading and Cytoskeleton Rearrangement." In Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Radiation Injury, 639–43. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3520-1_125.

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Carey, Shawn P., Jonathan M. Charest, and Cynthia A. Reinhart-King. "Forces During Cell Adhesion and Spreading: Implications for Cellular Homeostasis." In Cellular and Biomolecular Mechanics and Mechanobiology, 29–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/8415_2010_22.

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Humphries, Martin J., Zohreh Mostafavi-Pour, Mark R. Morgan, Nicholas O. Deakin, Anthea J. Messent, and Mark D. Bass. "Integrin-Syndecan Cooperation Governs the Assembly of Signalling Complexes during Cell Spreading." In Signalling Networks in Cell Shape and Motility, 178–92. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/047001766x.ch14.

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Conference papers on the topic "Cell spreading"

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Weafer, Paul, Maarten H. van Es, Suzanne P. Jarvis, and Patrick J. McGarry. "Compression Force Measurement During Cell Spreading Using a Modified Atomic Force Microscope." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53741.

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Mechanical forces play a critical role in the regulation of cell spreading and cytoskeletal organization. It has been demonstrated that the force required to compress a spread cell is significantly higher than that required to compress a cell with a rounded morphology [1]. This increase in force can not be attributed to morphological changes alone [2], highlighting the importance of cytoskeletal remodeling during cell spreading in the resistance of cells to compressive forces.
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Yang, Ling, Qiang Zhou, and Xianlong Hong. "Congestion-Driven Placement Improvement Using Cell Spreading." In 2006 International Conference on Communications, Circuits and Systems. IEEE, 2006. http://dx.doi.org/10.1109/icccas.2006.285164.

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Barmawi, A. M. "Strengthening Dynamic Cell Spreading (DCS) Image Steganography." In 2013 International Conference on Information and Network Security (ICINS 2013). Institution of Engineering and Technology, 2013. http://dx.doi.org/10.1049/cp.2013.2467.

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Shi, Jian, Benlian Xu, Mingli Lu, Peiyi Zhu, and Jihong Zhu. "Multiple Cell Tracking by Ripple Spreading Optimization." In 2018 International Conference on Control, Automation and Information Sciences (ICCAIS). IEEE, 2018. http://dx.doi.org/10.1109/iccais.2018.8570642.

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Hu, Jia, and 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.

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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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Vernerey, Franck J. "Biophysical Model of the Coupled Mechanisms of Cell Adhesion, Contraction and Spreading." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80309.

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Recent research has shown that cell spreading is highly dependent on the contractility of its cytoskeleton and the mechanical properties of its surrounding environment. This extended abstract introduces a mathematical formulation of cell spreading and contraction that couples the processes of stress fiber formation, protrusion growth through actin polymerization at the cell edge and dynamics of cross-membrane protein (integrins) enabling cell-substrate attachment. The evolving cell’s cytoskeleton is modeled as a mixture of fluid, proteins and filaments that can exchange mass and generate contraction. In particular, besides self-assembling into stress fibers, actin monomers are able to polymerize into an actin meshwork at the cell’s boundary in order to push the membrane forward and generate protrusion. These processes are possible via the development of cell-substrate attachment complexes that arise from the mechano-sensitive equilibrium of membrane proteins, known as integrins. Numerical simulations show that the proposed model is able to capture the dependency of cell spreading and contraction on substrate stiffness and chemistry. The very good agreement between model predictions and experimental observations suggests that mechanics plays a strong role into the coupled mechanisms of contraction, adhesion and spreading of adherent cells.
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Li, Jianrong, Tianle Cheng, and Martin Y. M. Chiang. "Finite Element Modelling of Cell Adhesion Mediated by Receptor-Ligand Binding." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206297.

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The process of cell adhesion and spreading on the extracellular matrix (ECM) protein layer is mediated by the interaction of cell receptors and ECM ligands [1]. Receptors diffuse along the cell membrane surface and interact with ligands in ECM to form bonds. Cells spread and the adhesion zone grows as bond formation at the adhesion front increases to a critical level. This process involves coupling of reaction-diffusion and mechanical contact between cells and ECM. In this study, a novel numerical algorithm is developed to implement this coupling into the finite element method for modeling the process of cell adhesion and spreading. By taking the mass diffusion and the user-defined gap conductance features provided in a commercial FEM code, Abaqus [2], the process has been solved in an integrated and fully coupled manner. Preliminary results have been obtained from the simulation of cell spreading on a rigid substrate. The influence of glycocalyx layer (present at cell surface) on the adhesion development has also been incorporated into the modeling.
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Wang, Xueyan, Yici Cai, and Qiang Zhou. "Cell spreading optimization for force-directed global placers." In 2017 IEEE International Symposium on Circuits and Systems (ISCAS). IEEE, 2017. http://dx.doi.org/10.1109/iscas.2017.8050572.

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Wang, Sifei, Qiang Zhou, Xu Qian, Yici Cai, and Wenchao Gao. "GPCS: Global placement based on cell spreading method." In 2013 International Conference on Communications, Circuits and Systems (ICCCAS). IEEE, 2013. http://dx.doi.org/10.1109/icccas.2013.6765261.

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Robu, A., A. Neagu, and L. Stoicu-Tivadar. "The influence of cell-substrate and cell-medium interfacial tension on the cell spreading." In 2011 15th IEEE International Conference on Intelligent Engineering Systems (INES). IEEE, 2011. http://dx.doi.org/10.1109/ines.2011.5954714.

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Reports on the topic "Cell spreading"

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Ivanova, Svetlana I., Stoyan A. Chakarov, and Roumen G. Pankov. Formation of Fibrillar Adhesions Correlates with Spreading but Does not Depend on Cell Polarization. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, November 2018. http://dx.doi.org/10.7546/crabs.2018.11.08.

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Research, Gratis. The Mystery behind Bacterial Retrons. Gratis Research, December 2020. http://dx.doi.org/10.47496/gr.blog.05.

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Retron-mediated cell killing serves as a defensive strategy to prevent the spreading of phage infection in bacteria and the combined action of retron and CRISPR-based gene editing appear to be a potent gene-editing tool.
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