Relevant bibliographies by topics / Migration Adhesion

Academic literature on the topic 'Migration Adhesion'

Author: Grafiati
Published: 6 September 2023

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Journal articles on the topic "Migration Adhesion"

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Aguilar-Cuenca, Rocio, Clara Llorente-Gonzalez, Carlos Vicente, and Miguel Vicente-Manzanares. "Microfilament-coordinated adhesion dynamics drives single cell migration and shapes whole tissues." F1000Research 6 (February 17, 2017): 160. http://dx.doi.org/10.12688/f1000research.10356.1.

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Cell adhesion to the substratum and/or other cells is a crucial step of cell migration. While essential in the case of solitary migrating cells (for example, immune cells), it becomes particularly important in collective cell migration, in which cells maintain contact with their neighbors while moving directionally. Adhesive coordination is paramount in physiological contexts (for example, during organogenesis) but also in pathology (for example, tumor metastasis). In this review, we address the need for a coordinated regulation of cell-cell and cell-matrix adhesions during collective cell migration. We emphasize the role of the actin cytoskeleton as an intracellular integrator of cadherin- and integrin-based adhesions and the emerging role of mechanics in the maintenance, reinforcement, and turnover of adhesive contacts. Recent advances in understanding the mechanical regulation of several components of cadherin and integrin adhesions allow us to revisit the adhesive clutch hypothesis that controls the degree of adhesive engagement during protrusion. Finally, we provide a brief overview of the major impact of these discoveries when using more physiological three-dimensional models of single and collective cell migration.
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Peacock, Justin G., Ann L. Miller, William D. Bradley, Olga C. Rodriguez, Donna J. Webb, and Anthony J. Koleske. "The Abl-related Gene Tyrosine Kinase Acts through p190RhoGAP to Inhibit Actomyosin Contractility and Regulate Focal Adhesion Dynamics upon Adhesion to Fibronectin." Molecular Biology of the Cell 18, no. 10 (October 2007): 3860–72. http://dx.doi.org/10.1091/mbc.e07-01-0075.

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In migrating cells, actin polymerization promotes protrusion of the leading edge, whereas actomyosin contractility powers net cell body translocation. Although they promote F-actin–dependent protrusions of the cell periphery upon adhesion to fibronectin (FN), Abl family kinases inhibit cell migration on FN. We provide evidence here that the Abl-related gene (Arg/Abl2) kinase inhibits fibroblast migration by attenuating actomyosin contractility and regulating focal adhesion dynamics. arg−/− fibroblasts migrate at faster average speeds than wild-type (wt) cells, whereas Arg re-expression in these cells slows migration. Surprisingly, the faster migrating arg−/− fibroblasts have more prominent F-actin stress fibers and focal adhesions and exhibit increased actomyosin contractility relative to wt cells. Interestingly, Arg requires distinct functional domains to inhibit focal adhesions and actomyosin contractility. The kinase domain–containing Arg N-terminal half can act through the RhoA inhibitor p190RhoGAP to attenuate stress fiber formation and cell contractility. However, Arg requires both its kinase activity and its cytoskeleton-binding C-terminal half to fully inhibit focal adhesions. Although focal adhesions do not turn over efficiently in the trailing edge of arg−/− cells, the increased contractility of arg−/− cells tears the adhesions from the substrate, allowing for the faster migration observed in these cells. Together, our data strongly suggest that Arg inhibits cell migration by restricting actomyosin contractility and regulating its coupling to the substrate through focal adhesions.
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González-Tarragó, Víctor, Alberto Elosegui-Artola, Elsa Bazellières, Roger Oria, Carlos Pérez-González, and Pere Roca-Cusachs. "Binding of ZO-1 to α5β1 integrins regulates the mechanical properties of α5β1–fibronectin links." Molecular Biology of the Cell 28, no. 14 (July 7, 2017): 1847–52. http://dx.doi.org/10.1091/mbc.e17-01-0006.

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Fundamental processes in cell adhesion, motility, and rigidity adaptation are regulated by integrin-mediated adhesion to the extracellular matrix (ECM). The link between the ECM component fibronectin (fn) and integrin α5β1 forms a complex with ZO-1 in cells at the edge of migrating monolayers, regulating cell migration. However, how this complex affects the α5β1-fn link is unknown. Here we show that the α5β1/ZO-1 complex decreases the resistance to force of α5β1–fn adhesions located at the edge of migrating cell monolayers while also increasing α5β1 recruitment. Consistently with a molecular clutch model of adhesion, this effect of ZO-1 leads to a decrease in the density and intensity of adhesions in cells at the edge of migrating monolayers. Taken together, our results unveil a new mode of integrin regulation through modification of the mechanical properties of integrin–ECM links, which may be harnessed by cells to control adhesion and migration.
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Longley, R. L., A. Woods, A. Fleetwood, G. J. Cowling, J. T. Gallagher, and J. R. Couchman. "Control of morphology, cytoskeleton and migration by syndecan-4." Journal of Cell Science 112, no. 20 (October 15, 1999): 3421–31. http://dx.doi.org/10.1242/jcs.112.20.3421.

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Syndecan-4 is a widely expressed transmembrane heparan sulfate proteoglycan which localizes to focal adhesions. Previous studies showed that the syndecan-4 cytoplasmic domain can associate with and potentiate the activity of protein kinase C, which is required for focal adhesion formation. To examine further the role of syndecan-4 in cell adhesion, we expressed syndecan-4 cDNA constructs in CHO-K1 cells. Syndecan-2 transfection was used to confirm effects seen were specific for syndecan-4. Cells overexpressing full length syndecan-4 core protein exhibited a more flattened, fibroblastic morphology, with increased focal adhesion formation and decreased cell motility. Expression of a syndecan-4 core protein with either a partial or complete deletion of the cytoplasmic domain or of an antisense construct led to markedly decreased spreading and focal adhesion formation, a more epithelioid morphology, and decreased motility. Overexpression of syndecan-2 changed the adhesive phenotype, but did not markedly alter focal adhesion and microfilament bundle formation. The data suggest that syndecan-4 is a regulator of focal adhesion and stress fiber formation, and influences both morphology and migration.
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Ventre, Maurizio, Carlo Fortunato Natale, Carmela Rianna, and Paolo Antonio Netti. "Topographic cell instructive patterns to control cell adhesion, polarization and migration." Journal of The Royal Society Interface 11, no. 100 (November 6, 2014): 20140687. http://dx.doi.org/10.1098/rsif.2014.0687.

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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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Powner, Dale, Petra M. Kopp, Susan J. Monkley, David R. Critchley, and Fedor Berditchevski. "Tetraspanin CD9 in cell migration." Biochemical Society Transactions 39, no. 2 (March 22, 2011): 563–67. http://dx.doi.org/10.1042/bst0390563.

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Tetraspanin CD9 is associated with integrin adhesion receptors and it was reported that CD9 regulates integrin-dependent cell migration and invasion. Pro- and anti-migratory effects of CD9 have been linked to adhesion-dependent signalling pathways, including phosphorylation of FAK (focal adhesion kinase) and activation of phosphoinositide 3-kinase, p38 MAPK (mitogen-activated protein kinase) and JNK (c-Jun N-terminal kinase). In the present paper, we describe a novel mechanism whereby CD9 specifically controls localization of talin1, one of the critical regulators of integrin activation, to focal adhesions: CD9-deficiency leads to impaired localization of talin1 to focal adhesions and correlates with increased motility of breast cancer cells.
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Banisadr, Afsheen, Mariam Eick, Pranjali Beri, Alison D. Parisian, Benjamin Yeoman, Jesse K. Placone, Adam J. Engler, and Frank Furnari. "EGFRvIII uses intrinsic and extrinsic mechanisms to reduce glioma adhesion and increase migration." Journal of Cell Science 133, no. 24 (November 26, 2020): jcs247189. http://dx.doi.org/10.1242/jcs.247189.

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ABSTRACTA lack of biological markers has limited our ability to identify the invasive cells responsible for glioblastoma multiforme (GBM). To become migratory and invasive, cells must downregulate matrix adhesions, which could be a physical marker of invasive potential. We engineered murine astrocytes with common GBM mutations, e.g. Ink4a (Ink) or PTEN deletion and expressing a constitutively active EGF receptor truncation (EGFRvIII), to elucidate their effect on adhesion. While loss of Ink or PTEN did not affect adhesion, counterparts expressing EGFRvIII were significantly less adhesive. EGFRvIII reduced focal adhesion size and number, and these cells – with more labile adhesions – displayed enhanced migration. Regulation appears to depend not on physical receptor association to integrins but, rather, on the activity of the receptor kinase, resulting in transcriptional integrin repression. Interestingly, EGFRvIII intrinsic signals can be propagated by cytokine crosstalk to cells expressing wild-type EGFR, resulting in reduced adhesion and enhanced migration. These data identify potential intrinsic and extrinsic mechanisms that gliomas use to invade surrounding parenchyma.
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Yamana, Norikazu, Yoshiki Arakawa, Tomohiro Nishino, Kazuo Kurokawa, Masahiro Tanji, Reina E. Itoh, James Monypenny, et al. "The Rho-mDia1 Pathway Regulates Cell Polarity and Focal Adhesion Turnover in Migrating Cells through Mobilizing Apc and c-Src." Molecular and Cellular Biology 26, no. 18 (September 15, 2006): 6844–58. http://dx.doi.org/10.1128/mcb.00283-06.

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ABSTRACT Directed cell migration requires cell polarization and adhesion turnover, in which the actin cytoskeleton and microtubules work critically. The Rho GTPases induce specific types of actin cytoskeleton and regulate microtubule dynamics. In migrating cells, Cdc42 regulates cell polarity and Rac works in membrane protrusion. However, the role of Rho in migration is little known. Rho acts on two major effectors, ROCK and mDia1, among which mDia1 produces straight actin filaments and aligns microtubules. Here we depleted mDia1 by RNA interference and found that mDia1 depletion impaired directed migration of rat C6 glioma cells by inhibiting both cell polarization and adhesion turnover. Apc and active Cdc42, which work together for cell polarization, localized in the front of migrating cells, while active c-Src, which regulates adhesion turnover, localized in focal adhesions. mDia1 depletion impaired localization of these molecules at their respective sites. Conversely, expression of active mDia1 facilitated microtubule-dependent accumulation of Apc and active Cdc42 in the polar ends of the cells and actin-dependent recruitment of c-Src in adhesions. Thus, the Rho-mDia1 pathway regulates polarization and adhesion turnover by aligning microtubules and actin filaments and delivering Apc/Cdc42 and c-Src to their respective sites of action.
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Wang, Shujie, Takashi Watanabe, Kenji Matsuzawa, Akira Katsumi, Mai Kakeno, Toshinori Matsui, Feng Ye, et al. "Tiam1 interaction with the PAR complex promotes talin-mediated Rac1 activation during polarized cell migration." Journal of Cell Biology 199, no. 2 (October 15, 2012): 331–45. http://dx.doi.org/10.1083/jcb.201202041.

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Migrating cells acquire front-rear polarity with a leading edge and a trailing tail for directional movement. The Rac exchange factor Tiam1 participates in polarized cell migration with the PAR complex of PAR3, PAR6, and atypical protein kinase C. However, it remains largely unknown how Tiam1 is regulated and contributes to the establishment of polarity in migrating cells. We show here that Tiam1 interacts directly with talin, which binds and activates integrins to mediate their signaling. Tiam1 accumulated at adhesions in a manner dependent on talin and the PAR complex. The interactions of talin with Tiam1 and the PAR complex were required for adhesion-induced Rac1 activation, cell spreading, and migration toward integrin substrates. Furthermore, Tiam1 acted with talin to regulate adhesion turnover. Thus, we propose that Tiam1, with the PAR complex, binds to integrins through talin and, together with the PAR complex, thereby regulates Rac1 activity and adhesion turnover for polarized migration.
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Kim, Sarah Hyun Ji, and Daniel A. Hammer. "Integrin crosstalk allows CD4+ T lymphocytes to continue migrating in the upstream direction after flow." Integrative Biology 11, no. 10 (October 2019): 384–93. http://dx.doi.org/10.1093/intbio/zyz034.

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Abstract In order to perform critical immune functions at sites of inflammation, circulatory T lymphocytes must be able to arrest, adhere, migrate and transmigrate on the endothelial surface. This progression of steps is coordinated by cellular adhesion molecules (CAMs), chemokines, and selectins presented on the endothelium. Two important interactions are between Lymphocyte Function-associated Antigen-1 (LFA-1) and Intracellular Adhesion Molecule-1 (ICAM-1) and also between Very Late Antigen-4 (VLA-4) and Vascular Cell Adhesion Molecule-1 (VCAM-1). Recent studies have shown that T lymphocytes and other cell types can migrate upstream (against the direction) of flow through the binding of LFA-1 to ICAM-1. Since upstream migration of T cells depends on a specific adhesive pathway, we hypothesized that mechanotransduction is critical to migration, and that signals might allow T-cells to remember their direction of migration after the flow is terminated. Cells on ICAM-1 surfaces migrate against the shear flow, but the upstream migration reverts to random migration after the flow is stopped. Cells on VCAM-1 migrate with the direction of flow. However, on surfaces that combine ICAM-1 and VCAM-1, cells crawl upstream at a shear rate of 800 s−1 and continue migrating in the upstream direction for at least 30 minutes after the flow is terminated—we call this ‘migrational memory’. Post-flow upstream migration on VCAM-1/ICAM-1 surfaces is reversed upon the inhibition of PI3K, but conserved with cdc42 and Arp2/3 inhibitors. Using an antibody against VLA-4, we can block migrational memory on VCAM-1/ICAM-1 surfaces. Using a soluble ligand for VLA-4 (sVCAM-1), we can promote migrational memory on ICAM-1 surfaces. These results indicate that, while upstream migration under flow requires LFA-1 binding to immobilized ICAM-1, signaling from VLA-4 and PI3K activity is required for the migrational memory of CD4+ T cells. These results indicate that crosstalk between integrins potentiates the signal of upstream migration.
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Dissertations / Theses on the topic "Migration Adhesion"

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Burthem, John. "Hairy cell adhesion and migration." Thesis, University of Liverpool, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240394.

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Sundar, Rajan Vinoth Edal Joseph. "Adhesion and transendothelial migration of cancer cells." Thesis, Université Grenoble Alpes (ComUE), 2016. http://www.theses.fr/2016GREAV065/document.

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Les métastases sont responsables de 90 % des décès causés par le cancer. Les métastases sont des foyers cancéreux secondaires qui se forment à distance de la tumeur d’origine. Des cellules cancéreuses quittent la tumeur primaire, rejoignent la circulation sanguine puis colonisent des organes voisins par migration à travers l’endothélium vasculaire. Ce phénomène d’adhésion à l’endothélium et de migration à travers l’endothélium appelé l’extravasation est une étape clé du processus métastatique. L’identification des molécules impliquées constitue une priorité dans le but d’élaborer de nouvelles drogues anticancéreuses. Nous avons précédemment montré que la molécule d’adhésion cellulaire InterCellular Adhesion Molecule-1 (ICAM-1) exprimée par les cellules endothéliales, est impliquée dans l’interaction des cellules de cancer de la vessie (BCs) avec l’endothélium. Cependant les ligands d’ICAM-1 n’ont pas été étudiés. Dans cette étude, nous utilisons des tests d'adhésion cellulaire et la microscopie à force atomique (AFM) afin d’identifier les ligands d’ICAM-1 et de mesurer les forces impliquées dans l’interaction ligand-ICAM-1. Nous avons identifié que les protéines MUC1 et CD43 exprimées par les BCs les plus invasives se lient à ICAM-1 en développant des forces d’intensité différente selon le couple considéré. Une analyse détaillée des événements de rupture suggère que CD43 est fortement lié au cytosquelette et que son interaction avec ICAM-1 correspond principalement à des sauts brusques. Au contraire, MUC1 semble être lié faiblement au cytosquelette et ses interactions avec ICAM-1 sont principalement associées à la formation de filaments membranaires ou « tethers ». Les forces mises en jeu lors de la migration des cellules cancéreuses à travers l'endothélium ont été étudiées par microscopie de forces de traction (TFM). Les résultats préliminaires montrent que les tractions exercées par les cellules cancéreuses lors de l’extravasation sont mesurables par TFM
Cancer metastasis is associated with 90% cancer-associated deaths, when cancer cells escape from the primary tumor and form metastatic colonies in secondary sites. Extravasation is an important step in cancer metastasis, where cancer cells carried in blood, adhere and transmigrate through the endothelium. Therefore identifying the key molecules involved during the adhesion process could enable to develop new anticancer cancer drugs able to inhibit the adhesion of cancer cells to the endothelium. We have previously shown that InterCellular Adhesion Molecule-1 (ICAM-1) expressed by endothelial cells is involved in the interactions of bladder cancer cells (BCs) with the endothelium. However the ICAM-1 ligands have never been investigated. In this study, we combined adhesion assays and Atomic Force Microscopy (AFM) to identify the ligands involved and to quantify the forces relevant in such interactions. We report the expression of MUC1 and CD43 on BCs and demonstrate that these ligands interact with ICAM-1 to mediate cancer cell-endothelial cell adhesion in the case of the more invasive BCs. AFM experiments were performed to quantify the force ranges involved by MUC1 and CD43 during their interaction with ICAM-1. AFM measurements combined with a Gaussian Mixture Model showed distinct force ranges for the interaction of ICAM-1 with MUC1 and ICAM-1 with CD43. Furthermore, a detailed analysis of the rupture events suggests that CD43 is strongly connected to the cytoskeleton and that its interaction with ICAM-1 mainly corresponds to force ramps followed by sudden jumps. On the contrary, MUC1 seems to be weakly connected to the cytoskeleton as its interactions with ICAM-1 are mainly associated with the formation of tethers. The forces involved during the transmigration of cancer cells through the endothelium was investigated using Traction Force Microscopy (TFM). Preliminary results showed that tractions exerted by cancer cells during transmigration can be studied and quantified using TFM
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Baghdadchi, Negin. "CYTOKINE CONTROL OF GLIOMA ADHESION AND MIGRATION." CSUSB ScholarWorks, 2014. https://scholarworks.lib.csusb.edu/etd/93.

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Glioblastoma multiforme (GBM) is the most lethal primary central nervous system tumor, with median survival after diagnosis of less than 12 months because dissemination into the brain parenchyma limits the long-term effectiveness of surgical resection, and because GBM cells are resistant to radiation and chemotherapy. This sad dismal prognosis for patients with GBM emphasizes the need for greater understand of the fundamental biology of the disease. Invasion is one of the major causes of treatment failure and death from glioma, because disseminated tumor cells provide the seeds for tumor recurrence. Inflammation is increasingly recognized as an important component of invasion. In the brain, inflammation can occur by activation of microglia, the resident macrophages of the brain, or by tumor-associated blood macrophages. Therefore, we hypothesize that activity of the innate immune system in the brain can influence tumor progression by secreting cytokines such as Tumor Necrosis Factor alpha (TNF-α). In this study, we show that patient-derived glioma spheres undergo morphological changes in response to TNF‑α that are associated with changes in migration behavior in vitro. These morphological changes include appearance of tumor islands in site different from where the primary tumor cells were seeded. We further showed that TNF‑α treated cells significantly increased expression of cell adhesion molecules such as CD44 and VCAM-1. Furthermore, we demonstrate increased cell density also caused increased in expression of cell adhesion molecules. The extent to which these are recapitulated in vivo will be investigated.
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Chen, Ning. "Role of cell adhesion molecules in melanoma transendothelial migration." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ58734.pdf.

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Golé, Laurent. "Migration of Dictyostelium Amoeba : role of Adhesion and Quorum sensing." Phd thesis, Université Claude Bernard - Lyon I, 2011. http://tel.archives-ouvertes.fr/tel-00846586.

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This thesis focuses on the analysis of the role of adhesion between substrate and cell and factors of Quorum sensing on the migration of Dictyostelium amoeba. Tools to automate the recordings of videomicroscopy and image analysis have been developed to work with very large samples of cells and toquantify cell migration. A microfluidic device for cell detachment in hydrodynamic flow combined witha motorized stage has allowed a statistical study of adhesion but also the dynamics of detachment. The analysis of the migration of Dictyostelium in non nutritive medium highlights the role of density on celldifferentiation and migration capacity. We observe the presence of a maximum speed of migration after6 hours of starvation. We show that the adhesion to glass is twice as low in deprivation buffer as inthe nutrient medium. The experiences of migration in growth medium revealed the presence of a factorof detection of density secreted by the cells and regulating their random migration. The diffusion coefficient, the persistence of the movement and morphology of cells vary depending on the concentrationof this factor. This factor does not affect cell adhesion but only the dynamics of detachment. Finally, the testing protocol developed allowed us to make a comparative study of migration by varying otherparameters such as surface or the chemical composition of experimental medium. This work concludesby outlining the possible role of adhesion to the migration of Dictyostelium in nutrient medium.
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Boespflug, Nicholas. "ATF3 regulates neutrophil migration in mice." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1382372804.

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Li, Yi-Yang Cheung H. Tak. "Basement membrane and its components on lymphocyte adhesion, migration, and proliferation." Normal, Ill. Illinois State University, 1992. http://wwwlib.umi.com/cr/ilstu/fullcit?p9234466.

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Thesis (Ph. D.)--Illinois State University, 1992.
Title from title page screen, viewed January 27, 2006. Dissertation Committee: H. Tak Cheung (chair), Anthony Otsuka, Alan Katz, Brian Wilkinson, David Weber. Includes bibliographical references (leaves 108-120) and abstract. Also available in print.
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Li, ShuShun. "Thrombospondin 1, an autocrine regulator in T cell adhesion and migration." Doctoral thesis, Umeå : Klinisk mikrobiologi, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-599.

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Cichon, Monika Agnieszka. "Axl regulates adhesion, migration and stem-like properties of cancer cells." Thesis, Queen Mary, University of London, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610930.

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Vielkind, Susina. "Role of the GTPase Rho in T cell adhesion and migration." Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406052.

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Books on the topic "Migration Adhesion"

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McGrath, John. CELL ADHESION AND MIGRATION IN SKIN DISEASE. Edited by Jonathan Barker. Abingdon, UK: Taylor & Francis, 2001. http://dx.doi.org/10.4324/9780203304594.

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Chen, Ning. Role of cell adhesion molecules in melanoma transendothelial migration. Ottawa: National Library of Canada, 2001.

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Hennigan, Shauna M. The effects of transendothelial migration on neutrophil function and programmed cell death. Dublin: University College Dublin, 1996.

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Lalor, Patricia Frances. The ability of VCAM-1 and ICAM-1 to support capture, adhesion and migration of flowing lymphocytes. Birmingham: University of Birmingham, 1998.

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Chander, Ashok Coil. Integrin-Linked Kinase, ECM Composition, and Substrate Rigidity Regulate Focal Adhesion - Actin Coupling, Modulating Survival, Proliferation and Migration: Towards a Biophysical Cancer Biomarker. [New York, N.Y.?]: [publisher not identified], 2012.

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McGrath, John, and Jonathan Barker. Cell Adhesion and Migration in Skin Disease (Cell Adhesion and Communication). CRC, 2001.

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McGrath, John, and Jonathan Barker. Cell Adhesion and Migration in Skin Disease. Taylor & Francis Group, 2001.

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McGrath, John, and Jonathan Barker. Cell Adhesion and Migration in Skin Disease. Taylor & Francis Group, 2001.

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McGrath, John, and Jonathan Barker. Cell Adhesion and Migration in Skin Disease. Taylor & Francis Group, 2001.

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Mierke, Claudia Tanja, and Akihiko Ito, eds. Editor’s Pick 2021: Highlights in Cell Adhesion and Migration. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-782-5.

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Book chapters on the topic "Migration Adhesion"

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Mondal, Chandrani, Julie Di Martino, and Jose Javier Bravo-Cordero. "Imaging Cell Adhesion and Migration." In Imaging from Cells to Animals In Vivo, 211–20. First edition. | Boca Raton : CRC Press, 2020. | Series: Series in cellular and clinical imaging: CRC Press, 2020. http://dx.doi.org/10.1201/9781315174662-15.

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McGettrick, Helen M., Lynn M. Butler, and Gerard B. Nash. "Analysis of Leukocyte Migration Through Monolayers of Cultured Endothelial Cells." In Adhesion Protein Protocols, 37–54. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-353-0_4.

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Steeber, Douglas A., Hariharan Subramanian, Jamison J. Grailer, Rochelle M. Conway, and Traci J. Storey. "L-selectin-mediated leukocyte adhesion and migration." In Adhesion Molecules: Function and Inhibition, 27–70. Basel: Birkhäuser Basel, 2007. http://dx.doi.org/10.1007/978-3-7643-7975-9_2.

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Carman, Christopher V. "High-Resolution Fluorescence Microscopy to Study Transendothelial Migration." In Integrin and Cell Adhesion Molecules, 215–45. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-166-6_15.

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Strutt, David, Ralf Schnabel, Franziska Fiedler, and Simone Prömel. "Adhesion GPCRs Govern Polarity of Epithelia and Cell Migration." In Adhesion G Protein-coupled Receptors, 249–74. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-41523-9_11.

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Bosanquet, David C., Keith G. Harding, and Wen G. Jiang. "ECIS, Cellular Adhesion and Migration in Keratinocytes." In Electric Cell-Substrate Impedance Sensing and Cancer Metastasis, 217–37. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4927-6_12.

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Lacoste, J., K. Young, and Claire M. Brown. "Live-Cell Migration and Adhesion Turnover Assays." In Methods in Molecular Biology, 61–84. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-056-4_3.

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Pijuan, Jordi, Anna Macià, and Anaïs Panosa. "Live Cell Adhesion, Migration, and Invasion Assays." In Methods in Molecular Biology, 313–29. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3052-5_20.

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Jutila, Mark A. "Selective lymphocyte migration into secondary lymphoid organs and inflamed tissues." In Vascular Adhesion Molecules and Inflammation, 141–60. Basel: Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-8743-4_8.

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Guadagno, Noemi A., and Cinzia Progida. "Probing the ER-Focal Adhesion Link During Cell Migration." In Cell Migration in Three Dimensions, 39–50. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2887-4_3.

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Conference papers on the topic "Migration Adhesion"

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Han, Sangyoon J., and 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.

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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.
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Jin, Quan, Claude Verdier, Pushpendra Singh, Nadine Aubry, and Alain Duperray. "Direct Simulation of the Migration of Leukocytes in Pressure Driven Flow." In ASME 2006 2nd Joint U.S.-European Fluids Engineering Summer Meeting Collocated With the 14th International Conference on Nuclear Engineering. ASMEDC, 2006. http://dx.doi.org/10.1115/fedsm2006-98415.

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We use the direct numerical simulation (DNS) approach to study the motion and deformation of leukocytes in pressure driven flows in a parallel plate channel in the case where there is an adhesion force between the leukocytes and the channel wall and when the adhesion force is absent. Two composite fluid models, consisting of a membrane, cytoplasm and a nucleus, are used to describe leukocytes. The first is the composite-drop model in which the cytoplasm and the nucleus are modeled as fluids, and the second is the drop-rigid-particle model in which the cytoplasm is modeled as a fluid and the nucleus as a rigid particle. The cytoplasm is modeled as a Newtonian fluid. The nucleus in the first model is assumed to be a viscoelastic liquid. The adhesion force is computed using two adhesion force models. In the first model, the adhesion force is given by a potential that varies as the fourth power of the distance between the cell and the adhesive wall. In the second model, the adhesion force is given by the Dembo’s kinetic adhesion model. The numerical code is based on the finite element method and the level-set method is used to track the cell membrane position. In the absence of the adhesion force, the equilibrium location of a freely suspended leukocyte in a pressure driven flow in a channel is shown to depend on the ratio of the cell to plasma viscosities. In presence of the adhesion force, the leukocyte is attracted to the layer of endothelial cells and, as it gets closer, it also deforms to get flatter under the shear forces. This deformation, in turn, further increases the adhesion force.
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Hirvonen, Liisa. "Super-resolution microscopy of macrophage adhesion and migration." In European Microscopy Congress 2020. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.emc2020.491.

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Baker, Brendon M., Colin K. Choi, Britta Trappmann, and Christopher S. Chen. "Engineered Fibrillar Extracellular Matrices for the Study of Directed Cell Migration." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80943.

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The biology of cell adhesion and migration has traditionally been studied on 2D glass or plastic surfaces. While such studies have shed light on the molecular mechanisms governing these processes [1], current knowledge is limited by the dissimilarity between the flat surfaces conventionally employed and the topographically complex extracellular matrix (ECM) cells routinely navigate within the body. On ECM-coated flat surfaces, cells are presented with an unlimited expanse of adhesive ligand and can spread and migrate freely. Conversely, the availability of ligand in vivo is generally restricted to ECM structures, forcing cells to form adhesions in prescribed locations distributed through 3D space depending on the geometry and organization of the surrounding matrix [2]. These physical constraints on cell adhesion likely have profound consequences on intracellular signaling and resulting migration, and calls into question whether the mechanisms and modes of cell motility observed on flat substrates are truly reflective of the in vivo scenario [3]. The topographies of ECMs found in vivo are varied but largely fibrillar, ranging from the tightly crosslinked fibers that form the sheet-like basement membrane, to the structure of fibrin-rich clots and collagenous connective tissues. Collagen comprises approximately 25% of the human body by mass, and as such, purified collagen has served as a popular setting for the study of cell migration within a fibrillar context for many decades [4]. However, a major limitation to the use of these gels is the inability to orthogonally dictate key structural features that impact cell behavior. For example, in contrast to the large range of fiber diameters found in vivo within connective tissue resulting from hierarchical collagen assembly and multiple types of collagens [3], collagen gels are limited to fibril diameters of ∼500nm. Furthermore, recreating the structural anisotropy common to connective tissues in collagen gels is technically challenging [5]. Thus, there remains a significant need for engineered fibrillar materials that afford precise and independent control of architectural and mechanical features for application in cell biology. In this work, we develop two approaches to fabricating fibrillar ECMs in order to study cell adhesion and migration in vitro.
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Zielinski, Rachel, Cosmin Mihai, and Samir Ghadiali. "Multi-Scale Modeling of Cancer Cell Migration and Adhesion During Epithelial-to-Mesenchymal Transition." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53511.

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Cancer is a leading cause of death in the US, and tumor cell metastasis and secondary tumor formation are key factors in the malignancy and prognosis of the disease. The regulation of cell motility plays an important role in the migration and invasion of cancer cells into surrounding tissues. The primary modes of increased motility in cancerous tissues may include collective migration of a group of epithelial cells during tumor growth and single cell migration of mesenchymal cells after detachment from the primary tumor site [1]. In epithelial cancers, metastasizing cells lose their cell-cell adhesions, detach from the tumor mass, begin expressing mesenchymal markers, and become highly motile and invasive, a process known as epithelial-to-mesenchymal transition (EMT) (Fig. 1) [2]. Although the cellular and biochemical signaling mechanisms underlying EMT have been studied extensively, there is limited information about the biomechanical mechanisms of EMT. In particular, it is not known how changes in cell mechanics (cell stiffness, cell-cell adhesion strength, traction forces) influence the detachment, migration and invasion processes that occur during metastasis.
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Buckingham, John, Reyda Gonzalez-Nieves, and Mary L. Cutler. "Abstract 5140: Rsu1 and the IPP adhesion complex can regulate adhesion and migration in glioma cell lines." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5140.

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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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Mai, Junyu, Song Li, and Xiang Zhang. "Protein Dot Array Patterning for Study of Cell Adhesion and Migration." In 2007 International Nano-Optoelectronics Workshop (iNOW). IEEE, 2007. http://dx.doi.org/10.1109/inow.2007.4302938.

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Al-Mrabt, N., TA Martin, and WG Jiang. "Abstract P1-02-03: JAM-2, Junctional Adhesion Molecule-2 Influences the Adhesion and Migration of Vascular Endothelial Cell." In Abstracts: Thirty-Third Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 8‐12, 2010; San Antonio, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/0008-5472.sabcs10-p1-02-03.

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Liu, Sen, Sheng-Nan Shen, Li Hui, and Fu-Hao Cui. "Analysis of the Adhered Particle Secondary Migration on the Slider Air Bearing Surface." In ASME 2016 Conference on Information Storage and Processing Systems. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/isps2016-9623.

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An entrapped particle on the slider air bearings damages the surface of the slider or the disk. The study of particle movement on and the particle adhesion mechanism onto the slider surface is critical to reduce entrapped particle-induced damage. In this paper, we extend the previous work proposing a dynamical model of the adhesive particle redistribution and migration on the slider surface. The model predicts whether the adhered particle will remain stationary action of the aerodynamic forces. Further, particle behaviors after detachment are analyzed considering the effects of flow shear rate, particle diameter and properties. There are four particle movement styles on the slider surface. Finally, the particle migration trajectory and velocity with time on the slider surface are presented.
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Reports on the topic "Migration Adhesion"

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Chen, Chen, Peng Chen, Xia Liu, and Hua Li. Combined 5-Fluorouracil and Low Molecular Weight Heparin for the Prevention of Postoperative Proliferative Vitreoretinopathy in Patients with Retinal Detachment. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0117.

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Review question / Objective: The aim of this meta-analysis is to evaluate the efficacy and safety of intraoperative infusion of combined 5-fluorouracil and low molecular weight heparin (LMWH) for the prevention of postoperative proliferative vitreoretinopathy in patients with retinal detachment. Condition being studied: Postoperative proliferative vitreoretinopathy (PVR) is the primary cause of failure of retinal reattachment surgery. 5-fluorouracil (5-FU) inhibits the proliferation of fibroblasts, and suppresses collagen contraction. On the other hand, heparin reduces fibrin exudation, and inhibits the adhesion and migration of retinal pigment epithelial cells. We conduct this comprehensive literature search and meta-analysis to address whether intraoperative infusion of combined 5-FU and LWMH improves the primary success rate of pars plana vitrectomy, as well as reduces postoperative PVR. Our study aims to provide clinical evidence for retinal surgeons concerning their choice of intraoperative medication.
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Gothilf, Yoav, Yonathan Zohar, Susan Wray, and Hanna Rosenfeld. Inducing sterility in farmed fish by disrupting the development of the GnRH System. United States Department of Agriculture, October 2007. http://dx.doi.org/10.32747/2007.7696512.bard.

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Hypothalamic gonadotropinreleasing hormone (GnRH1) is the key hormone in the control of gametogenesis and gonadal growth in vertebrates. Developmentally, hypothalamic GnRHproducing neurons originate from the olfactory placode, migrate along olfactory axons into the forebrain, and continue to the preoptic area and hypothalamus where they function to stimulate gonadotropin secretion from the pituitary gland. An appropriate location of GnRH neurons within the hypothalamus is necessary for normal reproductive function in the adult; abnormal migration and targeting of GnRH neurons during embryogenesis results in hypogonadism and infertility. The developmental migration of GnRH neurons and axonal pathfinding in mammals are modulated by a plethora of factors, including receptors, secreted molecules, adhesion molecules, etc. Yet the exact mechanism that controls these developmental events is still unknown. We investigated these developmental events and the underlying mechanisms using a transgenic zebrafish model, Tg(gnrh1: EGFP), in which GnRH1 neurons and axons are fluorescently labeled. The role of factors that potentially affect the development of this system was investigated by testing the effect of their knockdown and mutation on the development of the GnRH1 system. In addition, their localization in relation to GnRH1 was described during development. These studies are expected to generate the scientific foundation that will lead to developing innovative technologies, based on the disruption of the early establishment of the GnRH system, for inducing sterility in farmed fish, which is highly desirable for economical and environmental reasons.
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Ori, Naomi, and Sarah Hake. Similarities and differences in KNOX function. United States Department of Agriculture, March 2008. http://dx.doi.org/10.32747/2008.7696516.bard.

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Hypothalamic gonadotropinreleasing hormone (GnRH1) is the key hormone in the control of gametogenesis and gonadal growth in vertebrates. Developmentally, hypothalamic GnRHproducing neurons originate from the olfactory placode, migrate along olfactory axons into the forebrain, and continue to the preoptic area and hypothalamus where they function to stimulate gonadotropin secretion from the pituitary gland. An appropriate location of GnRH neurons within the hypothalamus is necessary for normal reproductive function in the adult; abnormal migration and targeting of GnRH neurons during embryogenesis results in hypogonadism and infertility. The developmental migration of GnRH neurons and axonal pathfinding in mammals are modulated by a plethora of factors, including receptors, secreted molecules, adhesion molecules, etc. Yet the exact mechanism that controls these developmental events is still unknown. We investigated these developmental events and the underlying mechanisms using a transgenic zebrafish model, Tg(gnrh1: EGFP), in which GnRH1 neurons and axons are fluorescently labeled. The role of factors that potentially affect the development of this system was investigated by testing the effect of their knockdown and mutation on the development of the GnRH1 system. In addition, their localization in relation to GnRH1 was described during development. These studies are expected to generate the scientific foundation that will lead to developing innovative technologies, based on the disruption of the early establishment of the GnRH system, for inducing sterility in farmed fish, which is highly desirable for economical and environmental reasons.
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Haugh, Jason M. Integration of Soluble and Adhesive Gradient Signals in Directed Cell Migration. Fort Belvoir, VA: Defense Technical Information Center, November 2006. http://dx.doi.org/10.21236/ada467054.

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