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Статті в журналах з теми "Cell adhesion"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 25 липня 2025

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1

Lipke, Peter N., Jason M. Rauceo, and Albertus Viljoen. "Cell–Cell Mating Interactions: Overview and Potential of Single-Cell Force Spectroscopy." International Journal of Molecular Sciences 23, no. 3 (2022): 1110. http://dx.doi.org/10.3390/ijms23031110.

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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 brough

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2

Katoh, Kazuo. "FAK-Dependent Cell Motility and Cell Elongation." Cells 9, no. 1 (2020): 192. http://dx.doi.org/10.3390/cells9010192.

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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 attachmen

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3

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 (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 adh

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4

Young, Katherine A., Laura Biggins, and Hayley J. Sharpe. "Protein tyrosine phosphatases in cell adhesion." Biochemical Journal 478, no. 5 (2021): 1061–83. http://dx.doi.org/10.1042/bcj20200511.

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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 prot

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5

Nakamura, N., J. Tanaka, and K. Sobue. "Rous sarcoma virus-transformed cells develop peculiar adhesive structures along the cell periphery." Journal of Cell Science 106, no. 4 (1993): 1057–69. http://dx.doi.org/10.1242/jcs.106.4.1057.

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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 re

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6

Simmons, David L. "Dissecting the modes of interactions amongst cell adhesion molecules." Development 119, Supplement (1993): 193–203. http://dx.doi.org/10.1242/dev.119.supplement.193.

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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 endo

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7

Lotz, M. M., C. A. Burdsal, H. P. Erickson, and D. R. McClay. "Cell adhesion to fibronectin and tenascin: quantitative measurements of initial binding and subsequent strengthening response." Journal of Cell Biology 109, no. 4 (1989): 1795–805. http://dx.doi.org/10.1083/jcb.109.4.1795.

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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

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8

Mentzer, S. J., D. V. Faller, and S. J. Burakoff. "Interferon-gamma induction of LFA-1-mediated homotypic adhesion of human monocytes." Journal of Immunology 137, no. 1 (1986): 108–13. http://dx.doi.org/10.4049/jimmunol.137.1.108.

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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

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9

Willaert, Ronnie G., Yeseren Kayacan, and Bart Devreese. "The Flo Adhesin Family." Pathogens 10, no. 11 (2021): 1397. http://dx.doi.org/10.3390/pathogens10111397.

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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 mechan

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10

Murphy-Ullrich, J. E., and M. Höök. "Thrombospondin modulates focal adhesions in endothelial cells." Journal of Cell Biology 109, no. 3 (1989): 1309–19. http://dx.doi.org/10.1083/jcb.109.3.1309.

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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

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11

Hall, Jeffrey W., Bruno P. Lima, Gaetan G. Herbomel, et al. "An intramembrane sensory circuit monitors sortase A–mediated processing of streptococcal adhesins." Science Signaling 12, no. 580 (2019): eaas9941. http://dx.doi.org/10.1126/scisignal.aas9941.

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Bacterial adhesins mediate adhesion to substrates and biofilm formation. Adhesins of the LPXTG family are posttranslationally processed by the cell membrane–localized peptidase sortase A, which cleaves the LPXTG motif. This generates a short C-terminal peptide (C-pep) that remains in the cell membrane, whereas the mature adhesin is incorporated into the cell wall. Genes encoding adhesins of the oral bacteriumStreptococcus gordoniiwere differentially expressed depending on whether the bacteria were isolated from saliva or dental plaque and appeared to be coordinately regulated. Deletion ofsspAa

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12

Tozluoglu, Melda, Yanlan Mao, Paul A. Bates, and Erik Sahai. "Cost–benefit analysis of the mechanisms that enable migrating cells to sustain motility upon changes in matrix environments." Journal of The Royal Society Interface 12, no. 106 (2015): 20141355. http://dx.doi.org/10.1098/rsif.2014.1355.

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Cells can move through extracellular environments with varying geometries and adhesive properties. Adaptation to these differences is achieved by switching between different modes of motility, including lamellipod-driven and blebbing motility. Further, cells can modulate their level of adhesion to the extracellular matrix (ECM) depending on both the level of force applied to the adhesions and cell intrinsic biochemical properties. We have constructed a computational model of cell motility to investigate how motile cells transition between extracellular environments with varying surface continu

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13

Bach, Cuc T. T., Sarah Creed, Jessie Zhong, et al. "Tropomyosin Isoform Expression Regulates the Transition of Adhesions To Determine Cell Speed and Direction." Molecular and Cellular Biology 29, no. 6 (2009): 1506–14. http://dx.doi.org/10.1128/mcb.00857-08.

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ABSTRACT The balance of transition between distinct adhesion types contributes to the regulation of mesenchymal cell migration, and the characteristic association of adhesions with actin filaments led us to question the role of actin filament-associating proteins in the transition between adhesive states. Tropomyosin isoform association with actin filaments imparts distinct filament structures, and we have thus investigated the role for tropomyosins in determining the formation of distinct adhesion structures. Using combinations of overexpression, knockdown, and knockout approaches, we establi

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14

Andreozzi, Elisa, and Gaylen A. Uhlich. "PchE Regulation of Escherichia coli O157:H7 Flagella, Controlling the Transition to Host Cell Attachment." International Journal of Molecular Sciences 21, no. 13 (2020): 4592. http://dx.doi.org/10.3390/ijms21134592.

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Shiga toxins and intimate adhesion controlled by the locus of enterocyte effacement are major enterohemorrhagic Escherichia coli (EHEC) virulence factors. Curli fimbriae also contribute to cell adhesion and are essential biofilm components. The transcriptional regulator PchE represses the expression of curli and their adhesion to HEp-2 cells. Past studies indicate that pchE also represses additional adhesins that contribute to HEp-2 cell attachment. In this study, we tested for pchE regulation of several tissue adhesins and their regulators. Three adhesin-encoding genes (eae, lpfA1, fliC) and

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15

van Steijn, Leonie, Inge M. N. Wortel, Clément Sire, Loïc Dupré, Guy Theraulaz, and Roeland M. H. Merks. "Computational modelling of cell motility modes emerging from cell-matrix adhesion dynamics." PLOS Computational Biology 18, no. 2 (2022): e1009156. http://dx.doi.org/10.1371/journal.pcbi.1009156.

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Lymphocytes have been described to perform different motility patterns such as Brownian random walks, persistent random walks, and Lévy walks. Depending on the conditions, such as confinement or the distribution of target cells, either Brownian or Lévy walks lead to more efficient interaction with the targets. The diversity of these motility patterns may be explained by an adaptive response to the surrounding extracellular matrix (ECM). Indeed, depending on the ECM composition, lymphocytes either display a floating motility without attaching to the ECM, or sliding and stepping motility with re

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16

Garrod, David, and Tomomi E. Kimura. "Hyper-adhesion: a new concept in cell–cell adhesion." Biochemical Society Transactions 36, no. 2 (2008): 195–201. http://dx.doi.org/10.1042/bst0360195.

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We have developed a new concept of cell–cell adhesion termed ‘hyper-adhesion’, the very strong adhesion adopted by desmosomes. This uniquely desmosomal property accounts for their ability to provide the intercellular links in the desmosome–intermediate filament complex. These links are targeted by diseases, resulting in disruption of the complex with severe consequences. Hyper-adhesion is characteristic of desmosomes in tissues and is believed to result from a highly ordered arrangement of the extracellular domains of the desmosomal cadherins that locks their binding interaction so that it is

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17

Greenwood, Jeffrey A., Anne B. Theibert, Glenn D. Prestwich, and Joanne E. Murphy-Ullrich. "Restructuring of Focal Adhesion Plaques by Pi 3-Kinase." Journal of Cell Biology 150, no. 3 (2000): 627–42. http://dx.doi.org/10.1083/jcb.150.3.627.

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Focal adhesions are an elaborate network of interconnecting proteins linking actin stress fibers to the extracellular matrix substrate. Modulation of the focal adhesion plaque provides a mechanism for the regulation of cellular adhesive strength. Using interference reflection microscopy, we found that activation of phosphoinositide 3-kinase (PI 3-kinase) by PDGF induces the dissipation of focal adhesions. Loss of this close apposition between the cell membrane and the extracellular matrix coincided with a redistribution of α-actinin and vinculin from the focal adhesion complex to the Triton X-

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18

Bialer, Magalí G., Gabriela Sycz, Florencia Muñoz González, Mariana C. Ferrero, Pablo C. Baldi, and Angeles Zorreguieta. "Adhesins of Brucella: Their Roles in the Interaction with the Host." Pathogens 9, no. 11 (2020): 942. http://dx.doi.org/10.3390/pathogens9110942.

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A central aspect of Brucella pathogenicity is its ability to invade, survive, and replicate in diverse phagocytic and non-phagocytic cell types, leading to chronic infections and chronic inflammatory phenomena. Adhesion to the target cell is a critical first step in the invasion process. Several Brucella adhesins have been shown to mediate adhesion to cells, extracellular matrix components (ECM), or both. These include the sialic acid-binding proteins SP29 and SP41 (binding to erythrocytes and epithelial cells, respectively), the BigA and BigB proteins that contain an Ig-like domain (binding t

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19

Akimov, Sergey S., Dmitry Krylov, Laurie F. Fleischman, and Alexey M. Belkin. "Tissue Transglutaminase Is an Integrin-Binding Adhesion Coreceptor for Fibronectin." Journal of Cell Biology 148, no. 4 (2000): 825–38. http://dx.doi.org/10.1083/jcb.148.4.825.

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The protein cross-linking enzyme tissue transglutaminase binds in vitro with high affinity to fibronectin via its 42-kD gelatin-binding domain. Here we report that cell surface transglutaminase mediates adhesion and spreading of cells on the 42-kD fibronectin fragment, which lacks integrin-binding motifs. Overexpression of tissue transglutaminase increases its amount on the cell surface, enhances adhesion and spreading on fibronectin and its 42-kD fragment, enlarges focal adhesions, and amplifies adhesion-dependent phosphorylation of focal adhesion kinase. These effects are specific for tissue

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20

NEWTON, SEAN C., and CLARKE F. MILLETTE. "Sertoli Cell Plasma Membrane Polypeptides Involved in Spermatogenic Cell‐Sertoli Cell Adhesion." Journal of Andrology 13, no. 2 (1992): 160–71. http://dx.doi.org/10.1002/j.1939-4640.1992.tb01651.x.

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ABSTRACT: This study concerns Sertoli cell‐spermatogenic cell adhesive interactions in the seminiferous tubule. Sertoli cell surface polypeptides involved in germ cell‐Sertoli cell adhesion were identified by serological inhibition of an in vitro Sertoli‐germ cell adhesion assay. This assay was modified from a previously reported adhesion assay, and employs a scanning laser cytometer for quantification of adherent cells. Reactivity of the polyclonal antiserum raised against rat Sertoli cells was also assessed via immunofluorescent microscopy. The addition of antiserum to the adhesion assay res

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21

Kirov, S. M., L. J. Hayward, and M. A. Nerrie. "Adhesion ofAeromonassp. to cell lines used as models for intestinal adhesion." Epidemiology and Infection 115, no. 3 (1995): 465–73. http://dx.doi.org/10.1017/s0950268800058623.

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SummaryAdhesion to HEp-2 cells has been shown to correlate with enteropathogenicity forAeromonasspecies. Such adhesion is thought to reflect the ability of strains to adhere to human intestinal enterocytes, although HEp-2 cells are not of intestinal origin. In this study strains ofAeromonas veroniibiotype sobria isolated from various sources were investigated in parallel assays for their ability to adhere to HEp-2 cells and to an intestinal cell line (Caco-2). Quantitative assays showed identical adhesion values were obtained with both cell lines. Adhesion was best when bacteria were grown at

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22

Banisadr, Afsheen, Mariam Eick, Pranjali Beri, et al. "EGFRvIII uses intrinsic and extrinsic mechanisms to reduce glioma adhesion and increase migration." Journal of Cell Science 133, no. 24 (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. EGFR

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23

Hillery, Cheryl A., J. Paul Scott, and Ming C. Du. "The Carboxy-Terminal Cell-Binding Domain of Thrombospondin Is Essential for Sickle Red Blood Cell Adhesion." Blood 94, no. 1 (1999): 302–9. http://dx.doi.org/10.1182/blood.v94.1.302.413k38_302_309.

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Sickle red blood cells (SS-RBCs) have enhanced adhesion to the plasma and subendothelial matrix protein thrombospondin-1 (TSP) under conditions of flow in vitro. TSP has at least four domains that mediate cell adhesion. The goal of this study was to map the site(s) on TSP that binds SS-RBCs. Purified TSP proteolytic fragments containing either the N-terminal heparin-binding domain, or the type 1, 2, or 3 repeats, failed to sustain SS-RBC adhesion (&lt;10% adhesion). However, a 140-kD thermolysin TSP fragment, containing the carboxy-terminal cell-binding domain in addition to the type 1, 2,

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24

Goodwin, Katharine, Emily E. Lostchuck, Kaitlyn M. L. Cramb, Teresa Zulueta-Coarasa, Rodrigo Fernandez-Gonzalez, and Guy Tanentzapf. "Cell–cell and cell–extracellular matrix adhesions cooperate to organize actomyosin networks and maintain force transmission during dorsal closure." Molecular Biology of the Cell 28, no. 10 (2017): 1301–10. http://dx.doi.org/10.1091/mbc.e17-01-0033.

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Tissue morphogenesis relies on the coordinated action of actin networks, cell–cell adhesions, and cell–extracellular matrix (ECM) adhesions. Such coordination can be achieved through cross-talk between cell–cell and cell–ECM adhesions. Drosophila dorsal closure (DC), a morphogenetic process in which an extraembryonic tissue called the amnioserosa contracts and ingresses to close a discontinuity in the dorsal epidermis of the embryo, requires both cell–cell and cell–ECM adhesions. However, whether the functions of these two types of adhesions are coordinated during DC is not known. Here we anal

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25

Douglas, L. Julia. "Adhesin - receptor interactions in the attachment ofCandida albicansto host epithelial cells." Canadian Journal of Botany 73, S1 (1995): 1147–53. http://dx.doi.org/10.1139/b95-371.

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The ability of Candida albicans to adhere to a variety of host surfaces is thought to be an important factor in the pathogenesis of candidosis. Adhesion of the yeast form of the fungus to epithelial cells can involve several kinds of adhesion – receptor interaction. Yeast adhesins are typically mannoproteins associated with fibrils or fimbriae on the fungal surface. Lectinlike interactions have been identified between the protein portion of two mannoprotein adhesins and glycosides containing L-fucose or N-acetylglucosamine. The fucoside-binding adhesin has been purified and shown to have an af

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26

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 mig

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27

CHAPLAIN, MARK A. J., MIROSŁAW LACHOWICZ, ZUZANNA SZYMAŃSKA, and DARIUSZ WRZOSEK. "MATHEMATICAL MODELLING OF CANCER INVASION: THE IMPORTANCE OF CELL–CELL ADHESION AND CELL–MATRIX ADHESION." Mathematical Models and Methods in Applied Sciences 21, no. 04 (2011): 719–43. http://dx.doi.org/10.1142/s0218202511005192.

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The process of invasion of tissue by cancer cells is crucial for metastasis — the formation of secondary tumours — which is the main cause of mortality in patients with cancer. In the invasion process itself, adhesion, both cell–cell and cell–matrix, plays an extremely important role. In this paper, a mathematical model of cancer cell invasion of the extracellular matrix is developed by incorporating cell–cell adhesion as well as cell–matrix adhesion into the model. Considering the interactions between cancer cells, extracellular matrix and matrix degrading enzymes, the model consists of a sys

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28

Alberici Delsin, Lara Elis, Cédric Plutoni, Anna Clouvel, et al. "MAP4K4 regulates forces at cell–cell and cell–matrix adhesions to promote collective cell migration." Life Science Alliance 6, no. 9 (2023): e202302196. http://dx.doi.org/10.26508/lsa.202302196.

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Collective cell migration is not only important for development and tissue homeostasis but can also promote cancer metastasis. To migrate collectively, cells need to coordinate cellular extensions and retractions, adhesion sites dynamics, and forces generation and transmission. Nevertheless, the regulatory mechanisms coordinating these processes remain elusive. Using A431 carcinoma cells, we identify the kinase MAP4K4 as a central regulator of collective migration. We show that MAP4K4 inactivation blocks the migration of clusters, whereas its overexpression decreases cluster cohesion. MAP4K4 r

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29

Labbate, Maurizio, Hua Zhu, Leena Thung, et al. "Quorum-Sensing Regulation of Adhesion in Serratia marcescens MG1 Is Surface Dependent." Journal of Bacteriology 189, no. 7 (2007): 2702–11. http://dx.doi.org/10.1128/jb.01582-06.

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ABSTRACT Serratia marcescens is an opportunistic pathogen and a major cause of ocular infections. In previous studies of S. marcescens MG1, we showed that biofilm maturation and sloughing were regulated by N-acyl homoserine lactone (AHL)-based quorum sensing (QS). Because of the importance of adhesion in initiating biofilm formation and infection, the primary goal of this study was to determine whether QS is important in adhesion to both abiotic and biotic surfaces, as assessed by determining the degree of attachment to hydrophilic tissue culture plates and human corneal epithelial (HCE) cells

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30

Gilmore, A. P., and L. H. Romer. "Inhibition of focal adhesion kinase (FAK) signaling in focal adhesions decreases cell motility and proliferation." Molecular Biology of the Cell 7, no. 8 (1996): 1209–24. http://dx.doi.org/10.1091/mbc.7.8.1209.

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It has been proposed that the focal adhesion kinase (FAK) mediates focal adhesion formation through tyrosine phosphorylation during cell adhesion. We investigated the role of FAK in focal adhesion structure and function. Loading cells with a glutathione-S-transferase fusion protein (GST-Cterm) containing the FAK focal adhesion targeting sequence, but not the kinase domain, decreased the association of endogenous FAK with focal adhesions. This displacement of endogenous FAK in both BALB/c 3T3 cells and human umbilical vein endothelial cells loaded with GST-Cterm decreased focal adhesion phospho

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31

Westhoff, M. A., B. Serrels, V. J. Fincham, M. C. Frame, and N. O. Carragher. "Src-Mediated Phosphorylation of Focal Adhesion Kinase Couples Actin and Adhesion Dynamics to Survival Signaling." Molecular and Cellular Biology 24, no. 18 (2004): 8113–33. http://dx.doi.org/10.1128/mcb.24.18.8113-8133.2004.

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ABSTRACT Integrin-associated focal adhesions not only provide adhesive links between cellular actin and extracellular matrix but also are sites of signal transmission into the cell interior. Many cell responses signal through focal adhesion kinase (FAK), often by integrin-induced autophosphorylation of FAK or phosphorylation by Src family kinases. Here, we used an interfering FAK mutant (4-9F-FAK) to show that Src-dependent FAK phosphorylation is required for focal adhesion turnover and cell migration, by controlling assembly of a calpain 2/FAK/Src/p42ERK complex, calpain activation, and prote

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Murphy-Ullrich, J. E., M. A. Pallero, N. Boerth, J. A. Greenwood, T. M. Lincoln, and T. L. Cornwell. "Cyclic GMP-dependent protein kinase is required for thrombospondin and tenascin mediated focal adhesion disassembly." Journal of Cell Science 109, no. 10 (1996): 2499–508. http://dx.doi.org/10.1242/jcs.109.10.2499.

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Focal adhesions are specialized regions of cell membranes that are foci for the transmission of signals between the outside and the inside of the cell. Intracellular signaling events are important in the organization and stability of these structures. In previous work, we showed that the counter-adhesive extracellular matrix proteins, thrombospondin, tenascin, and SPARC, induce the disassembly of focal adhesion plaques and we identified the active regions of these proteins. In order to determine the mechanisms whereby the anti-adhesive matrix proteins modulate cytoskeletal organization and foc

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Canalli, Andreia A., Carla F. Franco-Penteado, Fabiola Traina, et al. "Altered Red Cell and Platelet Adhesion in the Hemolytic Diseases: Hereditary Spherocytosis, Paroxysmal Nocturnal Hemoglobinuria and Sickle Cell Anemia." Blood 108, no. 11 (2006): 1238. http://dx.doi.org/10.1182/blood.v108.11.1238.1238.

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Abstract Increasing evidence exists to suggest that intravascular hemolysis may have important pathophysiological consequences resulting from reduced vascular nitric oxide (NO) bioavailability due to hemoglobin-mediated NO scavenging; such consequences may include endothelial dysfunction and vasculopathy. Hemolytic diseases such as hereditary spherocytosis (HS), paroxysmal nocturnal hemoglobinuria (PNH) and sickle cell anemia (SCA), despite having diverse etiologies, share a number of complications that include pulmonary and systolic arterial hypertension, cutaneous leg ulcerations and, in PNH

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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 (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 fo

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Oakes, Patrick W., Yvonne Beckham, Jonathan Stricker, and Margaret L. Gardel. "Tension is required but not sufficient for focal adhesion maturation without a stress fiber template." Journal of Cell Biology 196, no. 3 (2012): 363–74. http://dx.doi.org/10.1083/jcb.201107042.

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Focal adhesion composition and size are modulated in a myosin II–dependent maturation process that controls adhesion, migration, and matrix remodeling. As myosin II activity drives stress fiber assembly and enhanced tension at adhesions simultaneously, the extent to which adhesion maturation is driven by tension or altered actin architecture is unknown. We show that perturbations to formin and α-actinin 1 activity selectively inhibited stress fiber assembly at adhesions but retained a contractile lamella that generated large tension on adhesions. Despite relatively unperturbed adhesion dynamic

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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 (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 morphol

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Gallant, Nathan D., Kristin E. Michael, and Andrés J. García. "Cell Adhesion Strengthening: Contributions of Adhesive Area, Integrin Binding, and Focal Adhesion Assembly." Molecular Biology of the Cell 16, no. 9 (2005): 4329–40. http://dx.doi.org/10.1091/mbc.e05-02-0170.

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Mechanical interactions between a cell and its environment regulate migration, contractility, gene expression, and cell fate. We integrated micropatterned substrates to engineer adhesive area and a hydrodynamic assay to analyze fibroblast adhesion strengthening on fibronectin. Independently of cell spreading, integrin binding and focal adhesion assembly resulted in rapid sevenfold increases in adhesion strength to steady-state levels. Adhesive area strongly modulated adhesion strength, integrin binding, and vinculin and talin recruitment, exhibiting linear increases for small areas. However, a

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Chen, Tsute, Koji Nakayama, Lynn Belliveau, and Margaret J. Duncan. "Porphyromonas gingivalis Gingipains and Adhesion to Epithelial Cells." Infection and Immunity 69, no. 5 (2001): 3048–56. http://dx.doi.org/10.1128/iai.69.5.3048-3056.2001.

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ABSTRACT Porphyromonas gingivalis is one of the principal organisms associated with adult periodontitis. Bacterial surface proteins such as fimbriae and gingipain hemagglutinin domains have been implicated as adhesins that actuate colonization of epithelium lining the gingival sulcus. We investigated the genetics of P. gingivalis adhesion to monolayers of epithelial cells using wild-type and gingipain mutant strains. These experiments suggested that arginine-specific gingipain (Rgp) catalytic activity modulated adhesion. From the data obtained with rgp mutants, we constructed a working hypothe

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Usatyuk, Peter V., and Viswanathan Natarajan. "Regulation of reactive oxygen species-induced endothelial cell-cell and cell-matrix contacts by focal adhesion kinase and adherens junction proteins." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 6 (2005): L999—L1010. http://dx.doi.org/10.1152/ajplung.00211.2005.

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Oxidants, generated by activated neutrophils, have been implicated in the pathophysiology of vascular disorders and lung injury; however, mechanisms of oxidant-mediated endothelial barrier dysfunction are unclear. Here, we have investigated the role of focal adhesion kinase (FAK) in regulating hydrogen peroxide (H2O2)-mediated tyrosine phosphorylation of intercellular adhesion proteins and barrier function in endothelium. Treatment of bovine pulmonary artery endothelial cells (BPAECs) with H2O2 increased tyrosine phosphorylation of FAK, paxillin, β-catenin, and vascular endothelial (VE)-cadher

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Revach, Or-Yam, Inna Grosheva, and Benjamin Geiger. "Biomechanical regulation of focal adhesion and invadopodia formation." Journal of Cell Science 133, no. 20 (2020): jcs244848. http://dx.doi.org/10.1242/jcs.244848.

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ABSTRACTIntegrin adhesions are a structurally and functionally diverse family of transmembrane, multi-protein complexes that link the intracellular cytoskeleton to the extracellular matrix (ECM). The different members of this family, including focal adhesions (FAs), focal complexes, fibrillar adhesions, podosomes and invadopodia, contain many shared scaffolding and signaling ‘adhesome’ components, as well as distinct molecules that perform specific functions, unique to each adhesion form. In this Hypothesis, we address the pivotal roles of mechanical forces, generated by local actin polymeriza

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Petrie, Laurenne E., Allison C. Leonard, Julia Murphy, and Georgina Cox. "Development and validation of a high-throughput whole cell assay to investigate Staphylococcus aureus adhesion to host ligands." Journal of Biological Chemistry 295, no. 49 (2020): 16700–16712. http://dx.doi.org/10.1074/jbc.ra120.015360.

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Staphylococcus aureus adhesion to the host's skin and mucosae enables asymptomatic colonization and the establishment of infection. This process is facilitated by cell wall-anchored adhesins that bind to host ligands. Therapeutics targeting this process could provide significant clinical benefits; however, the development of anti-adhesives requires an in-depth knowledge of adhesion-associated factors and an assay amenable to high-throughput applications. Here, we describe the development of a sensitive and robust whole cell assay to enable the large-scale profiling of S. aureus adhesion to hos

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Hiscox, S., and W. G. Jiang. "Ezrin regulates cell-cell and cell-matrix adhesion, a possible role with E-cadherin/beta-catenin." Journal of Cell Science 112, no. 18 (1999): 3081–90. http://dx.doi.org/10.1242/jcs.112.18.3081.

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Ezrin, radixin, moesin and merlin form a subfamily of conserved proteins in the band 4.1 superfamily. The function of these proteins is to link the plasma membrane to the actin cytoskeleton. Merlin is defective or absent in schwannomas and meningiomas and has been suggested to function as a tumour suppressor. In this study, we have examined the role of ezrin as a potential regulator of the adhesive and invasive behaviour of tumour cells. We have shown that following inhibition of ezrin expression in colo-rectal cancer cells using antisense oligonucleotides, these cells displayed a reduced cell

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Wang, Chenlu, Sagar Chowdhury, Meghan Driscoll, Carole A. Parent, S. K. Gupta, and Wolfgang Losert. "The interplay of cell–cell and cell–substrate adhesion in collective cell migration." Journal of The Royal Society Interface 11, no. 100 (2014): 20140684. http://dx.doi.org/10.1098/rsif.2014.0684.

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Collective cell migration often involves notable cell–cell and cell–substrate adhesions and highly coordinated motion of touching cells. We focus on the interplay between cell–substrate adhesion and cell–cell adhesion. We show that the loss of cell-surface contact does not significantly alter the dynamic pattern of protrusions and retractions of fast migrating amoeboid cells ( Dictyostelium discoideum ), but significantly changes their ability to adhere to other cells. Analysis of the dynamics of cell shapes reveals that cells that are adherent to a surface may coordinate their motion with nei

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Bradley, William D., Samuel E. Hernández, Jeffrey Settleman, and Anthony J. Koleske. "Integrin Signaling through Arg Activates p190RhoGAP by Promoting Its Binding to p120RasGAP and Recruitment to the Membrane." Molecular Biology of the Cell 17, no. 11 (2006): 4827–36. http://dx.doi.org/10.1091/mbc.e06-02-0132.

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The Rho family GTPases RhoA (Rho), Rac1, and Cdc42 are essential effectors of integrin-mediated cell attachment and spreading. Rho activity, which promotes formation of focal adhesions and actin stress fibers, is inhibited upon initial cell attachment to allow sampling of the new adhesive environment. The Abl-related gene (Arg) tyrosine kinase mediates adhesion-dependent inhibition of Rho through phosphorylation and activation of the Rho inhibitor p190RhoGAP-A (p190). p190 phosphorylation promotes its binding to p120RasGAP (p120). Here, we elucidate the mechanism by which p120 binding regulate

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Taylor, James T., Rebekka Harting, Samer Shalaby, Charles M. Kenerley, Gerhard H. Braus, and Benjamin A. Horwitz. "Adhesion as a Focus in Trichoderma–Root Interactions." Journal of Fungi 8, no. 4 (2022): 372. http://dx.doi.org/10.3390/jof8040372.

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Fungal spores, germlings, and mycelia adhere to substrates, including host tissues. The adhesive forces depend on the substrate and on the adhesins, the fungal cell surface proteins. Attachment is often a prerequisite for the invasion of the host, hence its importance. Adhesion visibly precedes colonization of root surfaces and outer cortex layers, but little is known about the molecular details. We propose that by starting from what is already known from other fungi, including yeast and other filamentous pathogens and symbionts, the mechanism and function of Trichoderma adhesion will become a

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Zaidel-Bar, R., M. Cohen, L. Addadi, and B. Geiger. "Hierarchical assembly of cell–matrix adhesion complexes." Biochemical Society Transactions 32, no. 3 (2004): 416–20. http://dx.doi.org/10.1042/bst0320416.

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The adhesion of cells to the extracellular matrix is a dynamic process, mediated by a series of cell-surface and matrix-associated molecules that interact with each other in a spatially and temporally regulated manner. These interactions play a major role in tissue formation, cellular migration and the induction of adhesion-mediated transmembrane signals. In this paper, we show that the formation of matrix adhesions is a hierarchical process, consisting of several sequential molecular events. One of the earliest steps in surface recognition is mediated, in some cells, by a 1 μm-thick cell-surf

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Wallace, Charles S., Sophie A. Strike, and George A. Truskey. "Smooth muscle cell rigidity and extracellular matrix organization influence endothelial cell spreading and adhesion formation in coculture." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 3 (2007): H1978—H1986. http://dx.doi.org/10.1152/ajpheart.00618.2007.

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Efforts to develop functional tissue-engineered blood vessels have focused on improving the strength and mechanical properties of the vessel wall, while the functional status of the endothelium within these vessels has received less attention. Endothelial cell (EC) function is influenced by interactions between its basal surface and the underlying extracellular matrix. In this study, we utilized a coculture model of a tissue-engineered blood vessel to evaluate EC attachment, spreading, and adhesion formation to the extracellular matrix on the surface of quiescent smooth muscle cells (SMCs). EC

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Nybo, Kristie. "Cell Adhesion." BioTechniques 51, no. 4 (2011): 235–37. http://dx.doi.org/10.2144/000113747.

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Goridis, C. "Cell adhesion." Research in Immunology 141, no. 7 (1990): 796–98. http://dx.doi.org/10.1016/0923-2494(90)90010-v.

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Fleming, Stewart. "Cell adhesion." Journal of Pathology 170, no. 2 (1993): 205–9. http://dx.doi.org/10.1002/path.1711700217.

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