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1
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 of homotypic adhesions. Two monoclonal antibodies to distinct epitopes on the LFA-1 alpha-chain completely inhibited homotypic adhesions. Antibodies to a variety of other monocyte surface molecules, often present at higher cell surface density than LFA-1, did not inhibit homotypic adhesion. A panel of monoclonal antibodies that recognized different functional epitopes on the LFA-1 alpha-chain inhibited homotypic monocyte in a hierarchy identical to that observed in previous studies of cell-mediated cytotoxicity. These findings suggest that LFA-1 serves an adhesive function for human mononuclear phagocytes. In addition to providing a molecular basis for homotypic monocyte adhesions, the results suggest a more general role for LFA-1 in monocyte adhesion reactions.
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Willaert, Ronnie G., Yeseren Kayacan, 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 mechanisms of the Flo adhesins whose structure has been solved are discussed in detail. Finally, we identified from Pfam database datamining yeasts that could express Flo adhesins and are encountered in human infections and their adhesin architectures. These yeasts are discussed in relation to their adhesion characteristics and involvement in infections.
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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 accessible. There is a sequence, and perhaps functional, homology to other rhizosphere-competent Sordariomycetes. Specifically, Verticillium dahliae is a soil-borne pathogen that establishes itself in the xylem and causes destructive wilt disease. Metarhizium species are best-known as insect pathogens with biocontrol potential, but they also colonize roots. Verticillium orthologs of the yeast Flo8 transcription factor, Som1, and several other relevant genes are already under study for their roles in adhesion. Metarhizium encodes relevant adhesins. Trichoderma virens encodes homologs of Som1, as well as adhesin candidates. These genes should provide exciting leads toward the first step in the establishment of beneficial interactions with roots in the rhizosphere.
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Willaert, Ronnie. "Adhesins of Yeasts: Protein Structure and Interactions." Journal of Fungi 4, no. 4 (2018): 119. http://dx.doi.org/10.3390/jof4040119.
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The ability of yeast cells to adhere to other cells or substrates is crucial for many yeasts. The budding yeast Saccharomyces cerevisiae can switch from a unicellular lifestyle to a multicellular one. A crucial step in multicellular lifestyle adaptation is self-recognition, self-interaction, and adhesion to abiotic surfaces. Infectious yeast diseases such as candidiasis are initiated by the adhesion of the yeast cells to host cells. Adhesion is accomplished by adhesin proteins that are attached to the cell wall and stick out to interact with other cells or substrates. Protein structures give detailed insights into the molecular mechanism of adhesin-ligand interaction. Currently, only the structures of a very limited number of N-terminal adhesion domains of adhesins have been solved. Therefore, this review focuses on these adhesin protein families. The protein architectures, protein structures, and ligand interactions of the flocculation protein family of S. cerevisiae; the epithelial adhesion family of C. glabrata; and the agglutinin-like sequence protein family of C. albicans are reviewed and discussed.
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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 establish that Tm5NM1 preferentially stabilizes focal adhesions and drives the transition to fibrillar adhesions via stabilization of actin filaments. Moreover, our data suggest that the expression of Tm5NM1 is a critical determinant of paxillin phosphorylation, a signaling event that is necessary for focal adhesion disassembly. Thus, we propose that Tm5NM1 can regulate the feedback loop between focal adhesion disassembly and focal complex formation at the leading edge that is required for productive and directed cell movement.
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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. Our results demonstrate that while adhesion to the abiotic surface was AHL regulated, adhesion to the HCE cell biotic surface was not. Type I fimbriae were identified as the critical adhesin for non-QS-mediated attachment to the biotic HCE cell surface but played no role in adhesion to the abiotic surface. While we were not able to identify a single QS-regulated adhesin essential for attachment to the abiotic surface, four AHL-regulated genes involved in adhesion to the abiotic surface were identified. Interestingly, two of these genes, bsmA and bsmB, were also shown to be involved in adhesion to the biotic surface in a non-QS-controlled fashion. Therefore, the expression of these two genes appears to be cocontrolled by regulators other than the QS system for mediation of attachment to HCE cells. We also found that QS in S. marcescens regulates other potential cell surface adhesins, including exopolysaccharide and the outer membrane protein OmpX. We concluded that S. marcescens MG1 utilizes different regulatory systems and adhesins in attachment to biotic and abiotic surfaces and that QS is a main regulatory pathway in adhesion to an abiotic surface but not in adhesion to a biotic surface.
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TAKASHIMA, Yoshinori, Motofumi OSAKI, Tomoko SEKINE, Yasushi SHOJIMA, and Akira HARADA. "Materials Adhesion Based on Molecular Adhesive Techniques." Journal of The Adhesion Society of Japan 54, no. 6 (2018): 201–11. http://dx.doi.org/10.11618/adhesion.54.201.
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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 protein tyrosine phosphatases (PTPs) and protein tyrosine kinases. Several PTPs are implicated in the assembly and maintenance of cell adhesions, however, their signalling functions remain poorly defined. The PTPs can act by directly dephosphorylating adhesive complex components or function as scaffolds. In this review, we will focus on human PTPs and discuss their individual roles in major adhesion complexes, as well as Hippo signalling. We have collated PTP interactome and cell adhesome datasets, which reveal extensive connections between PTPs and cell adhesions that are relatively unexplored. Finally, we reflect on the dysregulation of PTPs and cell adhesions in disease.
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Simmons, David L. "Dissecting the modes of interactions amongst cell adhesion molecules." Development 119, Supplement (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 endothelial adhesin, CD31, and secondly the heterotypic adhesins ICAM-1, 2 and 3, which interact with the leukocyte integrin LFA-1.
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Saed, Ghassan M., and Michael P. Diamond. "Molecular Characterization of Postoperative Adhesions: The Adhesion Phenotype." Journal of the American Association of Gynecologic Laparoscopists 11, no. 3 (2004): 307–14. http://dx.doi.org/10.1016/s1074-3804(05)60041-2.
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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 ofsspAandsspB (sspAB), both of which encode LPXTG-containing adhesins, unexpectedly enhanced adhesion and biofilm formation. C-peps produced from a model LPXTG-containing adhesin localized to the cell membrane and bound to and inhibited the intramembrane sensor histidine kinase SGO_1180, thus preventing activation of the cognate response regulator SGO_1181. The absence of SspAB C-peps induced the expression of thescaCBAoperon encoding the lipoprotein adhesin ScaA, which was sufficient to preserve and even enhance biofilm formation. This C-pep–driven regulatory circuit also exists in pathogenic streptococci and is likely conserved among Gram-positive bacteria. This quality control mechanism ensures that the bacteria can form biofilms under diverse environmental conditions and may play a role in optimizing adhesion and biofilm formation.
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Iwasaki, T., and H. Miura. "Molecular dynamics analysis of adhesion strength of interfaces between thin films." Journal of Materials Research 16, no. 6 (2001): 1789–94. http://dx.doi.org/10.1557/jmr.2001.0247.
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We have developed a molecular-dynamics technique for determining the adhesion strength of the interfaces between different materials. This technique evaluates the adhesion strength by calculating the adhesive fracture energy defined as the difference between the total potential energy of the material-connected state and that of the material-separated state. The extended Tersoff-type potential is applied to calculate the adhesive fracture energy of metal/dielectric interfaces as well as metal/metal interfaces. We used the technique to determine the adhesion strength of the interfaces between ULSI-interconnect materials (Al and Cu) and diffusion-barrier materials (TiN and W). It was also applied to determine the adhesion strength of interfaces between the interconnect materials and a dielectric material (SiO2). Because the adhesion strength determined by this technique agrees well with that measured by scratch testing, this technique is considered to be effective for determining the adhesion strength.
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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 attachment, called focal adhesions. FAK has been suggested to play a role in the attachment of cells at adhesive micropatterns by affecting cell polarity. Therefore, the localization of FAK might play a key role in recognition of the border of the cell with the adhesive micropattern, thus regulating cell polarity and the cell axis. This review discusses the regulation and molecular mechanism of cell proliferation and cell elongation by FAK and its associated signal transduction proteins.
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Zamir, E., B. Z. Katz, S. Aota, K. M. Yamada, B. Geiger, and Z. Kam. "Molecular diversity of cell-matrix adhesions." Journal of Cell Science 112, no. 11 (1999): 1655–69. http://dx.doi.org/10.1242/jcs.112.11.1655.
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In this study we have examined for molecular heterogeneity of cell-matrix adhesions and the involvement of actomyosin contractility in the selective recruitment of different plaque proteins. For this purpose, we have developed a novel microscopic approach for molecular morphometry, based on automatic identification of matrix adhesions, followed by quantitative immunofluorescence and morphometric analysis. Particularly informative was fluorescence ratio imaging, comparing the local labeling intensities of different plaque molecules, including vinculin, paxillin, tensin and phosphotyrosine-containing proteins. Ratio imaging revealed considerable molecular heterogeneity between and within adhesion sites. Most striking were the differences between focal contacts, which are vinculin- and paxillin-rich and contain high levels of phosphotyrosine, and fibrillar adhesions, which are tensin-rich and contain little or no phosphotyrosine. Ratio imaging also revealed considerable variability in the molecular substructure of individual focal contacts, pointing to a non-uniform distribution of phosphotyrosine and the different plaque constituents. Studying the quantitative relationships between the various components of the submembrane plaque indicated that the levels of vinculin, paxillin and phosphotyrosine in adhesion sites are positively correlated with each other and negatively correlated with the levels of tensin. Tyrosine phosphorylation of focal contacts was highly sensitive to cellular contractility, and was diminished within 5 minutes after treatment with the kinase inhibitor H-7, an inhibitor of actomyosin contractility. This was followed by the loss of paxillin and vinculin from the focal adhesions. Tensin-rich fibrillar adhesions were relatively insensitive to H-7 treatment. These findings suggest a role for contractility in the generation of matrix adhesion diversity.
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von Fraunhofer, J. Anthony. "Adhesion and Cohesion." International Journal of Dentistry 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/951324.
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The phenomena of adhesion and cohesion are reviewed and discussed with particular reference to dentistry. This review considers the forces involved in cohesion and adhesion together with the mechanisms of adhesion and the underlying molecular processes involved in bonding of dissimilar materials. The forces involved in surface tension, surface wetting, chemical adhesion, dispersive adhesion, diffusive adhesion, and mechanical adhesion are reviewed in detail and examples relevant to adhesive dentistry and bonding are given. Substrate surface chemistry and its influence on adhesion, together with the properties of adhesive materials, are evaluated. The underlying mechanisms involved in adhesion failure are covered. The relevance of the adhesion zone and its importance with regard to adhesive dentistry and bonding to enamel and dentin is discussed.
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Ciobanasu, Corina, Bruno Faivre, and Christophe Le Clainche. "Actin Dynamics Associated with Focal Adhesions." International Journal of Cell Biology 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/941292.
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Cell-matrix adhesion plays a major role during cell migration. Proteins from adhesion structures connect the extracellular matrix to the actin cytoskeleton, allowing the growing actin network to push the plasma membrane and the contractile cables (stress fibers) to pull the cell body. Force transmission to the extracellular matrix depends on several parameters including the regulation of actin dynamics in adhesion structures, the contractility of stress fibers, and the mechanosensitive response of adhesion structures. Here we highlight recent findings on the molecular mechanisms by which actin assembly is regulated in adhesion structures and the molecular basis of the mechanosensitivity of focal adhesions.
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Kikuchi, Kiyoshi, Kentaro Setoyama, Seiya Takada, et al. "E8002 Inhibits Peripheral Nerve Adhesion by Enhancing Fibrinolysis of l-Ascorbic Acid in a Rat Sciatic Nerve Model." International Journal of Molecular Sciences 21, no. 11 (2020): 3972. http://dx.doi.org/10.3390/ijms21113972.
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Perineural adhesions leading to neuropathy are one of the most undesirable consequences of peripheral nerve surgery. However, there are currently no widely used compounds with anti-adhesive effects in the field of peripheral nerve surgery. E8002 is a novel, anti-adhesive, multi-layer membrane that contains L-ascorbic acid (AA). Here, we investigated the effect and mechanism of E8002 in a rat sciatic nerve adhesion model. A total of 21 rats were used. Six weeks after surgery, macroscopic adhesion scores were significantly lower in the E8002 group (adhesion procedure followed by nerve wrapping with E8002) compared to the E8002 AA(−) group (adhesion procedure followed by nerve wrapping with the E8002 membrane excluding AA) and adhesion group (adhesion procedure but no treatment). Correspondingly, a microscopic examination revealed prominent scar tissue in the E8002 AA(−) and adhesion groups. Furthermore, an in vitro study using human blood samples showed that AA enhanced tissue-type, plasminogen activator-mediated fibrinolysis. Altogether, these results suggest that E8002 may exert an anti-adhesive action via AA and the regulation of fibrinolysis.
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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 proteolysis of FAK. Expression of 4-9F-FAK in FAK-deficient fibroblasts also disrupts F-actin assembly associated with normal adhesion and spreading. In addition, we found that FAK's ability to regulate both assembly and disassembly of the actin and adhesion networks may be linked to regulation of the protease calpain. Surprisingly, we also found that the same interfering 4-9F-FAK mutant protein causes apoptosis of serum-deprived, transformed cells and suppresses anchorage-independent growth. These data show that Src-mediated phosphorylation of FAK acts as a pivotal regulator of both actin and adhesion dynamics and survival signaling, which, in turn, control apparently distinct processes such as cell migration and anchorage-independent growth. This also highlights that dynamic regulation of actin and adhesions (which include the integrin matrix receptors) is critical to signaling output and biological responses.
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Tam, Lik-ho, and Denvid Lau. "Molecular simulation of adhesion property recovery in the cellulose/phenolic adhesive interface: the role of water molecules." MRS Proceedings 1793 (2015): 59–66. http://dx.doi.org/10.1557/opl.2015.826.
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ABSTRACTCellulose is one of the most abundant substances in the world, and the major constituent in the wood structure. Phenolic adhesive is largely used in the wood manufacture for gluing the wood panels together. The cellulose/phenolic adhesive interface is a representative of the interface between the wood panels and adhesives in the wood products. As the wood panels and adhesive are sensitive to environmental humidity, the interfacial adhesion of such interface when subjected to a humid environment can be a major factor in the durability of final products. Here, the role of water molecules on the adhesion property of cellulose/phenolic adhesive interface is investigated by molecular dynamics simulations. The simulation results reveal that the adhesion energy between cellulose and phenolic adhesive can be reduced by 86.5% with saturated moisture ingress. Meanwhile, it is demonstrated that the adhesion energy can be recovered after the interface experiences further dry conditioning. The hydrogen bonds between the cellulose and phenolic adhesive are found to account for the strong interfacial adhesion, which can be interrupted in the presence of water molecules and recovered after further dry conditioning. The adhesion property between the wood panels and adhesives is mainly determined by water molecules absorbed at the bilayer interface, which should be considered in a wet condition.
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PARK, Hee Boong, Vita GOLUBOVSKAYA, Lihui XU, et al. "Activated Src increases adhesion, survival and alpha2-integrin expression in human breast cancer cells." Biochemical Journal 378, no. 2 (2004): 559–67. http://dx.doi.org/10.1042/bj20031392.
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Focal adhesion kinase (FAK) is an intracellular kinase that localizes to focal adhesions. FAK is overexpressed in human tumours, and FAK regulates both cellular adhesion and anti-apoptotic survival signalling. Disruption of FAK function by overexpression of the FAK C-terminal domain [FAK-CD, analogous to the FRNK (FAK-related non-kinase) protein] leads to loss of adhesion and apoptosis in tumour cells. We have shown that overexpression of an activated form of the Src tyrosine kinase suppressed the loss of adhesion induced by dominant-negative; adenoviral FAK-CD and decreased the apoptotic response in BT474 and MCF-7 breast cancer cell lines. This adhesion-dependent apoptosis was increased by the Src-family kinase inhibitor PP2 {4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine}. We have also shown that expression of activated Src in breast cancer cells increased the expression of α2-integrin and that overexpression of α2-integrin suppressed FAK-CD-mediated loss of adhesion. Our results suggest a model in which Src regulates adhesion and survival through enhanced expression of the α2-integrin. This provides a mechanism through which Src promotes cellular adhesion and alters the adhesive function of FAK.
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Tees, David F. J., and Douglas J. Goetz. "Leukocyte Adhesion: An Exquisite Balance of Hydrodynamic and Molecular Forces." Physiology 18, no. 5 (2003): 186–90. http://dx.doi.org/10.1152/nips.01444.2003.
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Leukocyte adhesion to the vascular endothelium involves a disruptive force exerted on the leukocyte by the flow of the blood and an adhesive force that forms at the leukocyte-endothelial interface. The relative strengths of these two competing forces govern leukocyte adhesion.
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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 host ligands. To validate the assay, and to gain insight into cellular factors contributing to adhesion, we profiled a sequence-defined S. aureus transposon mutant library, identifying mutants with attenuated adhesion to human-derived fibronectin, keratin, and fibrinogen. Our screening approach was validated by the identification of known adhesion-related proteins, such as the housekeeping sortase responsible for covalently linking adhesins to the cell wall. In addition, we also identified genetic loci that could represent undescribed anti-adhesive targets. To compare and contrast the genetic requirements of adhesion to each host ligand, we generated a S. aureus Genetic Adhesion Network, which identified a core gene set involved in adhesion to all three host ligands, and unique genetic signatures. In summary, this assay will enable high-throughput chemical screens to identify anti-adhesives and our findings provide insight into the target space of such an approach.
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Lipke, Peter N., and Peleg Ragonis-Bachar. "Sticking to the Subject: Multifunctionality in Microbial Adhesins." Journal of Fungi 9, no. 4 (2023): 419. http://dx.doi.org/10.3390/jof9040419.
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Bacterial and fungal adhesins mediate microbial aggregation, biofilm formation, and adhesion to host. We divide these proteins into two major classes: professional adhesins and moonlighting adhesins that have a non-adhesive activity that is evolutionarily conserved. A fundamental difference between the two classes is the dissociation rate. Whereas moonlighters, including cytoplasmic enzymes and chaperones, can bind with high affinity, they usually dissociate quickly. Professional adhesins often have unusually long dissociation rates: minutes or hours. Each adhesin has at least three activities: cell surface association, binding to a ligand or adhesive partner protein, and as a microbial surface pattern for host recognition. We briefly discuss Bacillus subtilis TasA, pilin adhesins, gram positive MSCRAMMs, and yeast mating adhesins, lectins and flocculins, and Candida Awp and Als families. For these professional adhesins, multiple activities include binding to diverse ligands and binding partners, assembly into molecular complexes, maintenance of cell wall integrity, signaling for cellular differentiation in biofilms and in mating, surface amyloid formation, and anchorage of moonlighting adhesins. We summarize the structural features that lead to these diverse activities. We conclude that adhesins resemble other proteins with multiple activities, but they have unique structural features to facilitate multifunctionality.
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Winograd-Katz, Sabina E., Shalev Itzkovitz, Zvi Kam, and Benjamin Geiger. "Multiparametric analysis of focal adhesion formation by RNAi-mediated gene knockdown." Journal of Cell Biology 186, no. 3 (2009): 423–36. http://dx.doi.org/10.1083/jcb.200901105.
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Cell adhesion to the extracellular matrix is mediated by elaborate networks of multiprotein complexes consisting of adhesion receptors, cytoskeletal components, signaling molecules, and diverse adaptor proteins. To explore how specific molecular pathways function in the assembly of focal adhesions (FAs), we performed a high-throughput, high-resolution, microscopy-based screen. We used small interfering RNAs (siRNAs) to target human kinases, phosphatases, and migration- and adhesion-related genes. Multiparametric image analysis of control and of siRNA-treated cells revealed major correlations between distinct morphological FA features. Clustering analysis identified different gene families whose perturbation induced similar effects, some of which uncoupled the interfeature correlations. Based on these findings, we propose a model for the molecular hierarchy of FA formation, and tested its validity by dynamic analysis of FA formation and turnover. This study provides a comprehensive information resource on the molecular regulation of multiple cell adhesion features, and sheds light on signaling mechanisms regulating the formation of integrin adhesions.
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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 polymerization or actomyosin-based contractility, in the formation, maturation and functionality of two members of the integrin adhesions family, namely FAs and invadopodia, which display distinct structures and functional properties. FAs are robust and stable ECM contacts, associated with contractile stress fibers, while invadopodia are invasive adhesions that degrade the underlying matrix and penetrate into it. We discuss here the mechanisms, whereby these two types of adhesion utilize a similar molecular machinery to drive very different – often opposing cellular activities, and hypothesize that early stages of FAs and invadopodia assembly use similar biomechanical principles, whereas maturation of the two structures, and their ‘adhesive’ and ‘invasive’ functionalities require distinct sources of biomechanical reinforcement.
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Guo, Jianhua, Niping Ma, Jiale Chen, and Ning Wei. "Efficient Non-Destructive Detection of Interface Adhesion State by Interfacial Thermal Conductance: A Molecular Dynamics Study." Processes 11, no. 4 (2023): 1032. http://dx.doi.org/10.3390/pr11041032.
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The state of interface adhesion, as measured by the void ratio, is a critical factor affecting the adhesion strength and heat dissipation efficiency of a system. However, non-destructive and rapid detection of the adhesion process remains a challenge. In this study, we used all-atom molecular dynamics simulations to investigate the interfacial thermal conductance of silicon and polymer at various adhesion void ratios, with the aim of achieving non-destructive and rapid detection of the adhesion process. Our results demonstrate a linear relationship between the interfacial thermal conductance and effective contact area at different temperatures, enabling the numerical value of interfacial thermal conductance to serve as an indicator of interfacial adhesion state. Furthermore, we also output the surface temperature of the adhesive interface. The non-uniformity of the surface temperature evolution can be used to identify the location of bubbles on the adhesive surface, which further reflects the bonding state of the interface. This project presents a novel approach and research framework for the non-destructive and rapid testing of the adhesion processes.
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Smith, Wendy D., Jonathan A. Pointon, Emily Abbot, et al. "Roles of Minor Pilin Subunits Spy0125 and Spy0130 in the Serotype M1 Streptococcus pyogenes Strain SF370." Journal of Bacteriology 192, no. 18 (2010): 4651–59. http://dx.doi.org/10.1128/jb.00071-10.
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ABSTRACT Adhesive pili on the surface of the serotype M1 Streptococcus pyogenes strain SF370 are composed of a major backbone subunit (Spy0128) and two minor subunits (Spy0125 and Spy0130), joined covalently by a pilin polymerase (Spy0129). Previous studies using recombinant proteins showed that both minor subunits bind to human pharyngeal (Detroit) cells (A. G. Manetti et al., Mol. Microbiol. 64:968-983, 2007), suggesting both may act as pilus-presented adhesins. While confirming these binding properties, studies described here indicate that Spy0125 is the pilus-presented adhesin and that Spy0130 has a distinct role as a wall linker. Pili were localized predominantly to cell wall fractions of the wild-type S. pyogenes parent strain and a spy0125 deletion mutant. In contrast, they were found almost exclusively in culture supernatants in both spy0130 and srtA deletion mutants, indicating that the housekeeping sortase (SrtA) attaches pili to the cell wall by using Spy0130 as a linker protein. Adhesion assays with antisera specific for individual subunits showed that only anti-rSpy0125 serum inhibited adhesion of wild-type S. pyogenes to human keratinocytes and tonsil epithelium to a significant extent. Spy0125 was localized to the tip of pili, based on a combination of mutant analysis and liquid chromatography-tandem mass spectrometry analysis of purified pili. Assays comparing parent and mutant strains confirmed its role as the adhesin. Unexpectedly, apparent spontaneous cleavage of a labile, proline-rich (8 of 14 residues) sequence separating the N-terminal ∼1/3 and C-terminal ∼2/3 of Spy0125 leads to loss of the N-terminal region, but analysis of internal spy0125 deletion mutants confirmed that this has no significant effect on adhesion.
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Ho, May, and Nicholas J. White. "Molecular mechanisms of cytoadherence in malaria." American Journal of Physiology-Cell Physiology 276, no. 6 (1999): C1231—C1242. http://dx.doi.org/10.1152/ajpcell.1999.276.6.c1231.
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Microbial pathogens subvert host adhesion molecules to disseminate or to enter host cells to promote their own survival. One such subversion is the cytoadherence of Plasmodium falciparum-infected erythrocytes (IRBC) to vascular endothelium, which protects the parasite from being removed by the spleen. The process results in microcirculatory obstruction and subsequent hypoxia, metabolic disturbances, and multiorgan failure, which are detrimental to the host. Understanding the molecular events involved in these adhesive interactions is therefore critical both in terms of pathogenesis and implications for therapeutic intervention. Under physiological flow conditions, cytoadherence occurs in a stepwise fashion through parasite ligands expressed on the surface of IRBC and the endothelial receptors CD36, intercellular adhesion molecule-1 (ICAM-1), P-selectin, and vascular adhesion molecule-1. Moreover, rolling on ICAM-1 and P-selectin increases subsequent adhesion to CD36, indicating that receptors can act synergistically. Cytoadherence may activate intracellular signaling pathways in both endothelial cells and IRBC, leading to gene expression of mediators such as cytokines, which could modify the outcome of the infection.
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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, above a threshold area, adhesion strength and focal adhesion assembly reached a saturation limit, whereas integrin binding transitioned from a uniform distribution to discrete complexes. Adhesion strength exhibited exponential increases with bound integrin numbers as well as vinculin and talin recruitment, and the relationship between adhesion strength and these biochemical events was accurately described by a simple mechanical model. Furthermore, adhesion strength was regulated by the position of an adhesive patch, comprised of bound integrins and cytoskeletal elements, which generated a constant 200-nN adhesive force. Unexpectedly, focal adhesion assembly, in particular vinculin recruitment, contributed only 30% of the adhesion strength. This work elucidates the roles of adhesive complex size and position in the generation of cell-extracellular matrix forces.
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Lungu, Mirela, Claudiu N. Lungu, Andreea Creteanu, and Mihaela C. Mehedinti. "Integrating Genomics and Molecular Biology in Understanding Peritoneal Adhesion." Current Issues in Molecular Biology 47, no. 6 (2025): 475. https://doi.org/10.3390/cimb47060475.
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Peritoneal adhesions following surgical injury remain a major clinical challenge, often resulting in severe complications, such as intestinal obstruction, chronic pain, and infertility. This review systematically integrates recent genomic and molecular biology insights into the pathogenesis of peritoneal adhesions, explicitly focusing on molecular pathways, including TGF-β signaling, COX-2-mediated inflammatory responses, fibrinolytic balance (tPA/PAI-1), angiogenesis pathways (VEGF, PDGF), and extracellular matrix remodeling (MMPs/TIMPs). Newly conducted transcriptomic and proteomic analyses highlight distinct changes in gene expression patterns in peritoneal fibroblasts during adhesion formation, pinpointing critical roles for integrins, cadherins, selectins, and immunoglobulin superfamily molecules. Recent studies indicate significant shifts in TGF-β isoforms expression, emphasizing isoform-specific impacts on fibrosis and scarring. These insights reveal substantial knowledge gaps, particularly the differential regulatory mechanisms involved in fibrosis versus normal reparative reperitonealization. Future therapeutic strategies could target these molecular pathways and inflammatory mediators to prevent or reduce adhesion formation. Further research into precise genetic markers and the exploration of targeted pharmacological interventions remain pivotal next steps in mitigating postoperative adhesion formation and improving clinical outcomes.
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Herrick, Sarah E., and Bettina Wilm. "Post-Surgical Peritoneal Scarring and Key Molecular Mechanisms." Biomolecules 11, no. 5 (2021): 692. http://dx.doi.org/10.3390/biom11050692.
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Post-surgical adhesions are internal scar tissue and a major health and economic burden. Adhesions affect and involve the peritoneal lining of the abdominal cavity, which consists of a continuous mesothelial covering of the cavity wall and majority of internal organs. Our understanding of the full pathophysiology of adhesion formation is limited by the fact that the mechanisms regulating normal serosal repair and regeneration of the mesothelial layer are still being elucidated. Emerging evidence suggests that mesothelial cells do not simply form a passive barrier but perform a wide range of important regulatory functions including maintaining a healthy peritoneal homeostasis as well as orchestrating events leading to normal repair or pathological outcomes following injury. Here, we summarise recent advances in our understanding of serosal repair and adhesion formation with an emphasis on molecular mechanisms and novel gene expression signatures associated with these processes. We discuss changes in mesothelial biomolecular marker expression during peritoneal development, which may help, in part, to explain findings in adults from lineage tracing studies using experimental adhesion models. Lastly, we highlight examples of where local tissue specialisation may determine a particular response of peritoneal cells to injury.
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Kesel, S., A. Mader, P. H. Seeberger, O. Lieleg, and M. Opitz. "Carbohydrate Coating Reduces Adhesion of Biofilm-Forming Bacillus subtilis to Gold Surfaces." Applied and Environmental Microbiology 80, no. 19 (2014): 5911–17. http://dx.doi.org/10.1128/aem.01600-14.
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ABSTRACTThe growth of bacterial biofilms in pipes and food tanks causes severe problems in industry. Biofilms growing on medical implants or catheters are of great concern, as they can cause serious infections and decrease the functionality of the medical device. The prevention of bacterial adhesion—the first step in colonization and biofilm formation—is therefore very important. Current research comprises alterations in surface properties, the prevention of adhesin biosynthesis, inhibition with receptor analogs, or the development of anti-adhesive vaccines. We present a new approach that allows us to study bacterial adhesion with high sensitivity in real-time while testing several different surfaces in parallel. Using the cantilever-array technique we demonstrate that coating of gold surfaces with mono- or disaccharides results in a reduction of the bacterial adhesion of the biofilm-forming bacteriumBacillus subtilisNCIB 3610 to these gold surfaces. This reduction in bacterial adhesion is independent of the studied carbohydrate. Using several mutant strains, we investigate the underlying molecular interactions, and our results suggest that adhesion to gold surfaces is mediated by thiol groups present in proteins of the bacterial cell membrane or biofilm matrix proteins expressed at low levels by the wild-type strain. Furthermore, our data indicate that the adhesion ofB. subtilisNCIB 3610 to carbohydrate-coated gold surfaces is facilitated by interactions between carbohydrates installed on the cantilever gold surface and an exopolysaccharide expressed by this strain. Understanding general and specific contributions of molecular interactions mediating bacterial adhesion will enable its prevention in the future.
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Mintz, Keith P. "Identification of an extracellular matrix protein adhesin, EmaA, which mediates the adhesion of Actinobacillus actinomycetemcomitans to collagen." Microbiology 150, no. 8 (2004): 2677–88. http://dx.doi.org/10.1099/mic.0.27110-0.
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Actinobacillus actinomycetemcomitans is an aetiologic agent in the development of periodontal and some systemic diseases in humans. This pathogen localizes to the underlying connective tissue of the oral cavity in individuals with periodontal disease. The adhesion of A. actinomycetemcomitans to extracellular matrix components of the connective tissue prompted this study to identify gene products mediating the interaction of A. actinomycetemcomitans to these molecules. A transposon mutagenesis system was optimized for use in A. actinomycetemcomitans and used to generate an insertional mutant library. A total of 2300 individual insertion transposon mutants were screened for changes in the adhesion to collagen and fibronectin. Mutants were identified which exhibited the following phenotypes: a decrease in collagen binding; a decrease in fibronectin binding; a decrease in binding to both proteins; and an increase in binding to both collagen and fibronectin. The identification of mutants defective in adhesion to the individual proteins indicates that distinct adhesins are expressed by this organism. Molecular analysis of these mutants implicated 11 independent loci in protein adhesion. One gene, emaA, is likely to encode a direct mediator of collagen adhesion, based on predicted protein features homologous to the collagen-binding protein YadA of Yersinia enterocolitica. EmaA was localized to the outer membrane, as expected for an adhesin. Reduction in fibronectin adhesion appeared to be influenced by abrogation of proteins involved in molybdenum-cofactor biosynthesis. Several other loci identified as reducing or increasing adhesion to both collagen and fibronectin are suggested to be involved in regulatory cascades that promote or repress expression of collagen and fibronectin adhesins. Collectively, the results support the hypothesis that A. actinomycetemcomitans host colonization involves afimbrial adhesins for extracellular matrix proteins, and that the expression of adhesion is modulated by global regulatory mechanisms.
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Kirchgatter, Karin, and Hernando A. Del Portillo. "Clinical and molecular aspects of severe malaria." Anais da Academia Brasileira de Ciências 77, no. 3 (2005): 455–75. http://dx.doi.org/10.1590/s0001-37652005000300008.
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The erythrocytic cycle of Plasmodium falciparum presents a particularity in relation to other Plasmodium species that infect man. Mature trophozoites and schizonts are sequestered from the peripheral circulation due to adhesion of infected erythrocytes to host endothelial cells. Modifications in the surface of infected erythrocytes, termed knobs, seem to facilitate adhesion to endothelium and other erythrocytes. Adhesion provides better maturation in the microaerophilic venous atmosphere and allows the parasite to escape clearance by the spleen which recognizes the erythrocytes loss of deformability. Adhesion to the endothelium, or cytoadherence, has an important role in the pathogenicity of the disease, causing occlusion of small vessels and contributing to failure of many organs. Cytoadherence can also describe adhesion of infected erythrocytes to uninfected erythrocytes, a phenomenon widely known as rosetting. Clinical aspects of severe malaria, as well as the host receptors and parasite ligands involved in cytoadherence and rosetting, are reviewed here. The erythrocyte membrane protein 1 of P. falciparum (PfEMP1) appears to be the principal adhesive ligand of infected erythrocytes and will be discussed in more detail. Understanding the role of host receptors and parasite ligands in the development of different clinical syndromes is urgently needed to identify vaccination targets in order to decrease the mortality rates of this disease.
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Byvalov, A. A., and I. V. Konyshev. "Yersinia pseudotuberculosis-derived adhesins." Russian Journal of Infection and Immunity 9, no. 3-4 (2019): 437–48. http://dx.doi.org/10.15789/2220-7619-2019-3-4-437-448.
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Around fifteen surface components referred to adhesins have been identified in Yersinia pseudotuberculosis combining primarily microbiological, molecular and genetic, as well as immunochemical and biophysical methods. Y. pseudotuberculosis-derived adhesins vary in structure and chemical composition but they are mainly presented by protein molecules. Some of them were shown to participate not only in adhesive but in other pathogen-related physiological functions in the host-parasite interplay. Adhesins can mediate bacterial adhesion to eukaryotic cell either directly or via the extracellular matrix components. These adhesion molecules are encoded by chromosomal DNA excepting YadA protein which gene is located in the calcium-dependence plasmid pYV common for pathogenic yersisniae. An optimum temperature for adhesin biosynthesis is located close to the body temperature of warm-blooded animals; however, at low temperature only invasin InvA, full-length smooth lipopolysaccharide and porin OmpF are produced in Y. pseudotuberculosis. Several adhesins (Psa, InvA) can be expressed at low pH (corresponds to intracellular content), thereby defining pathogenic yersiniae as facultative intracellular parasites. Three human Yersinia genus pathogens differ by ability to produce adhesins. Y. pseudotuberculosis adherence to host cells or extracellular matrix components is determined by a cumulative adhesion-based activity, which expression depends on chemical composition and physicochemical environmental conditions. It’s proposed that at the initial stage of infectious process adherence of Y. pseudotuberculosis to intestinal epithelium is mediated by InvA protein and “smooth” LPS form. These adhesins are produced in bacterial cells at low (lower than 30°С) temperature occurring in environment from which a pathogen invades into the host. At later stages of pathogenesis, after penetrating through intestinal epithelium, bacterial cells produce other adhesins, which promote survival and dissemination primarily into the mesenteric lymph nodes and, possibly, liver and spleen. At later stages of pathogenesis, after penetrating through intestinal epithelium, bacterial cells produce other adhesins, which promote survival and dissemination primarily into the mesenteric lymph nodes and, perhaps, liver and spleen. Qualitative and quantitative spectrum of Y. pseudotuberculosis adhesins is determined by environmental parameters (intercellular space, intracellular content within the diverse eukaryotic cells).
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Kang, Victor, Birgit Lengerer, Ruddy Wattiez, and Patrick Flammang. "Molecular insights into the powerful mucus-based adhesion of limpets ( Patella vulgata L.)." Open Biology 10, no. 6 (2020): 200019. http://dx.doi.org/10.1098/rsob.200019.
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Limpets ( Patella vulgata L.) are renowned for their powerful attachments to rocks on wave-swept seashores. Unlike adult barnacles and mussels, limpets do not adhere permanently; instead, they repeatedly transition between long-term adhesion and locomotive adhesion depending on the tide. Recent studies on the adhesive secretions (bio-adhesives) of marine invertebrates have expanded our knowledge on the composition and function of temporary and permanent bio-adhesives. In comparison, our understanding of the limpets' transitory adhesion remains limited. In this study, we demonstrate that suction is not the primary attachment mechanism in P. vulgata ; rather, they secrete specialized pedal mucus for glue-like adhesion. Through combined transcriptomics and proteomics, we identified 171 protein sequences from the pedal mucus. Several of these proteins contain conserved domains found in temporary bio-adhesives from sea stars, sea urchins, marine flatworms and sea anemones. Many of these proteins share homology with fibrous gel-forming glycoproteins, including fibrillin, hemolectin and SCO-spondin. Moreover, proteins with potential protein- and glycan-degrading domains could have an immune defence role or assist degrading adhesive mucus to facilitate the transition from stationary to locomotive states. We also discovered glycosylation patterns unique to the pedal mucus, indicating that specific sugars may be involved in transitory adhesion. Our findings elucidate the mechanisms underlying P. vulgata adhesion and provide opportunities for future studies on bio-adhesives that form strong attachments and resist degradation until necessary for locomotion.
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Wu, Ziwei, Zhipeng Li, Yixiao Li, Haoyu Wang, Jiang Yue, and Tieling Xing. "Biomimetic Design of Underwater Adhesives Based on Tea Polyphenol-Modified Gelatin." Biomimetics 10, no. 3 (2025): 149. https://doi.org/10.3390/biomimetics10030149.
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Although many tissue adhesives with good biocompatibility are currently available, their lack of wet adhesion capacity significantly hinders their clinical application. Therefore, further development and exploration of new medical adhesives are necessary. Inspired by the adhesion mechanism of marine mussels, through modifying gelatin protein with gallic acid (GA) for wet adhesion and cross-linking gelatin (Gel) molecular chains with tea polyphenols (TP), the adhesive TP-GA/Gel was developed. The adhesive exhibited an adhesion strength of up to 130.47 kPa to porcine skin tissues and maintained a high adhesion state in various aqueous environments, demonstrating excellent and reproducible adhesion. Additionally, TP-GA/Gel possessed outstanding antimicrobial, antioxidant, and biocompatibility properties. In an in vivo wound healing study with SD rats, the wound area treated with TP-GA/Gel adhesive decreased from 10.3 mm2 to 0.9 mm2 after 15 days, promoting effective and scarless wound healing. These results highlight the promising clinical potential of TP-GA/Gel as a medical adhesive.
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ENDO, Takeshi, and Atsushi SUDO. "Designs of Functional Materials -From Molecular Design to Molecular Engineering for Industrial Production." Journal of The Adhesion Society of Japan 49, no. 2 (2013): 63–69. http://dx.doi.org/10.11618/adhesion.49.63.
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MORI, Kunio. "The 21th Century Adhesion Technorogy - Molecular Adhesives -." Journal of The Adhesion Society of Japan 43, no. 6 (2007): 242–48. http://dx.doi.org/10.11618/adhesion.43.242.
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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 regulates p190 activation after adhesion. We show that p190 requires its p120-binding domain to undergo Arg-dependent activation in vivo. However, p120 binding does not activate p190RhoGAP activity in vitro. Instead, activation of p190 requires recruitment to the cell periphery. Integrin-mediated adhesion promotes relocalization of p190 and p120 to the cell periphery in wild-type fibroblasts, but not in arg−/− fibroblasts. A dominant-negative p120 fragment blocks p190:p120 complex formation, prevents activation of p190 by adhesion, and disrupts the adhesion-dependent recruitment of p190 to the cell periphery. Our results demonstrate that integrin signaling through Arg activates p190 by promoting its association with p120, resulting in recruitment of p190 to the cell periphery where it inhibits Rho.
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Schimmel, Lilian, and Emma Gordon. "The precise molecular signals that control endothelial cell–cell adhesion within the vessel wall." Biochemical Society Transactions 46, no. 6 (2018): 1673–80. http://dx.doi.org/10.1042/bst20180377.
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Endothelial cell–cell adhesion within the wall of the vasculature controls a range of physiological processes, such as growth, integrity and barrier function. The adhesive properties of endothelial cells are tightly controlled by a complex cascade of signals transmitted from the surrounding environment or from within the cells themselves, with the dynamic nature of cellular adhesion and the regulating signalling networks now beginning to be appreciated. Here, we summarise the current knowledge of the mechanisms controlling endothelial cell–cell adhesion in the developing and mature blood vasculature.
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Zhang, Jin, He Liu, Huan Xu та ін. "Molecular weight-modulated electrospun poly(ε-caprolactone) membranes for postoperative adhesion prevention". RSC Adv. 4, № 79 (2014): 41696–704. http://dx.doi.org/10.1039/c4ra07216b.
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Electrospun PCL membranes with various molecular weights behave distinctively for the prevention of surgery induced-adhesions, which finally helped acquire well-suited candidates for anti-adhesion biomaterial films.
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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 highly resistant to disruption. This ordered arrangement may be reflected by and dependent upon a similarly ordered molecular structure of the desmosomal plaque. Hyper-adhesion can be down-regulated to a more weakly adhesive state by cell signalling involving protein kinase C, which translocates to the desmosomal plaque. Down-regulation takes place in wound edge epithelium and appears to be accompanied by loss of the ordered arrangement causing desmosomes to adopt the type of weaker adhesion characteristic of adherens junctions. We review the evidence for hyper-adhesion and speculate on the molecular basis of its mechanism.
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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 brought into contact in an atomic force microscope (AFM), and the adhesive forces are monitored through the course of mating. The results have shown some remarkable characteristics of mating adhesins and add knowledge about the design and evolution of mating adhesins.
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TANAKA, Keiji. "Molecular Picture of Adhesive Interface." Journal of The Adhesion Society of Japan 56, no. 2 (2020): 42–47. http://dx.doi.org/10.11618/adhesion.56.42.
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AMAMOTO, Yoshifumi, and Yuichi MASUBUCHI. "Molecular Simulation on Polymer Adhesives." Journal of The Adhesion Society of Japan 53, no. 1 (2017): 19–23. http://dx.doi.org/10.11618/adhesion.53.19.
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Cooley, Marion A., Jill M. Broome, Christoph Ohngemach, Lewis H. Romer, and Michael D. Schaller. "Paxillin Binding Is Not the Sole Determinant of Focal Adhesion Localization or Dominant-Negative Activity of Focal Adhesion Kinase/Focal Adhesion Kinase-related Nonkinase." Molecular Biology of the Cell 11, no. 9 (2000): 3247–63. http://dx.doi.org/10.1091/mbc.11.9.3247.
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The carboxy-terminal 150 residues of the focal adhesion kinase (FAK) comprise the focal adhesion-targeting sequence, which is responsible for its subcellular localization. The mechanism of focal adhesion targeting has not been fully elucidated. We describe a mutational analysis of the focal adhesion-targeting sequence of FAK to further examine the mechanism of focal adhesion targeting and explore additional functions encoded by the carboxy-terminus of FAK. The results demonstrate that paxillin binding is dispensable for focal adhesion targeting of FAK. Cell adhesion-dependent tyrosine phosphorylation strictly correlated with the ability of mutants to target to focal adhesions. Focal adhesion targeting was also a requirement for maximal FAK-dependent tyrosine phosphorylation of paxillin and FAK-related nonkinase (FRNK)–dependent inhibition of endogenous FAK function. However, there were additional requirements for these latter functions because we identified mutants that target to focal adhesions, yet are defective for the induction of paxillin phosphorylation or the dominant-negative function of FRNK. Furthermore, the paxillin-binding activity of FRNK mutants did not correlate with their ability to inhibit FAK, suggesting that FRNK has other targets in addition to paxillin.
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Katz, Ben-Zion, Eli Zamir, Alexander Bershadsky, Zvi Kam, Kenneth M. Yamada, and Benjamin Geiger. "Physical State of the Extracellular Matrix Regulates the Structure and Molecular Composition of Cell-Matrix Adhesions." Molecular Biology of the Cell 11, no. 3 (2000): 1047–60. http://dx.doi.org/10.1091/mbc.11.3.1047.
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This study establishes that the physical state of the extracellular matrix can regulate integrin-mediated cytoskeletal assembly and tyrosine phosphorylation to generate two distinct types of cell-matrix adhesions. In primary fibroblasts, α5β1 integrin associates mainly with fibronectin fibrils and forms adhesions structurally distinct from focal contacts, independent of actomyosin-mediated cell contractility. These “fibrillar adhesions” are enriched in tensin, but contain low levels of the typical focal contact components paxillin, vinculin, and tyrosine-phosphorylated proteins. However, when the fibronectin is covalently linked to the substrate, α5β1integrin forms highly tyrosine-phosphorylated, “classical” focal contacts containing high levels of paxillin and vinculin. These experiments indicate that the physical state of the matrix, not just its molecular composition, is a critical factor in defining cytoskeletal organization and phosphorylation at adhesion sites. We propose that molecular organization of adhesion sites is controlled by at least two mechanisms: 1) specific integrins associate with their ligands in transmembrane complexes with appropriate cytoplasmic anchor proteins (e.g., fibronectin–α5β1integrin–tensin complexes), and 2) physical properties (e.g., rigidity) of the extracellular matrix regulate local tension at adhesion sites and activate local tyrosine phosphorylation, recruiting a variety of plaque molecules to these sites. These mechanisms generate structurally and functionally distinct types of matrix adhesions in fibroblasts.
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AlMotasem, Ahmed Tamer. "Influence of Alloying Additives on The Adhesive Properties of Steels: Atomic Level Simulation." JOURNAL OF ADVANCES IN PHYSICS 14, no. 3 (2018): 5734–40. http://dx.doi.org/10.24297/jap.v14i3.7601.
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In the present work we report atomistic molecular dynamics simulation results on adhesion force between self-mated iron/iron, iron/vanadium, iron-cementite and iron/titanium surfaces has been determined and we found that iron/cementite surface exhibits lower adhesive force than that of iron/iron surface. The results showed that adhesion, quantified by the work of adhesion, decreased as the vanadium content increased and highest reduction was obtained for 10 at.% vanadium and 7.5 at.% for titanium. Furthermore, the variation of adhesion force with temperature was studied in the temperature range between 300-700 K and we found that the adhesive force generally is lowered at higher temperature.
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Takahashi, Kunio. "Manipulation Mechanisms for Micro-Assembly Technology." Materials Science Forum 502 (December 2005): 327–34. http://dx.doi.org/10.4028/www.scientific.net/msf.502.327.
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Author has been working about mechanisms of some manipulation methods for micro-assembly, i.e., a mechanical method, an electro-adhesive method, and a capillary method. For the purpose of optimization and breakthrough of the micro-assembly technology, theoretical understanding of adhesion phenomenon is essential, because the adhesional force is proportional to the size of objects meanwhile gravitational force is proportional to the third power of it. Consequently the adhesion phenomenon is no more negligible for the smaller objects usually less than 1 mm, e.g., micro-objects. Author will introduce our analyses about the manipulation mechanisms and related basic approaches to the adhesion phenomena including an adhesion force measurement in Auger electron spectroscope, an elastic continuum approximation approach using contact mechanics, a quantum mechanics approach for surface energy, a molecular mechanics approach for surface and interfacial energies. Also it will be expressed that our data base project for the surface and interfacial energies is based on these basic approaches for the purpose of optimization and/or breakthrough of the micro-assembly technology.