Artykuły w czasopismach na temat „Adhesion”
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Willaert, Ronnie G., Yeseren Kayacan i Bart Devreese. "The Flo Adhesin Family". Pathogens 10, nr 11 (28.10.2021): 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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Lee, Y. K., i K. Y. Puong. "Competition for adhesion between probiotics and human gastrointestinal pathogens in the presence of carbohydrate". British Journal of Nutrition 88, S1 (wrzesień 2002): S101—S108. http://dx.doi.org/10.1079/bjn2002635.
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The adhesion ofLactobacillus rhamnosusGG to human enterocyte-like Caco-2 cells was not inhibited by eight carbohydrates tested, namelyN-acetyl-glucosamine, galactose, glucose, fructose, fucose, mannose, methyl-α-D-mannopyranoside and sucrose. The degree of hydrophobicity predicted the adhesion ofL. rhamnosusGG to Caco-2 cells.L. rhamnosusGG, however, was able to compete withEscherichia coliandSalmonellaspp. of low hydrophobicity and high adhesin–receptor interaction for adhesion to Caco-2 cells. The interference of adhesion of these gastrointestinal (GI) bacteria byL. rhamnosusGG was probably through steric hindrance, and the degree of inhibition was related to the distribution of the adhesin receptors and hydrophobins on the Caco-2 surface. A Carbohydrate Index for Adhesion (CIA) was used to depict the binding property of adhesins on bacteria surfaces. CIA was defined as the sum of the fraction of adhesion in the presence of carbohydrates, with reference to the adhesion measured in the absence of any carbohydrate. The degree of competition for receptor sites betweenLactobacillus caseiShirota and GI bacteria is a function of their CIA distance. There were at least two types of adhesins on the surface ofL. caseiShirota. The study provides a scientific basis for the screening and selection of probiotics that compete with selective groups of pathogens for adhesion to intestinal surfaces. It also provides a model for the characterisation of adhesins and adhesin–receptor interactions.
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Del Canto, Felipe, Douglas J. Botkin, Patricio Valenzuela, Vsevolod Popov, Fernando Ruiz-Perez, James P. Nataro, Myron M. Levine i in. "Identification of Coli Surface Antigen 23, a Novel Adhesin of Enterotoxigenic Escherichia coli". Infection and Immunity 80, nr 8 (29.05.2012): 2791–801. http://dx.doi.org/10.1128/iai.00263-12.
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ABSTRACTEnterotoxigenicEscherichia coli(ETEC) is an important cause of diarrhea, mainly in developing countries. Although there are 25 different ETEC adhesins described in strains affecting humans, between 15% and 50% of the clinical isolates from different geographical regions are negative for these adhesins, suggesting that additional unidentified adhesion determinants might be present. Here, we report the discovery of Coli Surface Antigen 23 (CS23), a novel adhesin expressed by an ETEC serogroup O4 strain (ETEC 1766a), which was negative for the previously known ETEC adhesins, albeit it has the ability to adhere to Caco-2 cells. CS23 is encoded by an 8.8-kb locus which contains 9 open reading frames (ORFs), 7 of them sharing significant identity with genes required for assembly of K88-related fimbriae. This gene locus, namedaal(adhesion-associatedlocus), is required for the adhesion ability of ETEC 1766a and was able to confer this adhesive phenotype to a nonadherentE. coliHB101 strain. The CS23 major structural subunit, AalE, shares limited identity with known pilin proteins, and it is more closely related to the CS13 pilin protein CshE, carried by human ETEC strains. Our data indicate that CS23 is a new member of the diverse adhesin repertoire used by ETEC strains.
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Nakamura, N., J. Tanaka i K. Sobue. "Rous sarcoma virus-transformed cells develop peculiar adhesive structures along the cell periphery". Journal of Cell Science 106, nr 4 (1.12.1993): 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 reflection microscopy. They were more easily destroyed by incubating the cells with RGD-containing peptide than were the focal adhesions. In contrast to focal adhesions and podosomes, actin bundles were not detected within the peripheral adhesions, where pp60v-src and tyrosine-phosphorylated proteins accumulated. Expression of the integrin was determined by the substratum composition when BY1 cells were cultured in serum-free culture medium. Under such conditions, BY1 cells expressed the peripheral adhesions within 3 hours on adhesion molecule-coated glass. On the other hand, in serum-containing medium, they first developed focal adhesions transiently at their early stage of adhesion, and then the peripheral adhesions were predominantly expressed within 12 hours. Podosomes were formed in a time course similar to that of the peripheral adhesions. These findings suggest that the peripheral adhesion is a class of stable adhesive structure distinct from the focal adhesion or podosome of BY1 cells. Similar close contact-type peripheral adhesions with the integrin were also observed in a variety of cultured cells such as normal fibroblasts at their logarithmic growth phase, phorbol ester-treated fibroblasts, and several malignant tumor cells, with poorly organized focal adhesions and stress fibers. These findings further suggest that the peripheral adhesions may be widely involved in the adhesion of cells that inadequately develop stress fibers and focal adhesions.
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Orazov, Mekan R., Viktor E. Radzinsky, Marina B. Khamoshina, Михалева M. Mikhaleva i Sevinc Ya Ismailzade. "Anti-adhesive barriers in clinical practice: personalized patient management". Gynecology 23, nr 6 (15.12.2021): 480–84. http://dx.doi.org/10.26442/20795696.2021.6.201292.
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The adhesive process is an urgent problem of operative gynecology. The number of women suffering from complications of the adhesive process is growing every year, not to mention the deaths associated with this problem. Polygenic etiology, low efficiency of treatment of the adhesion process determined the priority of searching for methods to prevent the process of adhesion formation or, at least, to reduce the severity of postoperative adhesion, at least a decrease in the severity of postoperative adhesion. The review presents the current paradigm of the pathogenesis of the formation of postoperative adhesions and the possibility of preventing adhesive disorders in gynecological patients.
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Douglas, L. Julia. "Adhesin - receptor interactions in the attachment ofCandida albicansto host epithelial cells". Canadian Journal of Botany 73, S1 (31.12.1995): 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 affinity for glycosphingolipid receptors carrying the H blood-group antigen. A fimbrial adhesin has also been described that binds to gangliosides containing a βGalNAc(1–4)βGal disaccharide sequence. Other mannoprotein adhesins proposed recently include the factor 6 epitope present on serotype A strains of C. albicans and an integrin analogue. Adhesin expression appears to be regulated by a number of environmental signals, including osmolarity and the availability of iron and sugars. Additional adhesion-dependent signals might trigger further responses such as the initiation of morphogenesis. Key words: Candida albicans, yeast adhesion, epithelial cell adhesion.
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Al-Kaabi, Arshad F. Jassem. "Evaluating The Effect of Humidity on Adhesion Strength of Skin Adhesive". Molecular and Cellular Biomedical Sciences 4, nr 3 (2.11.2020): 135. http://dx.doi.org/10.21705/mcbs.v4i3.148.
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Background: Skin adhesive has been used for attaching certain medical application to the human skin for functional and/or esthetic purposes. Silicone adhesive is the most common type of skin adhesives that are recently used. This study aims to evaluate the possible effect of humidity on the performance of silicone skin adhesive.Materials and Methods: Twenty-four silicone samples were divided into 2 main groups based on relative humidity (RH) exposure, namely 43% RH and 98% RH. Six samples from each group were tested for adhesion strength after 1 hour of adhesion, and the other 6 samples were tested after 2 hours of adhesion by conducting 180 degree peel test. The data were statistically analyzed for significant difference. Results: The results showed that at 43% RH, the adhesion strength was higher than the 98% RH group. The results also showed that at both humidity settings the adhesion strength after the first hours of adhesion was lower than the adhesion strength after the second hour.Conclusion: The silicone skin adhesive performance can be affected by the increase of relative humidity which needs more time of application to skin to reach the best adhesion function.Keywords: adhesions strength, humidity effect on adhesion, silicone adhesive, skin adhesives
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Taylor, James T., Rebekka Harting, Samer Shalaby, Charles M. Kenerley, Gerhard H. Braus i Benjamin A. Horwitz. "Adhesion as a Focus in Trichoderma–Root Interactions". Journal of Fungi 8, nr 4 (6.04.2022): 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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Kikuchi, Kiyoshi, Kentaro Setoyama, Seiya Takada, Shotaro Otsuka, Kazuki Nakanishi, Kosuke Norimatsu, Akira Tani i in. "E8002 Inhibits Peripheral Nerve Adhesion by Enhancing Fibrinolysis of l-Ascorbic Acid in a Rat Sciatic Nerve Model". International Journal of Molecular Sciences 21, nr 11 (1.06.2020): 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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Lotz, M. M., C. A. Burdsal, H. P. Erickson i D. R. McClay. "Cell adhesion to fibronectin and tenascin: quantitative measurements of initial binding and subsequent strengthening response." Journal of Cell Biology 109, nr 4 (1.10.1989): 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 response required cytoskeletal involvement. By contrast to the marked strengthening of adhesion to FN, adhesion to TN was unchanged or weakened after 15 min at 37 degrees C. The absolute strength of adhesion achieved varied according to protein and cell type. When a mixed substratum of fibronectin and tenascin was tested, the presence of tenascin was found to reduce the level of the strengthening of cell adhesion normally observed at 37 degrees C on a substratum of fibronectin alone. Parallel analysis of corresponding interference reflection micrographs showed that differences in the area of cell surface within 10-15 nm of the substratum correlated closely with each of the changes in adhesion observed: after incubation for 15 min on fibronectin at 37 degrees C, glioma cells increased their surface area within close contact to the substrate by integral to 125-fold. Cells on tenascin did not increase their surface area of contact. The increased surface area of contact and the inhibitory activity of cytochalasin b suggest that the adhesive "strengthening" in the 15 min after initial binding brings additional adhesion molecules into the adhesive site and couples the actin cytoskeleton to the adhesion complex.
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Yushkov, Boris, Alexey Sarapultsev i German Sarapultsev. "Major Characteristics of Experimental Models of Abdominal Adhesions". Journal of Experimental and Clinical Surgery 13, nr 2 (29.06.2020): 157–62. http://dx.doi.org/10.18499/2070-478x-2020-13-2-157-162.
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The search for preventive and treatment methods for adhesions of the abdominal cavity and adhesive disease is one of the most important tasks of pharmaceutical and medical sciences; and the solution is based on experimental research studies involving animals. However, the varietyof adhesion modeling techniques, as well as specific features of experimental animals imply considerable difficulties to such research. The aim of the review was to describe and systematize experimental models of the adhesive process in the peritoneum applicable to small laboratory animals. The authors identify major models of adhesion induction, emphasizing the species differences of small laboratory animals that could affect the interpretation and extrapolation of the data obtained. The authors have proven that since adhesion is a complete product of the body inflammatory response to tissue damage, the treatment of adhesions should be solely based on surgical techniques, while therapeutic approaches might only prevent, slow down or reduce the intensity of adhesion processes.
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Young, Katherine A., Laura Biggins i Hayley J. Sharpe. "Protein tyrosine phosphatases in cell adhesion". Biochemical Journal 478, nr 5 (10.03.2021): 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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Seo, Su Hyun, Geun Joo Choi, Oh Haeng Lee i Hyun Kang. "Effect of methylene blue on experimental postoperative adhesion: A systematic review and meta-analysis". PLOS ONE 17, nr 5 (19.05.2022): e0268178. http://dx.doi.org/10.1371/journal.pone.0268178.
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Adhesion is a primary challenge following surgery, and the anti-adhesive effect of methylene blue (MB) has been investigated. This systematic review and meta-analysis aimed to evaluate the effect of MB on postoperative adhesions in experimental studies. We initially searched OVID-MEDLINE, EMBASE, and Google Scholar in February 2021, and then in May 2021. The anti-adhesive efficacy of MB was compared with that of the control (either placebo or nothing) after the surgical procedure. The primary and secondary outcomes were the macroscopic and microscopic adhesion scores, respectively. Traditional meta-analysis, meta-regression, and trial sequential analysis (TSA) were performed to analyze the retrieved outcomes. We included 13 experimental studies of 367 rats (200 rats received MB and 167 rats received placebo or nothing). The macroscopic adhesion scores were significantly lower in the MB-administered group than in the control group (standardized mean difference, 2.313; 95% confidence interval, 1.104 to3.523; I2 = 94.0%, Tau = 2.059). Meta-regression analysis showed that macroscopic adhesion tended to decrease with an increase in MB dose. TSA demonstrated that the cumulative Z curve crossed both the conventional test and trial sequential monitoring boundary for the macroscopic adhesion score. MB had a beneficial effect on intraperitoneal adhesion following laparotomy, and adhesions decreased with increase in dose.
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Mentzer, S. J., D. V. Faller i S. J. Burakoff. "Interferon-gamma induction of LFA-1-mediated homotypic adhesion of human monocytes." Journal of Immunology 137, nr 1 (1.07.1986): 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. "Adhesins of Yeasts: Protein Structure and Interactions". Journal of Fungi 4, nr 4 (27.10.2018): 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, Maha Mahmassani, Galina Schevzov, Justine Stehn, Lauren N. Cowell i in. "Tropomyosin Isoform Expression Regulates the Transition of Adhesions To Determine Cell Speed and Direction". Molecular and Cellular Biology 29, nr 6 (5.01.2009): 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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Kuznetsova, M. V., i J. S. Gizatullina. "Genetic adhesion profiles and adhesive variability of uropathogenic <i>Escherichia coli</i> strains". Russian Journal of Infection and Immunity 11, nr 3 (23.08.2020): 481–90. http://dx.doi.org/10.15789/2220-7619-gap-1413.
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Our study was aimed at investigating prevalence of adhesion genetic determinants among uropathogenic E. coli strains and assessing their correlation with level of specific and non-specific adhesion. E. coli bacterial cultures (n = 33) isolated from patients with urinary tract infection were examined. A phylogenetic group of strains was detected by using Clermont quadriplex-PCR method. Detection of fimbrial and afimbrial adhesin genes was carried out with end-point PCR. Level of erythrocyte-specific, non-specific hydrophobic and hydrophilic adhesion as well as biofilm formation were estimated by using standard methods. Adhesin genes were detected with the following frequencies: fimH — 75.76%, flu — 66.67%, iha — 39.40%, papC — 33.33%. Each of the genes sfaDE, upaG, afa/draBC and yqi was found with frequency 18.18%, whereas eaeA was not detected. Seven strains (21.21%) carried solely fimbrial adhesin genes, three strains (9.09%) — afimbrial adhesin genes, and twenty-one strains (63.64%) had genes of both adhesin types. Twenty-three individual adhesion genotypes were found among thirty-three UPEC strains. A combination of at least four genes were detected in 45.45% strains, among which 60% belonged to phylogroup B2. Odds ratio for adhesin gene prevalence in B2 group was calculated. It was shown that in B2 group yqi and sfaDE genes were detected by 14-fold more frequently (OR = 14.286) than in other phylogroups, and flu gene was observed at 10-fold higher rate (OR = 10.000). No correlation between such genes and level of adhesion to erythrocytes was found, whereas fimH+, papC+ and upaG+ strains had higher level of non-specific hydrophilic adhesion. It was shown that fimbrial adhesins accounted for bacterial adhesion and biofilm formation stronger than afimbrial ones. Thicker biofilm tended to form on latex catheter surface for strains with positive genetic profile for adhesin gene carriers.
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Samartsev, V. A., V. A. Gavrilov, B. S. Pushkarev, A. A. Parshakov, M. P. Kuznetsova i M. V. Kuznetsova. "Peritoneal adhesion: state of issue and modern methods of prevention". Perm Medical Journal 36, nr 3 (8.08.2019): 72–90. http://dx.doi.org/10.17816/pmj36372-90.
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Peritoneal adhesion (PA) is still an actual surgical issue. It is known that any surgical intervention causes abdominal adhesion that, in its turn, induces a number of complications such as adhesive intestinal obstruction. There is registered a high lethality among patients with the developed acute adhesive intestinal obstruction. Adhesive intestinal obstruction hurts health of patients, leading to eight (on average) days of hospitalization and intrahospital lethality of 3 % per episode. The cause of the development of a significant number of lethal cases is imperfection of preventive, diagnostic, therapeutic measures; 20 to 30 % of patients with adhesive intestinal obstruction need surgical treatment. Heavy expenses in the system of healthcare are required for treatment of peritoneal adhesions. The review presents the data regarding modern state of the problem, advanced tendencies in diagnosis, prevention and treatment of patients with peritoneal adhesions, their use in practical studies.
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Bodnar, O., V. Khashchuk, L. Vatamanescu i B. Bodnar. "OPTIMIZATION OF SURGICAL TREATMENT AND PREVENTION OF THE DEVELOPMENT OF ADHESIVE DISEASE OF THE ABDOMINAL CAVITY IN EXPERIMENTAL MODELING". Clinical anatomy and operative surgery 20, nr 2 (28.08.2021): 14–23. http://dx.doi.org/10.24061/1727-0847.20.2.2021.13.
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Experimental modeling of the adhesion process on animals makes it possible to study the mechanism of adhesion formation in the abdominal cavity, to fi nd ways to interrupt this process at a certain stage and to avoid the development of complications. The aim of this study was to optimize the methods of modeling the adhesion process, determining the levels of hyaluronic acid and N-peptide collagen typ III in serum and introducing intraoperative determination of local concentrations of circular muscles of the small intestine to improve peristaltic wave in the postoperative period and prevent adhesions. To solve these problems, three series of experimental studies were performed on 135 white nonlinear rats, aged 35±5 days, weighing 110.0±20.0 g. In the fi rst series of experimental studies it was found that the intensity of the occurrence and spread of adhesions in the abdominal cavity is directly proportional to the method of modeling the adhesion process, and more pronounced in mesothelial damage and small bowel ischemia. The second series of experimental studies shows that the separation of intraperitoneal adhesions without the use of barrier agents contributed to the development of adhesive conglomerates and massive hyperplastic adhesions, which leads to the development of intestinal obstruction, and the use of «Defensal» solution reduces but doesn’t prevent adhesions after relaparotomy. Intraoperative determination of the local concentration of circular muscles with partial adhesiolysis and the use of «Defensal» solution, the third series of experiments promotes faster regeneration of the damaged peritoneum and the absence of adhesive conglomerates and hyperplastic adhesions
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Simmons, David L. "Dissecting the modes of interactions amongst cell adhesion molecules". Development 119, Supplement (1.12.1993): 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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Bialer, Magalí G., Gabriela Sycz, Florencia Muñoz González, Mariana C. Ferrero, Pablo C. Baldi i Angeles Zorreguieta. "Adhesins of Brucella: Their Roles in the Interaction with the Host". Pathogens 9, nr 11 (12.11.2020): 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 to cell adhesion molecules in epithelial cells), the monomeric autotransporters BmaA, BmaB, and BmaC (binding to ECM components, epithelial cells, osteoblasts, synoviocytes, and trophoblasts), the trimeric autotransporters BtaE and BtaF (binding to ECM components and epithelial cells) and Bp26 (binding to ECM components). An in vivo role has also been shown for the trimeric autotransporters, as deletion mutants display decreased colonization after oral and/or respiratory infection in mice, and it has also been suggested for BigA and BigB. Several adhesins have shown unipolar localization, suggesting that Brucella would express an adhesive pole. Adhesin-based vaccines may be useful to prevent brucellosis, as intranasal immunization in mice with BtaF conferred high levels of protection against oral challenge with B. suis.
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Hall, Jeffrey W., Bruno P. Lima, Gaetan G. Herbomel, Tata Gopinath, LeAnna McDonald, Michael T. Shyne, John K. Lee i in. "An intramembrane sensory circuit monitors sortase A–mediated processing of streptococcal adhesins". Science Signaling 12, nr 580 (7.05.2019): 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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Labbate, Maurizio, Hua Zhu, Leena Thung, Rani Bandara, Martin R. Larsen, Mark D. P. Willcox, Michael Givskov, Scott A. Rice i Staffan Kjelleberg. "Quorum-Sensing Regulation of Adhesion in Serratia marcescens MG1 Is Surface Dependent". Journal of Bacteriology 189, nr 7 (19.01.2007): 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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Greenwood, Jeffrey A., Anne B. Theibert, Glenn D. Prestwich i Joanne E. Murphy-Ullrich. "Restructuring of Focal Adhesion Plaques by Pi 3-Kinase". Journal of Cell Biology 150, nr 3 (7.08.2000): 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-100–soluble fraction. In contrast, talin and paxillin remained localized to focal adhesions, suggesting that activation of PI 3-kinase induced a restructuring of the plaque rather than complete dispersion. Furthermore, phosphatidylinositol (3,4,5)-trisphosphate (PtdIns (3,4,5)-P3), a lipid product of PI 3-kinase, was sufficient to induce restructuring of the focal adhesion plaque. We also found that PtdIns (3,4,5)-P3 binds to α-actinin in PDGF-treated cells. Further evidence demonstrated that activation of PI 3-kinase by PDGF induced a decrease in the association of α-actinin with the integrin β subunit, and that PtdIns (3,4,5)-P3 could disrupt this interaction in vitro. Modification of focal adhesion structure by PI 3-kinase and its lipid product, PtdIns (3,4,5)-P3, has important implications for the regulation of cellular adhesive strength and motility.
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Murphy-Ullrich, J. E., i M. Höök. "Thrombospondin modulates focal adhesions in endothelial cells." Journal of Cell Biology 109, nr 3 (1.09.1989): 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 time of seeding onto fibronectin substrates resulted in an inhibition of focal adhesion formation. Furthermore, the addition of TSP to fully adherent cells in situ or prespread on fibronectin substrates caused a reduction in the number of cells, which were positive for focal adhesions, although there was no significant effect on cell spreading. In a dose-dependent manner, TSP reduced the number of cells with adhesion plaques to approximately 60% of control levels. The distribution of remaining adhesion plaques in TSP-treated cells was also altered: plaques were primarily limited to the periphery of cells and were not present in the central cell body, as in control cells treated with BSA. The observed effects were specific for TSP and were not observed with platelet factor 4, beta-thromboglobulin, or fibronectin. The TSP-mediated loss of adhesion plaques was neutralized by the addition of heparin, fucoidan, other heparin-binding proteins, and by a monoclonal antibody to the heparin binding domain of TSP, but not by antibodies to the core or carboxy-terminal regions of TSP. The interaction of the heparin-binding domain of TSP with cell-associated heparan sulfate appears to be an important mechanistic component for this activity of TSP. These data indicate that TSP may have a role in destabilizing cell adhesion through prevention of focal adhesion formation and by loss of preformed focal adhesions.
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Ventre, Maurizio, Carlo Fortunato Natale, Carmela Rianna i Paolo Antonio Netti. "Topographic cell instructive patterns to control cell adhesion, polarization and migration". Journal of The Royal Society Interface 11, nr 100 (6.11.2014): 20140687. http://dx.doi.org/10.1098/rsif.2014.0687.
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Topographic patterns are known to affect cellular processes such as adhesion, migration and differentiation. However, the optimal way to deliver topographic signals to provide cells with precise instructions has not been defined yet. In this work, we hypothesize that topographic patterns may be able to control the sensing and adhesion machinery of cells when their interval features are tuned on the characteristic lengths of filopodial probing and focal adhesions (FAs). Features separated by distance beyond the length of filopodia cannot be readily perceived; therefore, the formation of new adhesions is discouraged. If, however, topographic features are separated by a distance within the reach of filopodia extension, cells can establish contact between adjacent topographic islands. In the latter case, cell adhesion and polarization rely upon the growth of FAs occurring on a specific length scale that depends on the chemical properties of the surface. Topographic patterns and chemical properties may interfere with the growth of FAs, thus making adhesions unstable. To test this hypothesis, we fabricated different micropatterned surfaces displaying feature dimensions and adhesive properties able to interfere with the filopodial sensing and the adhesion maturation, selectively. Our data demonstrate that it is possible to exert a potent control on cell adhesion, elongation and migration by tuning topographic features’ dimensions and surface chemistry.
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Banisadr, Afsheen, Mariam Eick, Pranjali Beri, Alison D. Parisian, Benjamin Yeoman, Jesse K. Placone, Adam J. Engler i Frank Furnari. "EGFRvIII uses intrinsic and extrinsic mechanisms to reduce glioma adhesion and increase migration". Journal of Cell Science 133, nr 24 (26.11.2020): jcs247189. http://dx.doi.org/10.1242/jcs.247189.
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ABSTRACTA lack of biological markers has limited our ability to identify the invasive cells responsible for glioblastoma multiforme (GBM). To become migratory and invasive, cells must downregulate matrix adhesions, which could be a physical marker of invasive potential. We engineered murine astrocytes with common GBM mutations, e.g. Ink4a (Ink) or PTEN deletion and expressing a constitutively active EGF receptor truncation (EGFRvIII), to elucidate their effect on adhesion. While loss of Ink or PTEN did not affect adhesion, counterparts expressing EGFRvIII were significantly less adhesive. EGFRvIII reduced focal adhesion size and number, and these cells – with more labile adhesions – displayed enhanced migration. Regulation appears to depend not on physical receptor association to integrins but, rather, on the activity of the receptor kinase, resulting in transcriptional integrin repression. Interestingly, EGFRvIII intrinsic signals can be propagated by cytokine crosstalk to cells expressing wild-type EGFR, resulting in reduced adhesion and enhanced migration. These data identify potential intrinsic and extrinsic mechanisms that gliomas use to invade surrounding parenchyma.
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Lipke, Peter N., Jason M. Rauceo i Albertus Viljoen. "Cell–Cell Mating Interactions: Overview and Potential of Single-Cell Force Spectroscopy". International Journal of Molecular Sciences 23, nr 3 (20.01.2022): 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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SAFONOVA, M. A., i N. A. GOLOVNYOVA. "ADHESION FACTORS OF LACTIC ACID BACTERIA AND BIFIDOBACTERIA". Микробные биотехнологии: фундаментальные и прикладные аспекты 13 (21.10.2021): 103–18. http://dx.doi.org/10.47612/2226-3136-2021-13-103-118.
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The review presents data on adhesive and biofilm-generating capacity of lactic acid bacteria and bifidobacteria, promoting microbial colonization of gastrointestinal tract and their application as constituents of probiotics. The structural elements
involved in adhesion include pili-like formations, cell surface proteins (adhesins, S-layer proteins, moonlighting proteins), exopolysaccharides, lipoteichoic and teichoic acids. Methods of studying the adhesive properties of bacteria and the main
environmental factors affecting the expression of genes engaged in the mechanism of adhesion have been considered.
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Caykara, Tugce, Sara Fernandes, Adelaide Braga, Joana Rodrigues, Ligia R. Rodrigues i Carla Joana Silva. "Can Superhydrophobic PET Surfaces Prevent Bacterial Adhesion?" Nanomaterials 13, nr 6 (21.03.2023): 1117. http://dx.doi.org/10.3390/nano13061117.
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Prevention of bacterial adhesion is a way to reduce and/or avoid biofilm formation, thus restraining its associated infections. The development of repellent anti-adhesive surfaces, such as superhydrophobic surfaces, can be a strategy to avoid bacterial adhesion. In this study, a polyethylene terephthalate (PET) film was modified by in situ growth of silica nanoparticles (NPs) to create a rough surface. The surface was further modified with fluorinated carbon chains to increase its hydrophobicity. The modified PET surfaces presented a pronounced superhydrophobic character, showing a water contact angle of 156° and a roughness of 104 nm (a considerable increase comparing with the 69° and 4.8 nm obtained for the untreated PET). Scanning Electron Microscopy was used to evaluate the modified surfaces morphology, further confirming its successful modification with nanoparticles. Additionally, a bacterial adhesion assay using an Escherichia coli expressing YadA, an adhesive protein from Yersinia so-called Yersinia adhesin A, was used to assess the anti-adhesive potential of the modified PET. Contrarily to what was expected, adhesion of E. coli YadA was found to increase on the modified PET surfaces, exhibiting a clear preference for the crevices. This study highlights the role of material micro topography as an important attribute when considering bacterial adhesion.
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Akimov, Sergey S., Dmitry Krylov, Laurie F. Fleischman i Alexey M. Belkin. "Tissue Transglutaminase Is an Integrin-Binding Adhesion Coreceptor for Fibronectin". Journal of Cell Biology 148, nr 4 (21.02.2000): 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 transglutaminase and are not shared by its functional homologue, a catalytic subunit of factor XIII. Adhesive function of tissue transglutaminase does not require its cross-linking activity but depends on its stable noncovalent association with integrins. Transglutaminase interacts directly with multiple integrins of β1 and β3 subfamilies, but not with β2 integrins. Complexes of transglutaminase with integrins are formed inside the cell during biosynthesis and accumulate on the surface and in focal adhesions. Together our results demonstrate that tissue transglutaminase mediates the interaction of integrins with fibronectin, thereby acting as an integrin-associated coreceptor to promote cell adhesion and spreading.
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Andreozzi, Elisa, i Gaylen A. Uhlich. "PchE Regulation of Escherichia coli O157:H7 Flagella, Controlling the Transition to Host Cell Attachment". International Journal of Molecular Sciences 21, nr 13 (28.06.2020): 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 four master regulators (csgD, stpA, ler, flhDC) were controlled by pchE. pchE over-expression strongly up-regulated fliC but the marked flagella induction reduced the attachment of O157:H7 clinical isolate PA20 to HEp-2 cells, indicating that flagella were blocking cell attachments rather than functioning as an adhesin. Chemotaxis, motor, structural, and regulatory genes in the flagellar operons were all increased by pchE expression, as was PA20 motility. This study identifies new members in the pchE regulon and shows that pchE stimulates flagellar motility while repressing cell adhesion, likely to support EHEC movement to the intestinal surface early in infection. However, induced or inappropriate pchE-dependent flagellar expression could block cell attachments later during disease progression.
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NAKAMURA, Yoshinobu, Kazuhiro YAMAMURA i Syuji FUJII. "Adhesion Strength and Interfacial Adhesion of Pressure-Sensitive Adhesive". Journal of The Surface Finishing Society of Japan 63, nr 12 (2012): 728–32. http://dx.doi.org/10.4139/sfj.63.728.
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Kirov, S. M., L. J. Hayward i M. A. Nerrie. "Adhesion ofAeromonassp. to cell lines used as models for intestinal adhesion". Epidemiology and Infection 115, nr 3 (grudzień 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 22 °C compared with 37 °C and 7 °C. Some environmental isolates showed greater adhesion when grown at 7 °C than when grown at 37 °C. Filamentous structures on these strains are also optimally expressed under the above conditions (reported elsewhere). Mechanical shearing or trypsin treatment to remove surface structures from several adhesive strains grown at 22 °C decreased adhesion to cell lines by 50–80% providing further indirect evidence that filamentous adhesins may play a role in cell adhesion for thisAeromonasspecies.
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Westhoff, M. A., B. Serrels, V. J. Fincham, M. C. Frame i N. O. Carragher. "Src-Mediated Phosphorylation of Focal Adhesion Kinase Couples Actin and Adhesion Dynamics to Survival Signaling". Molecular and Cellular Biology 24, nr 18 (15.09.2004): 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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Lipke, Peter N., Caleen Ramsook, Melissa C. Garcia-Sherman, Desmond N. Jackson, Cho X. J. Chan, Michael Bois i Stephen A. Klotz. "Between Amyloids and Aggregation Lies a Connection with Strength and Adhesion". New Journal of Science 2014 (2.02.2014): 1–12. http://dx.doi.org/10.1155/2014/815102.
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We tell of a journey that led to discovery of amyloids formed by yeast cell adhesins and their importance in biofilms and host immunity. We begin with the identification of the adhesin functional amyloid-forming sequences that mediate fiber formation in vitro. Atomic force microscopy and confocal microscopy show 2-dimensional amyloid “nanodomains” on the surface of cells that are activated for adhesion. These nanodomains are arrays of adhesin molecules that bind multivalent ligands with high avidity. Nanodomains form when adhesin molecules are stretched in the AFM or under laminar flow. Treatment with anti-amyloid perturbants or mutation of the amyloid sequence prevents adhesion nanodomain formation and activation. We are now discovering biological consequences. Adhesin nanodomains promote formation and maintenance of biofilms, which are microbial communities. Also, in abscesses within candidiasis patients, we find adhesin amyloids on the surface of the fungi. In both human infection and a Caenorhabditis elegans infection model, the presence of fungal surface amyloids elicits anti-inflammatory responses. Thus, this is a story of how fungal adhesins respond to extension forces through formation of cell surface amyloid nanodomains, with key consequences for biofilm formation and host responses.
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Murphy-Ullrich, J. E., M. A. Pallero, N. Boerth, J. A. Greenwood, T. M. Lincoln i T. L. Cornwell. "Cyclic GMP-dependent protein kinase is required for thrombospondin and tenascin mediated focal adhesion disassembly". Journal of Cell Science 109, nr 10 (1.10.1996): 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 focal adhesion integrity, we examined the role of protein kinases in mediating the loss of focal adhesions by these proteins. Data from these studies show that cGMP-dependent protein kinase is necessary to mediate focal adhesion disassembly triggered by either thrombospondin or tenascin, but not by SPARC. In experiments using various protein kinase inhibitors, we observed that selective inhibitors of cyclic GMP-dependent protein kinase, KT5823 and Rp-8-Br-cGMPS, blocked the effects of both the active sequence of thrombospondin 1 (hep I) and the alternatively-spliced segment (TNfnA-D) of tenascin-C on focal adhesion disassembly. Moreover, early passage rat aortic smooth muscle cells which have high levels of cGMP-dependent protein kinase were sensitive to hep I treatment, in contrast to passaged cGMP-dependent protein kinase deficient cells which were refractory to hep I or TNfnA-D treatment, but were sensitive to SPARC. Transfection of passaged smooth muscle cells with the catalytic domain of PKG I alpha restored responsiveness to hep I and TNfnA-D. While these studies show that cGMP-dependent protein kinase activity is necessary for thrombospondin and tenascin-mediated focal adhesion disassembly, kinase activity alone is not sufficient to induce disassembly as transfection of the catalytic domain of the kinase in the absence of additional stimuli does not result in loss of focal adhesions.
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Tozluoglu, Melda, Yanlan Mao, Paul A. Bates i 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, nr 106 (maj 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 continuity, confinement and adhesion. Changes in migration strategy are an emergent property of cells as the ECM geometry and adhesion changes. The transition into confined environments with discontinuous ECM fibres is sufficient to induce shifts from lamellipod-based to blebbing motility, while changes in confinement alone within a continuous geometry are not. The geometry of the ECM facilitates plasticity, by inducing shifts where the cell has high marginal gain from a mode change, and conserving persistency where the cell can continue movement regardless of the motility mode. This regulation of cell motility is independent of global changes in cytoskeletal properties, but requires locally higher linkage between the actin network and the plasma membrane at the cell rear, and changes in internal cell pressure. In addition to matrix geometry, we consider how cells might transition between ECM of different adhesiveness. We find that this requires positive feedback between the forces cells apply on the adhesion points, and the strength of the cell–ECM adhesions on those sites. This positive feedback leads to the emergence of a small number of highly adhesive cores, similar to focal adhesions. While the range of ECM adhesion levels the cell can invade is expanded with this feedback mechanism; the velocities are lowered for conditions where the positive feedback is not vital. Thus, plasticity of cell motility sacrifices the benefits of specialization, for robustness.
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PARK, Hee Boong, Vita GOLUBOVSKAYA, Lihui XU, Xihui YANG, Jin Woo LEE, Sean SCULLY, Rolf Joseph CRAVEN i William G. CANCE. "Activated Src increases adhesion, survival and alpha2-integrin expression in human breast cancer cells". Biochemical Journal 378, nr 2 (1.03.2004): 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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Ohno, H., Y. Araki i K. Endo. "A New Method for Promoting Adhesion between Precious Metal Alloys and Dental Adhesives". Journal of Dental Research 71, nr 6 (czerwiec 1992): 1326–31. http://dx.doi.org/10.1177/00220345920710061001.
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A new, simple method of modifying the adherend metal surface by a liquid Ga-Sn alloy (Adlloy) was applied to dental precious and base-metal alloys for adhesion with 4-META adhesive resin. Adhesions of 4-META resin to three other surface states-as-polished, oxidized at high temperature, and electroplated tin-were also performed for comparison with the adhesion on Adlloy-modified surfaces. Bond strength measurements were made, and the durability against water at the adhering interface was evaluated. The Adlloy-modified gold alloys (Type IV and 14 K) and silverbasedalloys (Ag-Pd and Ag-Cu) showed not only high bond strengths but also excellent water durability at the adhesion interface. Surface modification by Adlloy, however, did not affect adhesion to Ag-In-Zn and base-metal (SUS, Co-Cr, and Ni-Cr) alloys. Adhesion to the tin-electroplated specimens was comparable with that to the Adlloy-modified specimens.
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Katoh, Kazuo. "FAK-Dependent Cell Motility and Cell Elongation". Cells 9, nr 1 (12.01.2020): 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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Chen, Tsute, Koji Nakayama, Lynn Belliveau i Margaret J. Duncan. "Porphyromonas gingivalis Gingipains and Adhesion to Epithelial Cells". Infection and Immunity 69, nr 5 (1.05.2001): 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 hypothesis predicting that attachment and detachment of P. gingivalis to epithelial cells were mediated by gingipain adhesin and Rgp catalytic domains, respectively. A membrane-based epithelial cell binding assay, used to locate adhesins in extracellular fractions of wild-type and mutant strains, recognized gingipain peptides as adhesins rather than fimbriae. We developed a capture assay that demonstrated the binding of gingipain adhesin peptides to oral epithelial cells. The adherence of fimbrillin to epithelial cells was detected after heat denaturation of cell fractions. The prediction that Rgp catalytic activities mediated detachment was substantiated when the high level of attachment of anrgp mutant was reduced in the presence of wild-type cell fractions that contained gingipain catalytic activities.
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Petrie, Laurenne E., Allison C. Leonard, Julia Murphy i 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, nr 49 (25.09.2020): 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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Mintz, Keith P. "Identification of an extracellular matrix protein adhesin, EmaA, which mediates the adhesion of Actinobacillus actinomycetemcomitans to collagen". Microbiology 150, nr 8 (1.08.2004): 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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Oakes, Patrick W., Yvonne Beckham, Jonathan Stricker i Margaret L. Gardel. "Tension is required but not sufficient for focal adhesion maturation without a stress fiber template". Journal of Cell Biology 196, nr 3 (30.01.2012): 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 dynamics and force transmission, impaired stress fiber assembly impeded focal adhesion compositional maturation and fibronectin remodeling. Finally, we show that compositional maturation of focal adhesions could occur even when myosin II–dependent cellular tension was reduced by 80%. We propose that stress fiber assembly at the adhesion site serves as a structural template that facilitates adhesion maturation over a wide range of tensions. This work identifies the essential role of lamellar actin architecture in adhesion maturation.
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Byvalov, A. A., i I. V. Konyshev. "Yersinia pseudotuberculosis-derived adhesins". Russian Journal of Infection and Immunity 9, nr 3-4 (15.11.2019): 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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Longley, R. L., A. Woods, A. Fleetwood, G. J. Cowling, J. T. Gallagher i J. R. Couchman. "Control of morphology, cytoskeleton and migration by syndecan-4". Journal of Cell Science 112, nr 20 (15.10.1999): 3421–31. http://dx.doi.org/10.1242/jcs.112.20.3421.
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Syndecan-4 is a widely expressed transmembrane heparan sulfate proteoglycan which localizes to focal adhesions. Previous studies showed that the syndecan-4 cytoplasmic domain can associate with and potentiate the activity of protein kinase C, which is required for focal adhesion formation. To examine further the role of syndecan-4 in cell adhesion, we expressed syndecan-4 cDNA constructs in CHO-K1 cells. Syndecan-2 transfection was used to confirm effects seen were specific for syndecan-4. Cells overexpressing full length syndecan-4 core protein exhibited a more flattened, fibroblastic morphology, with increased focal adhesion formation and decreased cell motility. Expression of a syndecan-4 core protein with either a partial or complete deletion of the cytoplasmic domain or of an antisense construct led to markedly decreased spreading and focal adhesion formation, a more epithelioid morphology, and decreased motility. Overexpression of syndecan-2 changed the adhesive phenotype, but did not markedly alter focal adhesion and microfilament bundle formation. The data suggest that syndecan-4 is a regulator of focal adhesion and stress fiber formation, and influences both morphology and migration.
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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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Revach, Or-Yam, Inna Grosheva i Benjamin Geiger. "Biomechanical regulation of focal adhesion and invadopodia formation". Journal of Cell Science 133, nr 20 (15.10.2020): 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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Lipke, Peter N., i Peleg Ragonis-Bachar. "Sticking to the Subject: Multifunctionality in Microbial Adhesins". Journal of Fungi 9, nr 4 (29.03.2023): 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.