Journal articles: 'Surface-mediated interaction'

1

Hyldgaard, P., and T. L. Einstein. "Surface-state–mediated three-adsorbate interaction." Europhysics Letters (EPL) 59, no. 2 (July 2002): 265–71. http://dx.doi.org/10.1209/epl/i2002-00236-0.

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Ribeiro, Sylvie, Christina Puckert, Clarisse Ribeiro, Andreia C. Gomes, Michael J. Higgins, and Senentxu Lanceros-Méndez. "Surface Charge-Mediated Cell–Surface Interaction on Piezoelectric Materials." ACS Applied Materials & Interfaces 12, no. 1 (December 11, 2019): 191–99. http://dx.doi.org/10.1021/acsami.9b17222.

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3

HUANG, WEN-MIN, HSIN-HUA LAI, CHENG-HUNG CHANG, and HSIU-HAU LIN. "CARRIER-MEDIATED EXCHANGE COUPLING AND FERMI SURFACE TOPOLOGY." International Journal of Modern Physics B 22, no. 01n02 (January 20, 2008): 88–93. http://dx.doi.org/10.1142/s0217979208046098.

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We investigate the carrier-mediated exchange coupling between two ferromagnets, sandwiching an intermediate thin layer with Rashba interaction. The effective exchange coupling is obtained by integrating out the itinerant carriers. It turns out that the magnetic trends depend sensitively upon the topology of the Fermi surface. As the topology changes from “wedding cake” to “donut”, the mediated exchange goes from the oscillatory Ruderman-Kittel-Kasuya-Yosida to the non-collinear spiral interactions accordingly. It is rather surprising that the Fermi surface topology determines which type of magnetic interaction becomes dominant. Finally, we also discuss potential applications for carrier-mediated exchange coupling across the junction.

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Godfrey, H. P., D. A. Frenz, L. S. Canfield, S. K. Akiyama, and S. A. Newman. "Non-chemotactic translocation of phagocytic cells mediated by a fibronectin-related human lymphokine." Journal of Immunology 143, no. 11 (December 1, 1989): 3691–96. http://dx.doi.org/10.4049/jimmunol.143.11.3691.

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Abstract A fibronectin (FN)-related human lymphokine, macrophage agglutination factor (MAggF), agglutinates monocytes at femtomolar concentrations. Similar concentrations of MAggF translocate monocytes and neutrophils through artificial extracellular matrices by a non-chemotactic adhesive process not dependent on intracellular metabolism (matrix-driven translocation). As is the case with matrix-driven translocation mediated by other FN, MAggF-mediated translocation depends on interaction of the lymphokine amino-terminal heparin-binding domain with cell surface heparin-like molecules. In contrast, lymphokine-mediated agglutination involves interactions between the MAggF cell-binding domain and integrin FN receptors recognizing the Arg-Gly-Asp sequence. MAggF-mediated translocation and agglutination are also dependent on the lymphokine gelatin-binding domain. The extremely high activity of MAggF in translocating and agglutinating monocytes may result from cooperative interactions between multiple lymphokine domains and multiple classes of cell surface receptor molecules. We suggest that MAggF-mediated matrix-driven translocation could act independently of or in addition to chemotaxis in recruiting monocytes and neutrophils to a tissue site of T cell-mediated inflammation. Subsequent interaction of MAggF and monocyte FN receptor could then detain monocytes there.

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Hyldgaard, Per, and T. L. Einstein. "Surface-state mediated three-adsorbate interaction: electronic nature and nanoscale consequences." Surface Science 532-535 (June 2003): 600–605. http://dx.doi.org/10.1016/s0039-6028(03)00173-0.

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Huang, Lizhi, Jianfeng Jia, Hongwei Liu, Yong Yuan, Jian Zhao, Shuai Chen, Weibin Fan, Eric R. Waclawik, Huaiyong Zhu, and Zhanfeng Zheng. "Surface-mediated selective photocatalytic aerobic oxidation reactions on TiO2 nanofibres." RSC Advances 5, no. 70 (2015): 56820–31. http://dx.doi.org/10.1039/c5ra07518a.

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Sionov, Ronit Vogt, Chrystelle Lamagna, and Zvi Granot. "Recognition of Tumor Nidogen-1 by Neutrophil C-Type Lectin Receptors." Biomedicines 10, no. 4 (April 15, 2022): 908. http://dx.doi.org/10.3390/biomedicines10040908.

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Neutrophil-mediated cytotoxicity toward tumor cells requires cell contact and is mediated by hydrogen peroxide. We have recently shown that Cathepsin G expressed on the neutrophil surface interacts with tumor RAGE, and this interaction facilitates neutrophil cytotoxicity. Interruption of the Cathepsin G–RAGE interaction led to 50–80% reduction in cytotoxicity, suggesting that additional interactions are also involved. Here we show that blocking antibodies to the C-type lectin receptors (CLRs) Clec4e and Dectin-1, but not those to NKG2D, attenuated murine neutrophil cytotoxicity towards murine tumor cells, suggesting a contributing role for these CLRs in neutrophil recognition of tumor cells. We further observed that the CLRs interact with tumor Nidogen-1 and Hspg2, two sulfated glycoproteins of the basement membrane. Both Nidogen-1 and Hspg2 were found to be expressed on the tumor cell surface. The knockdown of Nidogen-1, but not that of Hspg2, led to reduced susceptibility of the tumor cells to neutrophil cytotoxicity. Altogether, this study suggests a role for CLR–Nidogen-1 interaction in the recognition of tumor cells by neutrophils, and this interaction facilitates neutrophil-mediated killing of the tumor cells.

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Zheng, Mingzhe, and Sen-itiroh Hakomori. "Soluble Fibronectin Interaction with Cell Surface and Extracellular Matrix Is Mediated by Carbohydrate-to-Carbohydrate Interaction." Archives of Biochemistry and Biophysics 374, no. 1 (February 2000): 93–99. http://dx.doi.org/10.1006/abbi.1999.1613.

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Bansal, Rajeev K. "Approximation of surface–groundwater interaction mediated by vertical streambank in sloping terrains." Journal of Ocean Engineering and Science 2, no. 1 (March 2017): 18–27. http://dx.doi.org/10.1016/j.joes.2016.10.002.

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10

Shin, Youngho, Sungjun Bae, and Woojin Lee. "Formation of surface mediated iron colloids during U(VI) and nZVI interaction." Advances in environmental research 2, no. 3 (September 25, 2013): 167–77. http://dx.doi.org/10.12989/aer.2013.2.3.167.

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11

Brennan, Marian P., Marc Devocelle, Timothy J. Foster, and Dermot Cox. "Staphylococcus Epidermidis Induced Platelet Aggregation Is Mediated by the Fibrinogen Binding Surface Protein SdrG." Blood 104, no. 11 (November 16, 2004): 3532. http://dx.doi.org/10.1182/blood.v104.11.3532.3532.

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Abstract S. epidermidis is normally present on the surface of the skin, however in a hospital setting, it is responsible for many infections involving implanted medical devices resulting in potentially fatal complications such as infective endocarditis and septicemia. S. epidermidis has previously been shown to induce platelet aggregation (Ohshima et al. Microbiol Immunol 1991) through an unknown mechanism. The surface protein SdrG (serine-aspartate repeat G protein) is important in the initial colonization of the device, as it binds fibrinogen, which is one of the first proteins to coat foreign devices. We thus postulated that this SdrG fibrinogen complex may mediate the S. epidermidis interaction with platelets. In order to investigate the specific effects of SdrG on platelets, we expressed SdrG in Lactococcus lactis which does not activate platelets. L. lactis SdrG was able to support platelet adhesion in the absence of fibrinogen, and to a greater extent in the presence of fibrinogen suggesting both a direct interaction with the platelet and an indirect interaction via a fibrinogen bridge. Fibrinogen dependent adhesion was inhibited by both abciximab and tirofiban confirming an interaction with GPIIb/IIIa. Furthermore, SdrG when expressed in L. lactis can induce platelet aggregation with a lag time of 1.5 ± 0.4 min. This aggregation was inhibited by abciximab suggesting that it is true aggregation rather than agglutination. We have also shown this to be dependent on cyclooxygenase signalling, as it is inhibited by aspirin. SdrG binds to the C-terminus of the beta chain of fibrinogen (Ponnuraj K et al. , Cell 2003). We synthesized a 15-mer peptide mimicking the binding region of the fibrinogen beta chain in order to determine whether fibrinogen binding was important for this aggregation. The native fibrinopeptide NEEGFFSARGHRPLD increased the lag time for aggregation to 9.2 ± 1.4 min, however, the control peptide NEEGFFAARGHRPLD did not affect aggregation (1.4 ± 0.3 min). The lag time did not increase further with saturating concentrations of peptide concentrations suggesting instability of the peptide, or a second mechanism involved in the aggregation which is consistent with the fibrinogen independent interaction seen in the adhesion assay. This work shows that SdrG alone is sufficient to support platelet adhesion and aggregation. SdrG mediates platelet activation through a novel mechanism via GPIIb/IIIa, and an as yet unknown direct interaction. Thus SdrG appears to be the dominant virulence factor for S. epidermidis induced thrombosis, therefore, inhibition of these interactions have potential for treatment of thrombotic complications associated with S. epidermidis infections.

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12

XIE, RONG. "THEORETICAL STUDY ON ADSORBATE-INDUCED SURFACE STRESS IN THE SELF-ASSEMBLY OF ALKANETHIOLS ON GOLD." Surface Review and Letters 16, no. 06 (December 2009): 807–14. http://dx.doi.org/10.1142/s0218625x09013359.

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By using established statistical thermodynamic theory of adsorbate-induced surface stress of adsorption monolayer on metal surface, the surface stress Δg in the self-assembly of alkanethiols on Au (111) surface has been calculated. The quantitative relations of the surface stress Δg with the length N of the alkyl chain of the molecule and with the coverage θ of molecules on Au (111) have been theoretically studied, respectively. The calculated results agree with Berger et al.'s experiment. The qualitative discrepancy between the theory and experiment on the sign of the surface stress has been resolved. Among various components of the adsorbate–adsorbate interaction energies in the adlayer, the substrate-mediated interaction is significant for the adsorbate-induced surface stress, which shows that indirect contribution of the adsorption energy of alkanethiols through the substrate-mediated interaction is very important.

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13

Eckford, Paul D. W., and Christine E. Bear. "Targeting the regulation of CFTR channels." Biochemical Journal 435, no. 2 (March 29, 2011): e1-e4. http://dx.doi.org/10.1042/bj20110461.

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In this issue of the Biochemical Journal, Zhang et al. reveal a new strategy for modifying the regulated function of CFTR (cystic fibrosis transmembrane conductance regulator) on the apical surface of epithelial cells. Simply stated, these authors tested the idea that the cAMP-dependent channel activity of CFTR could be effectively enhanced by disruption of a protein–protein interaction which is normally inhibitory for the production of cAMP. This particular protein–protein interaction [between the PDZ motif of LPA2 (type 2 lysophosphatidic acid receptor) and the scaffold protein Nherf2 (Na+/H+ exchanger regulatory factor 2)] is localized in the CFTR interactome on the apical membrane of epithelial cells. Hence disruption of the LPA2–Nherf2 interaction should lead to a localized elevation in cAMP and, consequently, increased cAMP-dependent CFTR activity on the surface of epithelial cells. Zhang et al. confirmed these expectations for a small-molecule compound targeting the LPA2–Nherf2 interaction using relevant cultures and tissues thought to model the human respiratory epithelium. The success of this strategy depended on previous knowledge regarding the role for multiple PDZ-motif-mediated interactions in signalling (directly or indirectly) to CFTR. Given the number and diversity of such PDZ-mediated interactions, future structural and computational studies will be essential for guiding the design of specific pharmacological interventions.

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14

Linne, Christine, Daniele Visco, Stefano Angioletti-Uberti, Liedewij Laan, and Daniela J. Kraft. "Direct visualization of superselective colloid-surface binding mediated by multivalent interactions." Proceedings of the National Academy of Sciences 118, no. 36 (August 31, 2021): e2106036118. http://dx.doi.org/10.1073/pnas.2106036118.

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Reliably distinguishing between cells based on minute differences in receptor density is crucial for cell–cell or virus–cell recognition, the initiation of signal transduction, and selective targeting in directed drug delivery. Such sharp differentiation between different surfaces based on their receptor density can only be achieved by multivalent interactions. Several theoretical and experimental works have contributed to our understanding of this “superselectivity.” However, a versatile, controlled experimental model system that allows quantitative measurements on the ligand–receptor level is still missing. Here, we present a multivalent model system based on colloidal particles equipped with surface-mobile DNA linkers that can superselectively target a surface functionalized with the complementary mobile DNA-linkers. Using a combined approach of light microscopy and Foerster resonance energy transfer (FRET), we can directly observe the binding and recruitment of the ligand–receptor pairs in the contact area. We find a nonlinear transition in colloid-surface binding probability with increasing ligand or receptor concentration. In addition, we observe an increased sensitivity with weaker ligand–receptor interactions, and we confirm that the timescale of binding reversibility of individual linkers has a strong influence on superselectivity. These unprecedented insights on the ligand–receptor level provide dynamic information into the multivalent interaction between two fluidic membranes mediated by both mobile receptors and ligands and will enable future work on the role of spatial–temporal ligand–receptor dynamics on colloid-surface binding.

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15

Boukerche, H., O. Berthier-Vergnes, E. Tabone, JF Dore, LL Leung, and JL McGregor. "Platelet-melanoma cell interaction is mediated by the glycoprotein IIb- IIIa complex." Blood 74, no. 2 (August 1, 1989): 658–63. http://dx.doi.org/10.1182/blood.v74.2.658.bloodjournal742658.

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A human malignant melanoma cell line (M3Dau) was observed by electron microscopy to interact directly with human platelets and induced platelet aggregation. Fab fragments of a monoclonal antibody MoAb (LYP18), directed against the platelet glycoprotein (GP) IIb-IIIa complex, inhibited platelet-melanoma interactions and platelet-platelet aggregation. M3Dau melanoma cells bind LYP 18 and synthesize IIb-IIIa- like GPs. When the melanoma cells were preincubated with LYP 18, tumor- platelet interaction did not occur, suggesting that the interaction may be mediated by the IIb-IIIa-like GPs present on the melanoma cell surface. Glanzmann's thrombasthenic platelets, lacking GPIIb and IIIa, did not interact with melanoma cells, indicating that the platelet GPIIb-IIIa complex is also necessary for the platelet-melanoma cell interaction. This work demonstrates the importance of the IIb-IIIa-like GPs, present on M3Dau melanoma cells, in mediating tumor-platelet interactions.

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Heinzmann, David, Moritz Noethel, Saskia von Ungern-Sternberg, Ioannis Mitroulis, Meinrad Gawaz, Triantafyllos Chavakis, Andreas E. May, and Peter Seizer. "CD147 is a Novel Interaction Partner of Integrin αMβ2 Mediating Leukocyte and Platelet Adhesion." Biomolecules 10, no. 4 (April 2, 2020): 541. http://dx.doi.org/10.3390/biom10040541.

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Surface receptor-mediated adhesion is a fundamental step in the recruitment of leukocytes and platelets, as well as platelet–leukocyte interactions. The surface receptor CD147 is crucially involved in host defense against self-derived and invading targets, as well as in thrombosis. In the current study, we describe the previously unknown interaction of CD147 with integrin αMβ2 (Mac-1) in this context. Using binding assays, we were able to show a stable interaction of CD147 with Mac-1 in vitro. Leukocytes from Mac-1−/− and CD147+/− mice showed a markedly reduced static adhesion to CD147- and Mac-1-coated surfaces, respectively, compared to wild-type mice. Similarly, we observed reduced rolling and adhesion of monocytes under flow conditions when cells were pre-treated with antibodies against Mac-1 or CD147. Additionally, as assessed by antibody inhibition experiments, CD147 mediated the dynamic adhesion of platelets to Mac-1-coated surfaces. The interaction of CD147 with Mac-1 is a previously undescribed mechanism facilitating the adhesion of leukocytes and platelets.

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17

Chamekh, Mustapha. "CD40-CD40L Interaction in Immunity Against Protozoan Infections." Journal of Biomedicine and Biotechnology 2007 (2007): 1–6. http://dx.doi.org/10.1155/2007/59430.

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Activation of the immune system against protozoan infections relies particularly on two specific signals provided by cognate interaction of T cells with antigen presenting cells (APCs). The first signal is attributed to binding of the T-cell receptor (TCR) to peptide/MHC complexes on the surface of APCs, whereas the second signal is triggered through binding of several costimulatory molecules on the surface of APCs with their corresponding receptors on T cells. Among these costimulatory signallings, CD40/CD40L interactions have been particularly investigated in protozoan infection models with regard to their potential to amplify cell-mediated immunity against intracellular parasites. This article reviews current studies of the potential role of CD40/CD40L interaction in the modulation of immune responses against some protozoan parasites and highlights recent developments regarding manipulation of this interaction for promoting control of parasite infections.

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18

Boukerche, H., O. Berthier-Vergnes, E. Tabone, JF Dore, LL Leung, and JL McGregor. "Platelet-melanoma cell interaction is mediated by the glycoprotein IIb- IIIa complex." Blood 74, no. 2 (August 1, 1989): 658–63. http://dx.doi.org/10.1182/blood.v74.2.658.658.

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Abstract A human malignant melanoma cell line (M3Dau) was observed by electron microscopy to interact directly with human platelets and induced platelet aggregation. Fab fragments of a monoclonal antibody MoAb (LYP18), directed against the platelet glycoprotein (GP) IIb-IIIa complex, inhibited platelet-melanoma interactions and platelet-platelet aggregation. M3Dau melanoma cells bind LYP 18 and synthesize IIb-IIIa- like GPs. When the melanoma cells were preincubated with LYP 18, tumor- platelet interaction did not occur, suggesting that the interaction may be mediated by the IIb-IIIa-like GPs present on the melanoma cell surface. Glanzmann's thrombasthenic platelets, lacking GPIIb and IIIa, did not interact with melanoma cells, indicating that the platelet GPIIb-IIIa complex is also necessary for the platelet-melanoma cell interaction. This work demonstrates the importance of the IIb-IIIa-like GPs, present on M3Dau melanoma cells, in mediating tumor-platelet interactions.

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Seo, Hyodae. "Distinct Influence of Air–Sea Interactions Mediated by Mesoscale Sea Surface Temperature and Surface Current in the Arabian Sea." Journal of Climate 30, no. 20 (September 8, 2017): 8061–80. http://dx.doi.org/10.1175/jcli-d-16-0834.1.

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Abstract During the southwest monsoons, the Arabian Sea (AS) develops highly energetic mesoscale variability associated with the Somali Current (SC), Great Whirl (GW), and cold filaments (CF). The resultant high-amplitude anomalies and gradients of sea surface temperature (SST) and surface currents modify the wind stress, triggering the so-called mesoscale coupled feedbacks. This study uses a high-resolution regional coupled model with a novel coupling procedure that separates spatial scales of the air–sea coupling to show that SST and surface currents are coupled to the atmosphere at distinct spatial scales, exerting distinct dynamic influences. The effect of mesoscale SST–wind interaction is manifested most strongly in wind work and Ekman pumping over the GW, primarily affecting the position of GW and the separation latitude of the SC. If this effect is suppressed, enhanced wind work and a weakened Ekman pumping dipole cause the GW to extend northeastward, delaying the SC separation by 1°. Current–wind interaction, in contrast, is related to the amount of wind energy input. When it is suppressed, especially as a result of background-scale currents, depth-integrated kinetic energy, both the mean and eddy, is significantly enhanced. Ekman pumping velocity over the GW is overly negative because of a lack of vorticity that offsets the wind stress curl, further invigorating the GW. Moreover, significant changes in time-mean SST and evaporation are generated in response to the current–wind interaction, accompanied by a noticeable southward shift in the Findlater Jet. The significant increase in moisture transport in the central AS implies that air–sea interaction mediated by the surface current is a potentially important process for simulation and prediction of the monsoon rainfall.

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20

Tao, Feng, Qiang Chen, Yuko Sato, John Skinner, Pei Tang, and Roger A. Johns. "Inhalational Anesthetics Disrupt Postsynaptic Density Protein-95, Drosophila Disc Large Tumor Suppressor, and Zonula Occludens-1 Domain Protein Interactions Critical to Action of Several Excitatory Receptor Channels Related to Anesthesia." Anesthesiology 122, no. 4 (April 1, 2015): 776–86. http://dx.doi.org/10.1097/aln.0000000000000609.

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Abstract Background: The authors have shown previously that inhaled anesthetics disrupt the interaction between the second postsynaptic density protein-95, Drosophila disc large tumor suppressor, and zonula occludens-1 (PDZ) domain of postsynaptic density protein-95 (PSD-95) and the C-terminus of N-methyl-d-aspartate receptor subunits NR2A and NR2B. The study data indicate that PDZ domains may serve as a molecular target for inhaled anesthetics. However, the underlying molecular mechanisms remain to be illustrated. Methods: Glutathione S-transferase pull-down assay, coimmunoprecipitation, and yeast two-hybrid analysis were used to assess PDZ domain–mediated protein–protein interactions in different conditions. Nuclear magnetic resonance spectroscopy was used to investigate isoflurane-induced chemical shift changes in the PDZ1–3 domains of PSD-95. A surface plasmon resonance–based BIAcore (Sweden) assay was used to examine the ability of isoflurane to inhibit the PDZ domain–mediated protein–protein interactions in real time. Results: Halothane and isoflurane dose-dependently inhibited PDZ domain–mediated interactions between PSD-95 and Shaker-type potassium channel Kv1.4 and between α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor subunit GluA2 and its interacting proteins—glutamate receptor–interacting protein or protein interacting with c kinase 1. However, halothane and isoflurane had no effect on PDZ domain–mediated interactions between γ-aminobutyric acid type B receptor and its interacting proteins. The inhaled anesthetic isoflurane mostly affected the residues close to or in the peptide-binding groove of PSD-95 PDZ1 and PDZ2 (especially PDZ2), while barely affecting the peptide-binding groove of PSD-95 PDZ3. Conclusion: These results suggest that inhaled anesthetics interfere with PDZ domain–mediated protein–protein interactions at several receptors important to neuronal excitation, anesthesia, and pain processing.

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Purushothaman, Anurag, Shyam Kumar Bandari, Jian Liu, James A. Mobley, Elizabeth E. Brown, and Ralph D. Sanderson. "Fibronectin on the Surface of Myeloma Cell-derived Exosomes Mediates Exosome-Cell Interactions." Journal of Biological Chemistry 291, no. 4 (November 24, 2015): 1652–63. http://dx.doi.org/10.1074/jbc.m115.686295.

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Exosomes regulate cell behavior by binding to and delivering their cargo to target cells; however, the mechanisms mediating exosome-cell interactions are poorly understood. Heparan sulfates on target cell surfaces can act as receptors for exosome uptake, but the ligand for heparan sulfate on exosomes has not been identified. Using exosomes isolated from myeloma cell lines and from myeloma patients, we identify exosomal fibronectin as a key heparan sulfate-binding ligand and mediator of exosome-cell interactions. We discovered that heparan sulfate plays a dual role in exosome-cell interaction; heparan sulfate on exosomes captures fibronectin, and on target cells it acts as a receptor for fibronectin. Removal of heparan sulfate from the exosome surface releases fibronectin and dramatically inhibits exosome-target cell interaction. Antibody specific for the Hep-II heparin-binding domain of fibronectin blocks exosome interaction with tumor cells or with marrow stromal cells. Regarding exosome function, fibronectin-mediated binding of exosomes to myeloma cells activated p38 and pERK signaling and expression of downstream target genes DKK1 and MMP-9, two molecules that promote myeloma progression. Antibody against fibronectin inhibited the ability of myeloma-derived exosomes to stimulate endothelial cell invasion. Heparin or heparin mimetics including Roneparstat, a modified heparin in phase I trials in myeloma patients, significantly inhibited exosome-cell interactions. These studies provide the first evidence that fibronectin binding to heparan sulfate mediates exosome-cell interactions, revealing a fundamental mechanism important for exosome-mediated cross-talk within tumor microenvironments. Moreover, these results imply that therapeutic disruption of fibronectin-heparan sulfate interactions will negatively impact myeloma tumor growth and progression.

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Aliyu, Isah, King-Hwa Ling, Nur Md Hashim, Jia-Yong Lam, and Hui-Yee Chee. "Annexin II as a Dengue Virus Serotype 2 Interacting Protein Mediating Virus Interaction on Vero Cells." Viruses 11, no. 4 (April 9, 2019): 335. http://dx.doi.org/10.3390/v11040335.

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Recent evidence has demonstrated that dengue virus requires active filopodia formation for a successful infection. However, the cellular factor involved in the interaction has not been fully elucidated. We used a combination of virus overlay protein binding assay and LC-MS/MS, and identified annexin II as a dengue virus serotype 2 (DENV2) interacting protein on Vero cells, upon filopodia induction. Flow cytometry analysis showed annexin II on the Vero cells surface increased when DENV2 was added. The amount of annexin II in the plasma membrane fraction was reduced as the infection progressed. Antibody-mediated inhibition of infection and siRNA-mediated knockdown of annexin II expression significantly reduced DENV2 infection and production levels. Collectively, we demonstrated that annexin II is one of the host factor involved in DENV2 binding on Vero cells.

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Scopino, Kristen, Elliot Williams, Abdelrahman Elsayed, William A. Barr, Daniel Krizanc, Kelly M. Thayer, and Michael P. Weir. "A Ribosome Interaction Surface Sensitive to mRNA GCN Periodicity." Biomolecules 10, no. 6 (June 3, 2020): 849. http://dx.doi.org/10.3390/biom10060849.

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A longstanding challenge is to understand how ribosomes parse mRNA open reading frames (ORFs). Significantly, GCN codons are over-represented in the initial codons of ORFs of prokaryote and eukaryote mRNAs. We describe a ribosome rRNA-protein surface that interacts with an mRNA GCN codon when next in line for the ribosome A-site. The interaction surface is comprised of the edges of two stacked rRNA bases: the Watson–Crick edge of 16S/18S rRNA C1054 and the adjacent Hoogsteen edge of A1196 (Escherichia coli 16S rRNA numbering). Also part of the interaction surface, the planar guanidinium group of a conserved Arginine (R146 of yeast ribosomal protein Rps3) is stacked adjacent to A1196. On its other side, the interaction surface is anchored to the ribosome A-site through base stacking of C1054 with the wobble anticodon base of the A-site tRNA. Using molecular dynamics simulations of a 495-residue subsystem of translocating ribosomes, we observed base pairing of C1054 to nucleotide G at position 1 of the next-in-line codon, consistent with previous cryo-EM observations, and hydrogen bonding of A1196 and R146 to C at position 2. Hydrogen bonding to both of these codon positions is significantly weakened when C at position 2 is changed to G, A or U. These sequence-sensitive mRNA-ribosome interactions at the C1054-A1196-R146 (CAR) surface potentially contribute to the GCN-mediated regulation of protein translation.

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Roubey, R. A. S. "Mechanisms of autoantibody-mediated thrombosis." Lupus 7, no. 2_suppl (February 1998): 114–19. http://dx.doi.org/10.1177/096120339800700226.

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It is widely hypothesized that autoantibodies directly contribute to the prothrombotic state in the antiphospholipid syndrome (APS). The discovery that antiphospholipid autoantibodies are specific for phospholipid-binding plasma proteins (β2-glycoprotein I, prothrombin, etc.) has allowed a much more precise investigation of the interactions of autoantibodies and antigens, and the effects of these interaction on hemostastis. Recent studies suggest that two types of interactions may be important in the pathophysiology of APS: (1) antibody cross-linking of membrane bound antigens may alter the kinetics of phospholipid-dependent reactions; and (2) antibody cross-linking of antigens bound to cell surface receptors may trigger signal transduction and cellular activation. In light of these findings, previous reports implicating various mechanisms of autoantibody-mediated thrombosis are being re-evaluated.

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Kim, Moo-Kyung, Zhen-Yu Huang, Pyoung-Han Hwang, Brian A. Jones, Norihito Sato, Sharon Hunter, Tai-Hee Kim-Han, Randall G. Worth, Zena K. Indik, and Alan D. Schreiber. "Fcγ receptor transmembrane domains: role in cell surface expression, γ chain interaction, and phagocytosis." Blood 101, no. 11 (June 1, 2003): 4479–84. http://dx.doi.org/10.1182/blood.v101.11.4479.

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Abstract We constructed chimeric receptors to dissect the role of the transmembrane (TM) domain in cell surface expression of and phagocytosis by the γ chain–dependent Fcγ receptors FcγRIIIA and FcγRI. FcγR chimeras containing the TM and cytoplasmic (CY) domains of the γ chain were expressed on the cell surface and mediated an efficient phagocytic signal. In contrast, chimeras containing the FcγRIIIA TM were poorly expressed. Receptors containing the FcγRI TM and the γ chain CY but lacking the γ chain TM also were expressed efficiently and mediated phagocytosis, suggesting that a γ chain dimer induced by the γ chain TM is not required for efficient phagocytosis. Cotransfection of FcγRI or FcγRIIIA with the chimera CD8-γ-γ (EC-TM-CY) resulted in FcγR cell surface expression and phagocytosis, whereas CD8-CD8-γ, whose TM does not associate with FcγR, allowed cell surface expression of (but not phagocytosis by) FcγRI. CD8-CD8-γ also did not allow surface expression of FcγRIIIA. Exchanging FcγRI and CD8 TMs indicated that the C-terminal 11 amino acids of the FcγRI TM are essential for association of FcγRI with the γ chain and phagocytosis. The data indicate that specific sequences in the FcγRIIIA and FcγRI TMs govern their different interactions with the γ chain in cell surface expression and phagocytosis and that γ chain TM sequences are not required for γ chain–mediated phagocytosis. The data identify a specific region of the FcγRI TM and its asparagine as important for FcγRI cell surface expression in the absence of the γ chain and for distinguishing the FcγRI and FcγRIIIA phenotypes.

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GINÉS, Silvia, Marta MARIÑO, Josefa MALLOL, Enric I. CANELA, Chikao MORIMOTO, Christian CALLEBAUT, Ara HOVANESSIAN, Vicent CASADÓ, Carmen LLUIS, and Rafael FRANCO. "Regulation of epithelial and lymphocyte cell adhesion by adenosine deaminase–CD26 interaction." Biochemical Journal 361, no. 2 (January 8, 2002): 203–9. http://dx.doi.org/10.1042/bj3610203.

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The extra-enzymic function of cell-surface adenosine deaminase (ADA), an enzyme mainly localized in the cytosol but also found on the cell surface of monocytes, B cells and T cells, has lately been the subject of numerous studies. Cell-surface ADA is able to transduce co-stimulatory signals in T cells via its interaction with CD26, an integral membrane protein that acts as ADA-binding protein. The aim of the present study was to explore whether ADA—CD26 interaction plays a role in the adhesion of lymphocyte cells to human epithelial cells. To meet this aim, different lymphocyte cell lines (Jurkat and CEM T) expressing endogenous, or overexpressing human, CD26 protein were tested in adhesion assays to monolayers of colon adenocarcinoma human epithelial cells, Caco-2, which express high levels of cell-surface ADA. Interestingly, the adhesion of Jurkat and CEM T cells to a monolayer of Caco-2 cells was greatly dependent on CD26. An increase by 50% in the cell-to-cell adhesion was found in cells containing higher levels of CD26. Incubation with an anti-CD26 antibody raised against the ADA-binding site or with exogenous ADA resulted in a significant reduction (50–70%) of T-cell adhesion to monolayers of epithelial cells. The role of ADA—CD26 interaction in the lymphocyte—epithelial cell adhesion appears to be mediated by CD26 molecules that are not interacting with endogenous ADA (ADA-free CD26), since SKW6.4 (B cells) that express more cell-surface ADA showed lower adhesion than T cells. Adhesion stimulated by CD26 and ADA is mediated by T cell lymphocyte function-associated antigen. A role for ADA—CD26 interaction in cell-to-cell adhesion was confirmed further in integrin activation assays. FACS analysis revealed a higher expression of activated integrins on T cell lines in the presence of increasing amounts of exogenous ADA. Taken together, these results suggest that the ADA—CD26 interaction on the cell surface has a role in lymphocyte—epithelial cell adhesion.

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Maharana, Jitendra, Budheswar Dehury, Jyoti Ranjan Sahoo, Itishree Jena, Aritra Bej, Debashis Panda, Bikash Ranjan Sahoo, Mahesh Chandra Patra, and Sukanta Kumar Pradhan. "Structural and functional insights into CARDs of zebrafish (Danio rerio) NOD1 and NOD2, and their interaction with adaptor protein RIP2." Molecular BioSystems 11, no. 8 (2015): 2324–36. http://dx.doi.org/10.1039/c5mb00212e.

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Campisi, Sebastiano, Carine Chan-Thaw, and Alberto Villa. "Understanding Heteroatom-Mediated Metal–Support Interactions in Functionalized Carbons: A Perspective Review." Applied Sciences 8, no. 7 (July 17, 2018): 1159. http://dx.doi.org/10.3390/app8071159.

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Carbon-based materials show unique chemicophysical properties, and they have been successfully used in many catalytic processes, including the production of chemicals and energy. The introduction of heteroatoms (N, B, P, S) alters the electronic properties, often increasing the reactivity of the surface of nanocarbons. The functional groups on the carbons have been reported to be effective for anchoring metal nanoparticles. Although the interaction between functional groups and metal has been studied by various characterization techniques, theoretical models, and catalytic results, the role and nature of heteroatoms is still an object of discussion. The aim of this review is to elucidate the metal–heteroatoms interaction, providing an overview of the main experimental and theoretical outcomes about heteroatom-mediated metal–support interactions. Selected studies showing the effect of heteroatom–metal interaction in the liquid-phase alcohol oxidation will be also presented.

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Sen, J., P. Bossu, S. J. Burakoff, and A. K. Abbas. "T cell surface molecules regulating noncognate B lymphocyte activation. Role of CD2 and LFA-1." Journal of Immunology 148, no. 4 (February 15, 1992): 1037–42. http://dx.doi.org/10.4049/jimmunol.148.4.1037.

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Abstract A central event in humoral responses is the Ag-mediated interaction of Th cells and B cells. This interaction leads to the activation of both cell types and results in cytokine secretion by the T cells and proliferation and secretion of Ig by the B cells. The proliferative and differentiative responses of B cells are dependent on contact-mediated signals and cytokines provided by the activated Th cells. Although the role of cytokines in B cell activation and differentiation is understood, the nature of the signals delivered by the activated Th cells and the molecules involved in this process are not known. In this study we have examined Ag-mediated "cognate" T-B cell interactions as well as B cell activation induced by contact with preactivated and fixed Th lymphocytes. Our results indicate that both the T cell surface molecules lymphocyte function associated Ag-1 and CD2 are important in the activation of T cells by Ag presented by B lymphocytes. This indicates that B cells have similar characteristics as other APC. However, once the T cells are activated, contact-mediated stimulation of resting B lymphocytes (the noncognate phase) is dependent on CD2 but not lymphocyte function associated Ag-1. Two lines of evidence indicate this; first, it is inhibited by blocking of CD2 on the T cells and, second, such stimulation is not efficiently mediated by a CD2- Th cell line. Thus, CD2 plays an obligatory role at several discrete stages of T cell-mediated activation of resting B lymphocytes.

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Porter, Stace W., Qingping Xu, and Ann H. West. "Ssk1p Response Regulator Binding Surface on Histidine- Containing Phosphotransfer Protein Ypd1p." Eukaryotic Cell 2, no. 1 (February 2003): 27–33. http://dx.doi.org/10.1128/ec.2.1.27-33.2003.

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ABSTRACT Ypd1p, a histidine-containing phosphotransfer protein, plays an important role in a branched His-Asp phosphorelay signal transduction pathway that regulates cellular responses to hyperosmotic stress in Saccharomyces cerevisiae. Ypd1p is required for phosphoryl group transfer from the membrane-bound Sln1p sensor histidine kinase to two downstream response regulator proteins, Ssk1p and Skn7p. To investigate the molecular basis for interaction of Ypd1p with these response regulator domains, we used an approach that coupled alanine-scanning mutagenesis of surface-exposed residues in Ypd1p with a yeast two-hybrid interaction screen. Mutated residues that adversely affected the interaction of Ypd1p with the C-terminal response regulator domain of Ssk1p were identified and found to cluster on or near the αA helix in Ypd1p. Our results, supported by analysis of a modeled complex, identify a binding site on Ypd1p for response regulators that is composed of a cluster of conserved hydrophobic residues surrounded by less conserved polar residues. We propose that molecular interactions involving Ypd1p are mediated primarily through hydrophobic contacts, whereas binding specificity and strength of interaction may be influenced by select polar side chain interactions.

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Noual, A., R. Akiki, G. Lévêque, Y. Pennec, and B. Djafari-Rouhani. "Enhanced phonon-plasmon interaction in film-coupled dimer nanoridges mediated by surface acoustic waves." Optics Express 29, no. 26 (December 9, 2021): 43104. http://dx.doi.org/10.1364/oe.444430.

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Duan, Hou-Jian, Shi-Han Zheng, Pei-Hao Fu, Rui-Qiang Wang, Jun-Feng Liu, Guang-Hui Wang, and Mou Yang. "Indirect magnetic interaction mediated by Fermi arc and boundary reflection near Weyl semimetal surface." New Journal of Physics 20, no. 10 (October 10, 2018): 103008. http://dx.doi.org/10.1088/1367-2630/aae3f9.

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KABAKOV, A. E., V. A. SAENKO, and A. M. POVERENNY. "LDL-mediated interaction of DNA and DNA-anti-DNA immune complexes with cell surface." Clinical & Experimental Immunology 83, no. 3 (June 28, 2008): 359–63. http://dx.doi.org/10.1111/j.1365-2249.1991.tb05643.x.

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Graham, Andrew P., J. Peter Toennies, and Giorgio Benedek. "Evidence for long-range surface state mediated interaction between sodium atoms on copper (001)." Surface Science 556, no. 1 (May 2004): L143—L149. http://dx.doi.org/10.1016/j.susc.2004.03.010.

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Binda, Alicia V., Nadine Kabbani, Ridwan Lin, and Robert Levenson. "D2 and D3 Dopamine Receptor Cell Surface Localization Mediated by Interaction with Protein 4.1N." Molecular Pharmacology 62, no. 3 (September 1, 2002): 507–13. http://dx.doi.org/10.1124/mol.62.3.507.

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Hyldgaard, Per, and T. L. Einstein. "Surface-state mediated three-adsorbate interaction: exact and numerical results and simple asymptotic expression." Applied Surface Science 212-213 (May 2003): 856–60. http://dx.doi.org/10.1016/s0169-4332(03)00365-9.

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Wheeler, Christopher J., Jing-Yi Chen, Terry A. Potter, and Jane R. Parnes. "Mechanisms of CD8β-Mediated T Cell Response Enhancement: Interaction with MHC Class I/β2-Microglobulin and Functional Coupling to TCR/CD3." Journal of Immunology 160, no. 9 (May 1, 1998): 4199–207. http://dx.doi.org/10.4049/jimmunol.160.9.4199.

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Abstract CD8β expression results in enhanced IL-2 production and/or altered specificity in allogeneic MHC class I-restricted T cell hybridomas. Expression of chimeric CD8β-α molecules (extracellular CD8β, transmembrane and cytoplasmic CD8α) also results in enhancement of T hybridoma responses to alloantigen, suggesting that at least part of CD8β’s ability to influence responses similar to those of mature CD8+ T cells is mediated by its extracellular domain. Current data suggest that CD8β-mediated response enhancement proceeds through mechanisms similar to those mediated by CD8α, i.e., interacting with MHC class I and stabilizing CD8-associated Lck activity. In this study we present evidence that the extracellular portion of CD8β is capable of independent interaction with MHC class I/β2m dimers in the absence of CD8α. In addition, CD8β may enhance interaction with MHC class I/β2m when associated with CD8α. We also present evidence from T hybridoma responses suggesting that the extracellular portion of CD8β is uniquely capable of efficient interaction with the TCR/CD3 complex and may couple the TCR/CD3 complex to other surface components capable of enhancing TCR-mediated signals. This represents the first evidence that a critical coreceptor function can be preferentially associated with the CD8β subunit.

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Weeterings, Cees, Philip G. de Groot, Jelle Adelmeijer, and Ton Lisman. "The glycoprotein Ib-IX-V complex contributes to tissue factor–independent thrombin generation by recombinant factor VIIa on the activated platelet surface." Blood 112, no. 8 (October 15, 2008): 3227–33. http://dx.doi.org/10.1182/blood-2008-02-139113.

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Abstract Several lines of evidence suggest that recombinant factor VIIa (rFVIIa) is able to activate factor X on an activated platelet, in a tissue factor-independent manner. We hypothesized that, besides the anionic surface, a receptor on the activated platelet surface is involved in this process. Here, we showed that, in an ELISA setup, a purified extracellular fragment of GPIbα bound to immobilized rFVIIa. Surface plasmon resonance established a affinity constant (Kd) of approximately 20 nM for this interaction. In addition, CHO cells transfected with the GPIb-IX-V complex could adhere to immobilized rFVIIa, whereas wild-type CHO cells could not. Furthermore, platelets sti-mulated with a combination of collagen and thrombin adhered to immobilized rFVIIa under static conditions. Platelet adhesion was inhibited by treatment with O-sialoglycoprotein endopeptidase, which specifically cleaves GPIbα from the platelet surface. In addition, rFVIIa-mediated thrombin generation on the activated platelet surface was inhibited by cleaving GPIbα from its surface. In summary, 3 lines of evidence showed that rFVIIa interacts with the GPIb-IX-V complex, and this interaction enhanced tissue factor-independent thrombin generation mediated by rFVIIa on the activated platelet surface. The rFVIIa-GPIbα interaction could contribute to cessation of bleeding after administration of rFVIIa to patients with bleeding disorders.

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Chaudhri, Apoorvi, Yanping Xiao, Baogong Zhu, and Gordon J. Freeman. "PD-L1 binds with B7-1 only in cis on the same cell surface." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 154.11. http://dx.doi.org/10.4049/jimmunol.198.supp.154.11.

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Abstract Programmed death ligand 1 (PD-L1)-mediated immune suppression is a major regulator of peripheral tolerance and is often co-opted by tumors to evade immune attack. PD-L1 binds to PD-1 but in addition binds to B7-1 (CD80) to regulate T cell function. The binding interactions of the PD-L1-B7-1 pathway and its functional role need further investigation in order to understand differences between PD-1 and PD-L1 mediated tumor immunotherapy. We examined the molecular orientation for PD-L1 binding to B7-1 using cell to cell binding assays, ELISA, and flow cytometry. Surprisingly, we found that PD-L1 transfected cells did not bind to B7-1 transfected cells, whereas PD-L1 transfected cells bound to PD-1 transfected cells. As expected, B7-1 transfected cells bound to CD28 or cytotoxic T-lymphocyte antigen 4 (CTLA-4) transfected cells. By ELISA and flow cytometry with purified proteins, we found that PD-L1 and B7-1 had a strong binding interaction only when the PD-L1 molecule was accessible and flexible. On decreasing its accessibility, the binding was greatly reduced. We observed the PD-L1-B7-1 interaction competed for the binding of PD-L1 to PD-1. Further, we co-transfected PD-L1 and B7-1 on the same cell surface and confirmed the cis binding using a Nanobit Assay system. These results indicate that the PD-L1-B7-1 interaction can occur in cis when the molecules are on the same cell but not in trans when the molecules are on different cells. This binding orientation emphasizes the functional importance of co-expression of B7-1 and PD-L1 on the same cell. Interaction in cis competes for binding to other receptors and modulates their function. Our findings help in further understanding PD-L1 mediated immune suppression.

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Tolsma, Thomas O., Hallie P. Febvre, Deanna M. Olson, and Santiago M. Di Pietro. "Cargo-mediated recruitment of the endocytic adaptor protein Sla1 in S. cerevisiae." Journal of Cell Science 133, no. 19 (September 9, 2020): jcs247684. http://dx.doi.org/10.1242/jcs.247684.

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ABSTRACTEndocytosis of plasma membrane proteins is mediated by their interaction with adaptor proteins. Conversely, emerging evidence suggests that adaptor protein recruitment to the plasma membrane may depend on binding to endocytic cargo. To test this idea, we analyzed the yeast adaptor protein Sla1, which binds membrane proteins harboring the endocytic signal NPFxD via the Sla1 SHD1 domain. Consistently, SHD1 domain point mutations that disrupted NPFxD binding caused a proportional reduction in Sla1–GFP recruitment to endocytic sites. Furthermore, simultaneous SHD1 domain point mutation and deletion of the C-terminal LxxQxTG repeat (SR) region linking Sla1 to coat proteins Pan1 and End3 resulted in total loss of Sla1–GFP recruitment to the plasma membrane. These data suggest that multiple interactions are needed for recruitment of Sla1 to the membrane. Interestingly, a Sla1 fragment containing just the third SH3 domain, which binds ubiquitin, and the SHD1 domain displayed broad surface localization, suggesting plasma membrane recruitment is mediated by interaction with both NPFxD-containing and ubiquitylated plasma membrane proteins. Our results also imply that a Sla1 NPF motif adjacent to the SR region might regulate the Sla1–cargo interaction, mechanistically linking Sla1 cargo binding to endocytic site recruitment.

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Wang, Qingsong, Lan Jiang, Jingya Sun, Changji Pan, Weina Han, Guoyan Wang, Feifei Wang, Kaihu Zhang, Ming Li, and Yongfeng Lu. "Structure-Mediated Excitation of Air Plasma and Silicon Plasma Expansion in Femtosecond Laser Pulses Ablation." Research 2018 (December 9, 2018): 1–11. http://dx.doi.org/10.1155/2018/5709748.

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Femtosecond laser-induced surface structures upon multiple pulses irradiation are strongly correlated with the pulse number, which in turn significantly affects successive laser-material interactions. By recording the dynamics of femtosecond laser ablation of silicon using time-resolved shadowgraphy, here we present direct visualization of the excitation of air plasma induced by the reflected laser during the second pulse irradiation. The interaction of the air plasma and silicon plasma is found to enhance the shockwave expansion induced by silicon ablation in the longitudinal direction, showing anisotropic expansion dynamics in different directions. We further demonstrate the vanishing of air plasma as the pulse number increases because of the generation of a rough surface without light focusing ability. In the scenario, the interaction of air plasma and silicon plasma disappears; the expansion of the silicon plasma and shockwave restores its original characteristic that is dominated by the laser-material coupling. The results show that the excitation of air plasma and the laser-material coupling involved in laser-induced plasma and shockwave expansion are structure mediated and dependent on the pulse number, which is of fundamental importance for deep insight into the nature of laser-material interactions during multiple pulses ablation.

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Zhang, Yazhou, Yang Wang, Xiaofeng Li, Jianhong Zhang, Junhao Mao, Zhong Li, Jie Zheng, Lin Li, Steve Harris, and Dianqing Wu. "The LRP5 High-Bone-Mass G171V Mutation Disrupts LRP5 Interaction with Mesd." Molecular and Cellular Biology 24, no. 11 (June 1, 2004): 4677–84. http://dx.doi.org/10.1128/mcb.24.11.4677-4684.2004.

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ABSTRACT The mechanism by which the high-bone-mass (HBM) mutation (G171V) of the Wnt coreceptor LRP5 regulates canonical Wnt signaling was investigated. The mutation was previously shown to reduce DKK1-mediated antagonism, suggesting that the first YWTD repeat domain where G171 is located may be responsible for DKK-mediated antagonism. However, we found that the third YWTD repeat, but not the first repeat domain, is required for DKK1-mediated antagonism. Instead, we found that the G171V mutation disrupted the interaction of LRP5 with Mesd, a chaperone protein for LRP5/6 that is required for transport of the coreceptors to cell surfaces, resulting in fewer LRP5 molecules on the cell surface. Although the reduction in the number of cell surface LRP5 molecules led to a reduction in Wnt signaling in a paracrine paradigm, the mutation did not appear to affect the activity of coexpressed Wnt in an autocrine paradigm. Together with the observation that osteoblast cells produce autocrine canonical Wnt, Wnt7b, and that osteocytes produce paracrine DKK1, we think that the G171V mutation may cause an increase in Wnt activity in osteoblasts by reducing the number of targets for paracrine DKK1 to antagonize without affecting the activity of autocrine Wnt.

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Day, Christopher J., Elizabeth N. Tran, Evgeny A. Semchenko, Greg Tram, Lauren E. Hartley-Tassell, Preston S. K. Ng, Rebecca M. King, et al. "Glycan:glycan interactions: High affinity biomolecular interactions that can mediate binding of pathogenic bacteria to host cells." Proceedings of the National Academy of Sciences 112, no. 52 (December 16, 2015): E7266—E7275. http://dx.doi.org/10.1073/pnas.1421082112.

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Cells from all domains of life express glycan structures attached to lipids and proteins on their surface, called glycoconjugates. Cell-to-cell contact mediated by glycan:glycan interactions have been considered to be low-affinity interactions that precede high-affinity protein–glycan or protein–protein interactions. In several pathogenic bacteria, truncation of surface glycans, lipooligosaccharide (LOS), or lipopolysaccharide (LPS) have been reported to significantly reduce bacterial adherence to host cells. Here, we show that the saccharide component of LOS/LPS have direct, high-affinity interactions with host glycans. Glycan microarrays reveal that LOS/LPS of four distinct bacterial pathogens bind to numerous host glycan structures. Surface plasmon resonance was used to determine the affinity of these interactions and revealed 66 high-affinity host–glycan:bacterial–glycan pairs with equilibrium dissociation constants (KD) ranging between 100 nM and 50 µM. These glycan:glycan affinity values are similar to those reported for lectins or antibodies with glycans. Cell assays demonstrated that glycan:glycan interaction-mediated bacterial adherence could be competitively inhibited by either host cell or bacterial glycans. This is the first report to our knowledge of high affinity glycan:glycan interactions between bacterial pathogens and the host. The discovery of large numbers of glycan:glycan interactions between a diverse range of structures suggests that these interactions may be important in all biological systems.

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Lazarus, A. H., G. B. Mills, A. R. Crow, and T. L. Delovitch. "Antigen-induced Fc receptor-dependent and -independent B cell desensitization. An elevation in [Ca2+]i is not sufficient and protein kinase C activation is not required for these pathways of surface IgM-mediated desensitization." Journal of Immunology 147, no. 6 (September 15, 1991): 1739–45. http://dx.doi.org/10.4049/jimmunol.147.6.1739.

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Abstract The interaction of an Ag ligand with its B cell surface Ig (sIg) receptor can occur via an FcR-dependent or -independent pathway. We previously found that transfected TNP-specific B cells undergo both Ca2+ signaling and desensitization upon interaction with the thymus-dependent Ag TNP-OVA. Similarly, we showed that these B cells can also be desensitized by cross-linking sIg to the Fc gamma R via the formation of an Ag-antibody bridge. Thus, Ag-specific B cells can be desensitized by two different Ag-dependent events, one mediated by Ag-sIg interaction and the other by sIg-Fc gamma R cross-linking. Inasmuch as Ag-sIg and sIg-Fc gamma R interactions lead to positive and negative signaling, it was of interest to determine whether B cell desensitization mediated by these interactions occurs by one of the well known signaling pathways in B cells. We found that Ag-induced changes in [Ca2+]i could be readily dissociated from Ag-induced desensitization, indicating that a Ca(2+)-independent pathway is likely responsible for this pathway of desensitization. To determine if PKC plays a role in B cell desensitization mediated by either Ag or sIg-Fc gamma R interaction, PKC was downregulated by long term exposure to 12-O-tetradecanoylphorbol 13-acetate or inhibited by exposure of cells to staurosporine. The PKC down-regulated and inhibited cells underwent similar Ag- and Fc gamma R-dependent desensitization compared to cells containing active PKC. Taken together, these data indicate that Ag-induced desensitization of B cell signaling likely involves an event(s) that occurs either upstream or independent of Ag-induced elevations in [Ca2+]i and PKC activation.

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Acheson, A., J. L. Sunshine, and U. Rutishauser. "NCAM polysialic acid can regulate both cell-cell and cell-substrate interactions." Journal of Cell Biology 114, no. 1 (July 1, 1991): 143–53. http://dx.doi.org/10.1083/jcb.114.1.143.

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We have proposed previously that the polysialic acid (PSA) moiety of NCAM can influence membrane-membrane apposition, and thereby serve as a selective regulator of a variety of contact-dependent cell interactions. In this study, cell and tissue culture models are used to obtain direct evidence that the presence of PSA on the surface membrane can affect both cell-cell and cell-substrate interactions. Using a neuroblastoma/sensory neuron cell hybrid, it was found that removal of PSA with a specific neuraminidase (endo-N) augments cell-cell aggregation mediated by the L1 cell adhesion molecule as well as cell attachment to a variety of tissue culture substrates. In studies of embryonic spinal cord axon bundling, which involves both cell-cell and cell-substrate interactions, the pronounced defasciculation produced by removal of PSA is most easily explained by an increase in cell-substrate interaction. The fact that in both studies NCAM's intrinsic adhesion function was found not to be an important variable further illustrates that regulation of the cell surface by PSA can extend beyond binding mediated by the NCAM polypeptide.

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Tak, Young Joo, Woosun Jang, Norina A. Richter, and Aloysius Soon. "A rational computational study of surface defect-mediated stabilization of low-dimensional Pt nanostructures on TiN(100)." Physical Chemistry Chemical Physics 17, no. 15 (2015): 9680–86. http://dx.doi.org/10.1039/c4cp05930a.

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A rational computational platform to design surface defect-mediated low-dimensional Pt/TiN nanocatalysts for next generation high-performance fuel cell technology via strong electronic metal–support interaction.

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Tacke, Robert S., Stephen N. Waggoner, Annie Tosello-Trampont, and Young S. Hahn. "HCV Core/gC1qR Interaction Regulates LPS-Mediated MAPK Activation (134.66)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 134.66. http://dx.doi.org/10.4049/jimmunol.182.supp.134.66.

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Abstract Hepatitis C Virus (HCV) is a dangerous human pathogen that is able to establish chronic infection in its host. Studies of the immune response to the virus reveal a weak and severely delayed T and B cell response. HCV core protein is the first viral protein made following infection within hepatocytes. In addition to forming the viral capsid, HCV core protein is secreted from infected hepatocytes and is present at high levels in the peripheral blood of infected individuals. Previous data from our laboratory has shown that extracellular HCV core protein binds complement receptor gC1qR. This interaction results in the suppression of LPS-mediated IL-12 production in a PI3K dependant manner in human monocytes. Here we show that signaling through the gC1qR results in the suppression of LPS-mediated MAPK activation in a PI3K-dependent fashion. Further, we show that gC1qR-mediated signaling activates AKT, and that AKT is able to phosphorylate GSK-3β and MAPKKK family protein ASK1 at serines 9 and 83 respectively. Phosphorylation at these sites results in reduced activity of both kinases. Interestingly, both GSK-3β and ASK1 are important for LPS-mediated IL-12 production. These results suggest that HCV core protein binds gC1qR on the surface of human monocytes resulting in the activation of the PI3K/AKT pathway. AKT then inhibits LPS-mediated GSK-3β and ASK1 activation resulting in impaired MAPK activation and IL-12 production. NIH Grant RO1AI057591 supported this research.

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Capocefalo, Angela, Tanja Deckert-Gaudig, Francesco Brasili, Paolo Postorino, and Volker Deckert. "Unveiling the interaction of protein fibrils with gold nanoparticles by plasmon enhanced nano-spectroscopy." Nanoscale 13, no. 34 (2021): 14469–79. http://dx.doi.org/10.1039/d1nr03190b.

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A combined label-free spectroscopic approach at the nanoscale, based on tip-enhanced and surface-enhanced Raman spectroscopies, enabled to identify the key mechanisms in the degradation of amyloid fibrils mediated by gold nanoparticles.

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Lanzerstorfer, Peter, Ulrike Müller, Klavdiya Gordiyenko, Julian Weghuber, and Christof M. Niemeyer. "Highly Modular Protein Micropatterning Sheds Light on the Role of Clathrin-Mediated Endocytosis for the Quantitative Analysis of Protein-Protein Interactions in Live Cells." Biomolecules 10, no. 4 (April 2, 2020): 540. http://dx.doi.org/10.3390/biom10040540.

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Protein micropatterning is a powerful tool for spatial arrangement of transmembrane and intracellular proteins in living cells. The restriction of one interaction partner (the bait, e.g., the receptor) in regular micropatterns within the plasma membrane and the monitoring of the lateral distribution of the bait’s interaction partner (the prey, e.g., the cytosolic downstream molecule) enables the in-depth examination of protein-protein interactions in a live cell context. This study reports on potential pitfalls and difficulties in data interpretation based on the enrichment of clathrin, which is a protein essential for clathrin-mediated receptor endocytosis. Using a highly modular micropatterning approach based on large-area micro-contact printing and streptavidin-biotin-mediated surface functionalization, clathrin was found to form internalization hotspots within the patterned areas, which, potentially, leads to unspecific bait/prey protein co-recruitment. We discuss the consequences of clathrin-coated pit formation on the quantitative analysis of relevant protein-protein interactions, describe controls and strategies to prevent the misinterpretation of data, and show that the use of DNA-based linker systems can lead to the improvement of the technical platform.

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Zheng, Yongfang, Wendi Luo, Lanlan Yu, Shixian Chen, Kejing Mao, Qiaojun Fang, Yanlian Yang, Chen Wang, Hu Zhu, and Bin Tu. "Heterochirality-Mediated Cross-Strand Nested Hydrophobic Interaction Effects Manifested in Surface-Bound Peptide Assembly Structures." Journal of Physical Chemistry B 126, no. 3 (January 14, 2022): 723–33. http://dx.doi.org/10.1021/acs.jpcb.1c09747.

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Journal articles on the topic 'Surface-mediated interaction'

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