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Journal articles on the topic 'Microclusters'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 July 2024

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1

Campi, Gabriele, Rajat Varma, and Michael L. Dustin. "Actin and agonist MHC–peptide complex–dependent T cell receptor microclusters as scaffolds for signaling." Journal of Experimental Medicine 202, no. 8 (October 10, 2005): 1031–36. http://dx.doi.org/10.1084/jem.20051182.

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T cell receptor (TCR) microclusters form within seconds of T cell contact with supported planar bilayers containing intercellular adhesion molecule-1 and agonist major histocompatibility complex (MHC)–peptide complexes, and elevation of cytoplasmic Ca2+ is observed within seconds of the first detectable microclusters. At 0–30 s after contact, TCR microclusters are colocalized with activated forms of Lck, ZAP-70, and the linker for activation of T cells. By 2 min, activated kinases are reduced in the older central microclusters, but are abundant in younger peripheral microclusters. By 5 min, TCR in the central supramolecular activation cluster have reduced activated kinases, whereas faint peripheral TCR microclusters efficiently generated activated Lck and ZAP-70. TCR microcluster formation is resistant to inhibition by Src family kinase inhibitor PP2, but is abrogated by actin polymerization inhibitor latrunculin A. We propose that Src kinase–independent formation of TCR microclusters in response to agonist MHC–peptide provides an actin-dependent scaffold for signal amplification.

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2

Yu-Yang, Paul, A. Reddy, and Subhadip Raychaudhuri. "The effect of B cell receptor affinity on lipid mediated B cell receptor antigen microclustering (109.1)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 109.1. http://dx.doi.org/10.4049/jimmunol.186.supp.109.1.

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Abstract After encountering antigens (Ags), B-cell receptors(BCRs) with bound Ags assemble into microclusters then into a macrocluster. BCR recognition of antigen results in a monotonically increasing graded signaling response with increasing affinity for Ag, a robust feature that seems to be characterizing BCR-Ag affinity discrimination. Recent experiments indicate an important role of very early (within seconds) signaling events, such as formation of BCR-Ag microclusters, in this affinity discrimination process. Our current studies improve upon our most recent biophysical models for BCR-Ag microcluster and macrocluster formation by incorporating lipid-mediated BCR attraction factors. We examine the effect of (a) lipid and BCR concentration, and (b) varying attractive forces between different lipid and BCR pairings. Our studies indicate that a weak attraction between pairs of BCR molecules does not lead to microclusters. However, strong coupling between BCR and lipid (sphingolipids) molecules, that possibly arises upon antigen binding, generates microclusters of size similar to what has been observed in experiments. Our results indicate that microcluster size and number increase with increasing affinity while the formation times of such early BCR-Ag clusters decrease. These features can have important implications for the B cell affinity discrimination problem.

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3

Treanor, Bebhinn, David Depoil, Andreas Bruckbauer, and Facundo D. Batista. "Dynamic cortical actin remodeling by ERM proteins controls BCR microcluster organization and integrity." Journal of Experimental Medicine 208, no. 5 (April 11, 2011): 1055–68. http://dx.doi.org/10.1084/jem.20101125.

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Signaling microclusters are a common feature of lymphocyte activation. However, the mechanisms controlling the size and organization of these discrete structures are poorly understood. The Ezrin-Radixin-Moesin (ERM) proteins, which link plasma membrane proteins with the actin cytoskeleton and regulate the steady-state diffusion dynamics of the B cell receptor (BCR), are transiently dephosphorylated upon antigen receptor stimulation. In this study, we show that the ERM proteins ezrin and moesin influence the organization and integrity of BCR microclusters. BCR-driven inactivation of ERM proteins is accompanied by a temporary increase in BCR diffusion, followed by BCR immobilization. Disruption of ERM protein function using dominant-negative or constitutively active ezrin constructs or knockdown of ezrin and moesin expression quantitatively and qualitatively alters BCR microcluster formation, antigen aggregation, and downstream BCR signal transduction. Chemical inhibition of actin polymerization also altered the structure and integrity of BCR microclusters. Together, these findings highlight a crucial role for the cortical actin cytoskeleton during B cell spreading and microcluster formation and function.

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4

Lasserre, Rémi, Céline Cuche, Ronnie Blecher-Gonen, Evgeny Libman, Elise Biquand, Anne Danckaert, Deborah Yablonski, Andrés Alcover, and Vincenzo Di Bartolo. "Release of serine/threonine-phosphorylated adaptors from signaling microclusters down-regulates T cell activation." Journal of Cell Biology 195, no. 5 (November 21, 2011): 839–53. http://dx.doi.org/10.1083/jcb.201103105.

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Antigen recognition within immunological synapses triggers and sustains T cell activation by nucleating protein microclusters that gather T cell receptors (TCRs), kinases, and adaptors. Dissipation of these microclusters results in signal termination, but how this process is regulated is unclear. In this paper, we reveal that release of the adaptors SLP76 and GADS from signaling microclusters is induced by the serine/threonine protein kinase HPK1 and that phosphorylation of GADS plays a major role in this process. We found that HPK1 was recruited into microclusters and triggered their dissipation by inducing the phosphorylation of a threonine-containing motif of GADS, together with the previously described serine phosphorylation of SLP76. These events induced the cooperative binding of 14-3-3 proteins to SLP76–GADS complexes, leading to their uncoupling from the transmembrane adaptor LAT and consequently reducing microcluster persistence and activation-induced gene transcription. These results demonstrate that serine/threonine phosphorylation of multiple TCR-proximal effectors controls the stability of signaling microclusters, thereby determining the intensity of T cell responses.

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5

Ophir, Michael J., Beiyun C. Liu, and Stephen C. Bunnell. "The N terminus of SKAP55 enables T cell adhesion to TCR and integrin ligands via distinct mechanisms." Journal of Cell Biology 203, no. 6 (December 23, 2013): 1021–41. http://dx.doi.org/10.1083/jcb.201305088.

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The T cell receptor (TCR) triggers the assembly of “SLP-76 microclusters,” which mediate signals required for T cell activation. In addition to regulating integrin activation, we show that Src kinase–associated phosphoprotein of 55 kD (SKAP55) is required for microcluster persistence and movement, junctional stabilization, and integrin-independent adhesion via the TCR. These functions require the dimerization of SKAP55 and its interaction with the adaptor adhesion and degranulation-promoting adaptor protein (ADAP). A “tandem dimer” containing two ADAP-binding SKAP55 Src homology 3 (SH3) domains stabilized SLP-76 microclusters and promoted T cell adhesion via the TCR, but could not support adhesion to integrin ligands. Finally, the SKAP55 dimerization motif (DM) enabled the coimmunoprecipitation of the Rap1-dependent integrin regulator Rap1-GTP–interacting adaptor molecule (RIAM), the recruitment of talin into TCR-induced adhesive junctions, and “inside-out” signaling to β1 integrins. Our data indicate that SKAP55 dimers stabilize SLP-76 microclusters, couple SLP-76 to the force-generating systems responsible for microcluster movement, and enable adhesion via the TCR by mechanisms independent of RIAM, talin, and β1 integrins.

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6

Fooksman, David R., and Michael L. Dustin. "Affinity measured by microcluster." Journal of Experimental Medicine 207, no. 5 (May 3, 2010): 907–9. http://dx.doi.org/10.1084/jem.20100780.

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Like T cell activation, B cell activation is driven by aggregation of B cell receptors (BCRs) into microclusters. New work suggests that the early dynamics of BCR mobility and microcluster formation “translate” BCR affinity for antigen into B cell responsiveness.

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7

Sohn, Hae Won, Pavel Tolar, and Susan K. Pierce. "Membrane heterogeneities in the formation of B cell receptor–Lyn kinase microclusters and the immune synapse." Journal of Cell Biology 182, no. 2 (July 21, 2008): 367–79. http://dx.doi.org/10.1083/jcb.200802007.

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Antigen binding to the B cell receptors (BCRs) induces BCR clustering, phosphorylation of BCRs by the Src family kinase Lyn, initiation of signaling, and formation of an immune synapse. We investigated B cells as they first encountered antigen on a membrane using live cell high resolution total internal reflection fluorescence microscopy in conjunction with fluorescence resonance energy transfer. Newly formed BCR microclusters perturb the local membrane microenvironment, leading to association with a lipid raft probe. This early event is BCR intrinsic and independent of BCR signaling. Association of BCR microclusters with membrane-tethered Lyn depends on Lyn activity and persists as microclusters accumulate and form an immune synapse. Membrane perturbation and BCR–Lyn association correlate both temporally and spatially with the transition of microclustered BCRs from a “closed” to an “open” active signaling conformation. Visualization and analysis of the earliest events in BCR signaling highlight the importance of the membrane microenvironment for formation of BCR–Lyn complexes and the B cell immune synapse.

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8

Biggs, M. J. P., M. C. Milone, L. C. Santos, A. Gondarenko, and S. J. Wind. "High-resolution imaging of the immunological synapse and T-cell receptor microclustering through microfabricated substrates." Journal of The Royal Society Interface 8, no. 63 (April 13, 2011): 1462–71. http://dx.doi.org/10.1098/rsif.2011.0025.

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T-cell activation via antigen presentation is associated with the formation of a macromolecular membrane assembly termed the immunological synapse (IS). The genesis of the IS and the onset of juxtacrine signalling is characterized by the formation of cell membrane microclusters and the organization of such into segregated microdomains. A central zone rich in T-cell receptor (TCR)–major histocompatibility complex microclusters termed the central supramolecular activation cluster (cSMAC) forms the bullseye of this structure, while the cellular interface surrounding the cSMAC is characterized by regions enriched in adhesion and co-stimulatory molecules. In vitro , the study of dynamic TCR microcluster coalescence and IS genesis in T-cell populations is hampered by cell migration within the culture system and resolution constraints resulting from lateral cell–cell contact. Here, we detail a novel system describing the fabrication of micropit arrays designed to sequester single T-cell–antigen presenting cell (APC) conjugates and promote IS formation in the horizontal imaging plane for high-resolution studies of microcluster dynamics. We subsequently use this system to describe the formation of the cSMAC in T-cell populations and to investigate the morphology of the interfacial APC membrane.

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9

Xu, Jiaxuan, Jiang Wu, Taiyong Li, and Yang Nan. "Divergence-Based Locally Weighted Ensemble Clustering with Dictionary Learning and the L2,1-Norm." Entropy 24, no. 10 (September 21, 2022): 1324. http://dx.doi.org/10.3390/e24101324.

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Accurate clustering is a challenging task with unlabeled data. Ensemble clustering aims to combine sets of base clusterings to obtain a better and more stable clustering and has shown its ability to improve clustering accuracy. Dense representation ensemble clustering (DREC) and entropy-based locally weighted ensemble clustering (ELWEC) are two typical methods for ensemble clustering. However, DREC treats each microcluster equally and hence, ignores the differences between each microcluster, while ELWEC conducts clustering on clusters rather than microclusters and ignores the sample–cluster relationship. To address these issues, a divergence-based locally weighted ensemble clustering with dictionary learning (DLWECDL) is proposed in this paper. Specifically, the DLWECDL consists of four phases. First, the clusters from the base clustering are used to generate microclusters. Second, a Kullback–Leibler divergence-based ensemble-driven cluster index is used to measure the weight of each microcluster. With these weights, an ensemble clustering algorithm with dictionary learning and the L2,1-norm is employed in the third phase. Meanwhile, the objective function is resolved by optimizing four subproblems and a similarity matrix is learned. Finally, a normalized cut (Ncut) is used to partition the similarity matrix and the ensemble clustering results are obtained. In this study, the proposed DLWECDL was validated on 20 widely used datasets and compared to some other state-of-the-art ensemble clustering methods. The experimental results demonstrated that the proposed DLWECDL is a very promising method for ensemble clustering.

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10

Duncan, Michael A., and Dennis H. Rouvray. "Microclusters." Scientific American 261, no. 6 (December 1989): 110–15. http://dx.doi.org/10.1038/scientificamerican1289-110.

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11

Yokosuka, Tadashi, Masako Takamatsu, Wakana Kobayashi-Imanishi, Akiko Hashimoto-Tane, Miyuki Azuma, and Takashi Saito. "Programmed cell death 1 forms negative costimulatory microclusters that directly inhibit T cell receptor signaling by recruiting phosphatase SHP2." Journal of Experimental Medicine 209, no. 6 (May 28, 2012): 1201–17. http://dx.doi.org/10.1084/jem.20112741.

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Programmed cell death 1 (PD-1) is a negative costimulatory receptor critical for the suppression of T cell activation in vitro and in vivo. Single cell imaging elucidated a molecular mechanism of PD-1–mediated suppression. PD-1 becomes clustered with T cell receptors (TCRs) upon binding to its ligand PD-L1 and is transiently associated with the phosphatase SHP2 (Src homology 2 domain–containing tyrosine phosphatase 2). These negative costimulatory microclusters induce the dephosphorylation of the proximal TCR signaling molecules. This results in the suppression of T cell activation and blockade of the TCR-induced stop signal. In addition to PD-1 clustering, PD-1–TCR colocalization within microclusters is required for efficient PD-1–mediated suppression. This inhibitory mechanism also functions in PD-1hi T cells generated in vivo and can be overridden by a neutralizing anti–PD-L1 antibody. Therefore, PD-1 microcluster formation is important for regulation of T cell activation.

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12

Fehervari, Zoltan. "Preexisting microclusters." Nature Immunology 15, no. 9 (August 19, 2014): 824. http://dx.doi.org/10.1038/ni.2969.

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13

Gawdzik, Barbara, Joanna Drzeżdżon, Tatsiana Siarhei, Artur Sikorski, Anna Malankowska, Paweł Kowalczyk, and Dagmara Jacewicz. "Catalytic Activity of New Oxovanadium(IV) Microclusters with 2-Phenylpyridine in Olefin Oligomerization." Materials 14, no. 24 (December 12, 2021): 7670. http://dx.doi.org/10.3390/ma14247670.

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So far, few microclusters containing vanadium have been described in the literature. In this report, the synthesis protocol for the preparation of oxovanadium (IV) microclusters with 2-phenylpyridine is shown for the first time. Moreover, the crystal structure of these microclusters is also studied through the use of X-rays. The morphology of the prepared crystals is investigated using a field-emission Scanning Electron Microscope (SEM). The new compound, after activation by modified methylaluminoxane as the catalytic system, is investigated regarding the oligomerizations of 3-buten-1-ol, 2-chloro-2-propen-1-ol, allyl alcohol, and 2,3-dibromo-2-propen-1-ol. The products of oligomerization are tested by the TG-FTIR and MALDI-TOF-MS methods. Moreover, the values of catalytic activities for the new oxovanadium(IV) microclusters with 2-phenylpyridine are determined for the 3-buten-1-ol, 2-chloro-2-propen-1-ol, allyl alcohol, and 2,3-dibromo-2-propen-1-ol oligomerizations. Oxovanadium(IV) microclusters with 2-phenylpyridine are shown to be very highly active precatalysts for the oligomerization of allyl alcohol, 2,3-dibromo-2-propen-1-ol, and 3-buten-1-ol. However, in the case of 2-chloro-2-propen-1-ol oligomerization, the new microclusters are seen as highly active precatalysts.

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14

Ophir, Michael, Ken Nguyen, and Stephen Bunnell. "The SKAP55 dimer stabilizes TCR-induced SLP-76 microclusters (121.27)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 121.27. http://dx.doi.org/10.4049/jimmunol.188.supp.121.27.

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Abstract The adapter molecule SKAP55 enables the formation of T-cell:APC conjugates, facilitates T-cell cytokine production, and is required for optimal T cell proliferation in response to antigen. However, the molecular basis for the involvement of SKAP55 in these events remains unclear. Here, we demonstrate that both endogenous SKAP55 and exogenous SKAP55 chimeras enter T cell receptor (TCR)-induced signaling microclusters containing the adapter protein SLP-76. Using a SKAP55-deficient Jurkat T cell line, we demonstrate that SKAP55 is required for both the persistence and the movement of SLP-76 microclusters. Furthermore, the recruitment of SKAP55 into microclusters requires the presence of both SLP-76 and ADAP, an intermediary adapter protein capable of interacting with both SLP-76 and SKAP55. In addition, we show that SKAP55 homodimerizes via an N-terminal dimerization motif (DM). Our structure-function analyses indicate that the dimerization domain and the ADAP-interacting Src-homology domain 3 (SH3) domain of SKAP55 are both required for the recruitment of SKAP55 into SLP-76 microclusters, and for the stabilization of SLP-76 microclusters. Importantly, an artificial tandem dimer composed of two functional SH3 domains joined by a flexible linker was sufficient for entry into, and stabilization of these signaling complexes. This data indicates that SKAP55 could contribute to T-cell activation by increasing the overall avidity and stability of TCR-induced SLP-76 microclusters.

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15

Wang, Q., Q. Sun, Z.-J. Yu, and Yoshiyuki Kawazoe. "Capacitance of Microclusters." Materials Transactions, JIM 40, no. 11 (1999): 1224–27. http://dx.doi.org/10.2320/matertrans1989.40.1224.

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16

Halicioglu, T., and C. W. Bauschlicher. "Physics of microclusters." Reports on Progress in Physics 51, no. 6 (June 1, 1988): 883–921. http://dx.doi.org/10.1088/0034-4885/51/6/003.

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17

Anagnostatos, G. S. "Mixed alkali microclusters." Zeitschrift f�r Physik D Atoms, Molecules and Clusters 26, S1 (March 1993): 110–12. http://dx.doi.org/10.1007/bf01425634.

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18

Liu, Wanli. "A PI(4,5)P2-derived “gasoline engine model” for the sustained B cell receptor activation." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 151.11. http://dx.doi.org/10.4049/jimmunol.204.supp.151.11.

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Abstract To efficiently initiate activation responses against rare ligands in the microenvironment, lymphocytes employ sophisticated mechanisms involving signaling amplification. Recently, a signaling amplification mechanism initiated from phosphatidylinositol (PI) 4, 5-biphosphate [PI(4,5)P2] hydrolysis and synthesis for sustained B cell activation has been reported. Antigen and B cell receptor (BCR) recognition triggered the prompt reduction of PI(4,5)P2 density within the BCR microclusters, which led to the positive feedback for the synthesis of PI(4,5)P2 outside of the BCR microclusters. At single molecule level, the diffusion of PI(4,5)P2 was slow, allowing for the maintenance of a PI(4,5)P2 density gradient between the inside and outside of the BCR microclusters and the persistent supply of PI(4,5)P2 from outside to inside of the BCR microclusters. Here, we review studies that have contributed to uncovering the molecular mechanisms of PI(4,5)P2-derived signaling amplification model. Based on these studies, our recent work supported a “gasoline engine model” in which the activation of B cell signaling inside the microclusters is similar to the working principle of burning gasoline within the engine chamber of a gasoline engine.

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19

Yi, Jason, Xufeng S. Wu, Travis Crites, and John A. Hammer. "Actin retrograde flow and actomyosin II arc contraction drive receptor cluster dynamics at the immunological synapse in Jurkat T cells." Molecular Biology of the Cell 23, no. 5 (March 2012): 834–52. http://dx.doi.org/10.1091/mbc.e11-08-0731.

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Actin retrograde flow and actomyosin II contraction have both been implicated in the inward movement of T cell receptor (TCR) microclusters and immunological synapse formation, but no study has integrated and quantified their relative contributions. Using Jurkat T cells expressing fluorescent myosin IIA heavy chain and F-tractin—a novel reporter for F-actin—we now provide direct evidence that the distal supramolecular activation cluster (dSMAC) and peripheral supramolecular activation cluster (pSMAC) correspond to lamellipodial (LP) and lamellar (LM) actin networks, respectively, as hypothesized previously. Our images reveal concentric and contracting actomyosin II arcs/rings at the LM/pSMAC. Moreover, the speeds of centripetally moving TCR microclusters correspond very closely to the rates of actin retrograde flow in the LP/dSMAC and actomyosin II arc contraction in the LM/pSMAC. Using cytochalasin D and jasplakinolide to selectively inhibit actin retrograde flow in the LP/dSMAC and blebbistatin to selectively inhibit actomyosin II arc contraction in the LM/pSMAC, we demonstrate that both forces are required for centripetal TCR microcluster transport. Finally, we show that leukocyte function–associated antigen 1 clusters accumulate over time at the inner aspect of the LM/pSMAC and that this accumulation depends on actomyosin II contraction. Thus actin retrograde flow and actomyosin II arc contraction coordinately drive receptor cluster dynamics at the immunological synapse.

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20

Liu, Wanli, and LiLing Xu. "FcγRIIB-mediated dissociation of BCR-CD19 microclusters and hyperreactivity of lupus B cells (HUM7P.303)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 184.12. http://dx.doi.org/10.4049/jimmunol.192.supp.184.12.

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Abstract B cell activation is regulated through the interplay between the B cell receptor (BCR) and the inhibitory co-receptor FcγRIIB or activating co-receptor CD19. Recent studies suggest that the BCR microcluster is converted to a signaling active state upon its colocalization with CD19 microclusters to activate B cells. Here using TIRF microscopy-based live cell imaging techniques, we show that FcγRIIB can inhibit B cell activation by a previously uncharacterized mechanism of blocking the spatial-temporal colocalization of BCR and CD19 microclusters within the immunological synapse (IS). This inhibitory function of FcγRIIB mainly relies on its transmembrane domain (TM). Indeed, human primary B cells from SLE patients homozygous for the gene encoding FcγRIIB-I232T lose the ability to block the synaptic colocalization of BCR with CD19, leading to the dis-regulated recruitment of pCD19, pSyk and pPI3K to membrane proximal signalosome. Furthermore, FcγRIIB-I232T homozygous SLE patients are more likely to develop severe clinical symptoms characterized by high anti-ds DNA antibody titers and the involvement of kidney, central nervous system, gastrointestinal tract, lung and heart compared to patients carrying either one or both WT copies of FcγRIIB. These observations may explain the hyper-reactive features of SLE patient B cells and provide a potential target through FcγRIIB for the prophylactic diagnosis, evaluation of disease progression and potential therapies.

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21

Sykulev, Yuri, Maria Steblyanko, Nadia Anikeeva, and James Keen. "Quantitation of activating signaling microclusters’ size and dynamics and their influence on killing kinetics by cytotoxic lymphocytes (TECH2P.915)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 206.25. http://dx.doi.org/10.4049/jimmunol.194.supp.206.25.

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Abstract Stimulation of cytotoxic lymphocytes via activating receptors results in aggregation of the receptors and recruitment of proximal signaling proteins at distinct location of the contact surface term signaling microclusters. The microclusters that are initially arise in the periphery of the contact surface then move centripetally to the center and signal when they are on the move. We examined the size and dynamics of CD16 activating signaling microclusters at the interface of CD16.NK-92 cells and supported lipid bilayers containing anti-CD16 antibody and ICAM-1, a ligand for integrin receptors, at different densities. We have found that variations in the ligation of integrins but not CD16 receptor significantly affect the microclusters’ size and their displacement and mobility. These and other data provided evidence that integrin signaling effectively modulate activating receptor proximal signaling and regulate the kinetics of cytolytic granule delivery and killing kinetics by cytotoxic lymphocytes.

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22

Acevedo-Alvarez, Carlos A. "Los Clúster del Sistema Regional de Innovación Antioqueño: Más Debilidades que Fortalezas en su Desempeño." TecnoLógicas, no. 23 (December 20, 2009): 187. http://dx.doi.org/10.22430/22565337.244.

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En este artículo se realiza inicialmente una contextualización internacional del origen, estado actual y perspectivas del concepto de sistema regional de innovación (SRI). Luego se mostrarán características de los SRI exitosos o de los países desarrollados frente a las características de los SRI de países en desarrollo. Posteriormente se mostrará cómo el proceso de identificación, apoyo, implementación y consolidación de los Microclusters en Antioquia (Eje central de las actividades del SRI Antioqueño) no obedece a una estrategia de desarrollo regional ya que no involucra toda su institucionalidad (incluyendo los entornos científico, productivo, social, tecnológico y financiero). Finalmente, se establece el panorama actual (análisis DOFA, haciendo énfasis en las deficiencias e insuficiencias) de la política de microcluster como eje central de las actividades del SRI antioqueño.

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23

Schneider, E., K. Zhou, G. Gilbert, and Y. S. Weinstein. "Imperfect construction of microclusters." Journal of Modern Optics 61, no. 1 (September 20, 2013): 32–35. http://dx.doi.org/10.1080/09500340.2013.829875.

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24

Anagnastatos, G. S. "Light mixed alkali microclusters." HNPS Proceedings 3 (December 5, 2019): 154. http://dx.doi.org/10.12681/hnps.2382.

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25

Garz�n, I. L., and J. Jellinek. "Melting of gold microclusters." Zeitschrift f�r Physik D Atoms, Molecules and Clusters 20, no. 1-4 (March 1991): 235–38. http://dx.doi.org/10.1007/bf01543981.

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26

Montano, P. A., J. Zhao, M. Ramanathan, G. K. Shenoy, W. Schulze, and J. Urban. "Structure of silver microclusters." Chemical Physics Letters 164, no. 2-3 (December 1989): 126–30. http://dx.doi.org/10.1016/0009-2614(89)85003-1.

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27

EL-BAYYARI, ZUHEIR, HÜSEYIN OYMAK, and HATICE KÖKTEN. "ON THE STRUCTURAL AND ENERGETIC FEATURES OF SMALL METAL CLUSTERS: Nin, Cun, Pdn, Ptn, AND Pbn; n=3–13." International Journal of Modern Physics C 15, no. 06 (July 2004): 917–30. http://dx.doi.org/10.1142/s0129183104006339.

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Using an empirical potential energy function parametrized for each of the Ni , Cu , Pd , Pt , and Pb systems, minimum-energy structures of Ni n, Cu n, Pd n, Pt n, and Pb n (n=3–13) microclusters have been determined by performing molecular-dynamics simulations. The structural and energetic features of the obtained microclusters have been investigated.

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Koylass, Nicholas Robert, Elizabeth DeRiso, Andrea L. Szymczak-Workman, Angela Montecalvo, Joanne M. Murphy, Maria-Cristina Seminario, Stephen C. Bunnell, and Lawrence P. Kane. "Polyubiquitin-dependent recruitment of NEMO/IKKγ into T cell receptor signaling microclusters is controlled by IKKβ kinase activity." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 80.1. http://dx.doi.org/10.4049/jimmunol.204.supp.80.1.

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Abstract The IkB kinase (IKK) complex coordinates inflammatory responses by activating canonical NFkB downstream of immune receptors. This complex consists of the kinases IKKa/β and the dimeric adaptor subunit NEMO (NFkB essential modulator protein). NEMO mutations cause immunodeficiencies and impair antigen receptor function. Canonical NFkB activation by immunoreceptors, such as the T cell receptor (TCR), requires the assembly of the Carma1/Bcl10/Malt1 (CBM) signalosome. While, functional studies and in vitro interactions, place the IKK complex downstream of the CBM signalosome, the spatial relationship between these complexes has never been observed in intact immune cells. We observed that NEMO is recruited into TCR microclusters and membrane compartments within ~70 seconds of TCR engagement. Point mutations impacting the K63-linked and linear polyubiquitin ubiquitin-binding domains of NEMO selectively impair NEMO recruitment into TCR microclusters. We verified the involvement of these polyubiquitin chains by showing that inhibitors of either the K63-specific Uev1A/Ubc13 ubiquitin E2 ligase or the linear ubiquitin activating complex (LUBAC) prevent NEMO from entering TCR microclusters. To examine whether the entire IKK complex is recruited to the TCR, we co-expressed IKKb chimeras with NEMO. We observed that wild-type (WT), but not kinase-dead, IKKb caused NEMO microclusters to disappear. Similarly, the treatment of cells expressing WT IKKb with inhibitors of IKKβ or its upstream activator, TAK1, restored the recruitment of IKKβ and NEMO into microclusters. These results suggest that the IKK complex is recruited to the TCR via linear- and K63-linked polyubiquitin chains and then dissociates from the TCR via IKKβ activity.

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29

Shafinaz Zainal Abidin, Mastura, Shahjahan Shahjahan, and Abdul Manaf Hashim. "Synthesis of Germanium Dioxide Microclusters on Silicon Substrate in Non-aqueous Solution by Electrochemical Deposition." Indonesian Journal of Electrical Engineering and Computer Science 6, no. 1 (April 1, 2017): 193. http://dx.doi.org/10.11591/ijeecs.v6.i1.pp193-199.

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<p>We report the formation of crystalline germanium dioxide (GeO<sub>2</sub>) microclusters on n-Si (100) electrodeposited in non-aqueous electrolyte (a mixture of 5 vol.% germanium tetrachloride (GeCl<sub>4</sub>) and dipropylene glycol (C<sub>6</sub>H<sub>14</sub>O<sub>3</sub>) ) at current density of 20 mA/cm<sup>2</sup> for 200 sec. Pt, C and Ge are used as an anode while Si acts as a cathode. Field- emission scanning electron microscopy (FESEM) images show that the deposited GeO<sub>2</sub> microclusters are having rounded-mushroom-shaped particles with the smallest size of 660 nm. Energy dispersive x-ray (EDX) spectra reveal that the particles are only composed of Ge and O elements. Raman spectra confirm the formation of crystalline GeO<sub>2</sub> with trigonal bonding structures in all samples. The photoluminescence (PL) spectra show two significant emission peaks in visible range at 2.27 eV and 2.96 eV, which seems to be attributed by GeO<sub>2</sub> and Si defects. C<sub>6</sub>H<sub>14</sub>O<sub>3 </sub>seems to contribute to the formation of GeO<sub>2</sub> due to its hygroscopic nature. Such microcluster structures shall provide some potential applications for electronic and optical devices on Si platform.</p>

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30

Yang, Fuqian. "Nucleation in a liquid droplet." Physical Chemistry Chemical Physics 22, no. 18 (2020): 9990–97. http://dx.doi.org/10.1039/d0cp00559b.

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31

MARUYAMA, K., T. TSUZUKI, M. YAO, and H. ENDO. "PHOTOINDUCED PHENOMENA OF CHALCOGEN MICROCLUSTERS CONFINED IN THE ZEOLITE CAGES." Surface Review and Letters 03, no. 01 (February 1996): 711–15. http://dx.doi.org/10.1142/s0218625x96001285.

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Photoacoustic spectroscopy measurements have been carried out on the Se-ring microclusters confined in the cages of zeolite 4A. The shift of photoabsorption edge and the new absorption bands around 1.5 and 1.9 eV appeared by illumination of the light having the band-gap energy at low temperature. These phenomena may be associated with the distortion of Se ring and the formation of dangling bonds. Mixing of S or Te to the Se microclusters causes appreciable change in the photoinduced phenomena.

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32

Endo, H., K. Maruyama, T. Tsuzuki, and M. Yao. "EXAFS Study of Chalcogen Microclusters." Japanese Journal of Applied Physics 32, S2 (January 1, 1993): 773. http://dx.doi.org/10.7567/jjaps.32s2.773.

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33

Boo, T. B., H. H. Kwong, and Yuan Ping Feng. "Computational Study of GaAs Microclusters." Key Engineering Materials 227 (August 2002): 177–82. http://dx.doi.org/10.4028/www.scientific.net/kem.227.177.

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34

Delaly, P., P. Ballone, and J. Buttet. "Metallic bonding in magnesium microclusters." Physical Review B 45, no. 7 (February 15, 1992): 3838–41. http://dx.doi.org/10.1103/physrevb.45.3838.

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35

Jiang, P., F. Jona, and P. M. Marcus. "Surface effects in metal microclusters." Physical Review B 36, no. 12 (October 15, 1987): 6336–38. http://dx.doi.org/10.1103/physrevb.36.6336.

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36

Feuston, B. P., R. K. Kalia, and P. Vashishta. "Structural correlations in silicon microclusters." Physical Review B 37, no. 11 (April 15, 1988): 6297–304. http://dx.doi.org/10.1103/physrevb.37.6297.

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37

Anagnostatos, G. S. "FERMION-BOSON CLASSIFICATION IN MICROCLUSTERS." HNPS Proceedings 2 (February 18, 2020): 407. http://dx.doi.org/10.12681/hnps.2867.

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Mlcroclusters composed of atoms with non delocallzed odd number of valence electrons possess the usual magic numbers for fermions in a central potential and those with an even number of valence electrons possess the magic numbers for bosons coming from the packing of atoms in nested icosahedral or octahedral or tetrahedral shells. On the other hand, mlcroclusters composed of atoms with delocallzed valence electrons, either with an odd or with an even number of electrons, exhibit electronic magic numbers (according to the jelllum model) but also magic numbers coming from the (same, as above) packings of their bosonlc ion cores. Finally, through the present work, an alternative approach to study atomic nuclei as quantum clusters appears possible and promising.

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38

Zhang, F. S., E. Suraud, F. Calvo, and F. Spiegelmann. "Vibrational properties of sodium microclusters." Chemical Physics Letters 300, no. 5-6 (February 1999): 595–602. http://dx.doi.org/10.1016/s0009-2614(98)01415-8.

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39

Phan, Tri Giang, and Robert Brink. "Micromanaging Memory with Immunoglobulin Microclusters." Immunity 32, no. 6 (June 2010): 732–33. http://dx.doi.org/10.1016/j.immuni.2010.06.009.

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40

ZHANG, F. S., and F. WANG. "THERMODYNAMICAL PROPERTIES OF SODIUM MICROCLUSTERS." International Journal of Modern Physics B 19, no. 15n17 (July 10, 2005): 2657–62. http://dx.doi.org/10.1142/s0217979205031481.

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Isomerization, pseudo-rotation and phase transition in sodium microclusters Nan are investigated for several sizes ( n =4, 8, and 20) using distance dependent tight-binding molecular dynamics simulations with a particular attention to Na4.

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41

Selby, K., V. Kresin, J. Masui, M. Vollmer, A. Scheidemann, and W. D. Knight. "Optical spectra of sodium microclusters." Zeitschrift f�r Physik D Atoms, Molecules and Clusters 19, no. 1-4 (March 1991): 43–45. http://dx.doi.org/10.1007/bf01448251.

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42

Fujima, N., and T. Yamaguchi. "Electronic states of Mn microclusters." Zeitschrift f�r Physik D Atoms, Molecules and Clusters 19, no. 1-4 (March 1991): 185–87. http://dx.doi.org/10.1007/bf01448287.

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43

Suzdalev, I. P., and V. K. Imshennik. "Microclusters nucleation in porous materials." Nuclear Instruments and Methods in Physics Research Section B: Beam Interactions with Materials and Atoms 76, no. 1-4 (April 1993): 318–20. http://dx.doi.org/10.1016/0168-583x(93)95222-q.

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Anagnostatos, G. S. "Magic numbers in semiconductor microclusters." Physics Letters A 143, no. 6-7 (January 1990): 332–36. http://dx.doi.org/10.1016/0375-9601(90)90349-s.

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45

Anagnostatos, G. S. "Fermion/boson classification in microclusters." Physics Letters A 157, no. 1 (July 1991): 65–72. http://dx.doi.org/10.1016/0375-9601(91)90410-a.

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46

Katayama, Yoshinori, Kenji Maruyama, and Hirohisa Endo. "Microclusters confined in zeolite cage." Journal of Non-Crystalline Solids 117-118 (February 1990): 485–88. http://dx.doi.org/10.1016/0022-3093(90)90980-z.

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47

Weber, Michele, Bebhinn Treanor, David Depoil, Hisaaki Shinohara, Naomi E. Harwood, Masaki Hikida, Tomohiro Kurosaki, and Facundo D. Batista. "Phospholipase C-γ2 and Vav cooperate within signaling microclusters to propagate B cell spreading in response to membrane-bound antigen." Journal of Experimental Medicine 205, no. 4 (March 24, 2008): 853–68. http://dx.doi.org/10.1084/jem.20072619.

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B cell receptor (BCR) recognition of membrane-bound antigen initiates a spreading and contraction response, the extent of which is controlled through the formation of signaling-active BCR-antigen microclusters and ultimately affects the outcome of B cell activation. We followed a genetic approach to define the molecular requirements of BCR-induced spreading and microcluster formation. We identify a key role for phospholipase C-γ2 (PLCγ2), Vav, B cell linker, and Bruton's tyrosine kinase in the formation of highly coordinated “microsignalosomes,” the efficient assembly of which is absolutely dependent on Lyn and Syk. Using total internal reflection fluorescence microscopy, we examine at high resolution the recruitment of PLCγ2 and Vav to microsignalosomes, establishing a novel synergistic relationship between the two. Thus, we demonstrate the importance of cooperation between components of the microsignalosome in the amplification of signaling and propagation of B cell spreading, which is critical for appropriate B cell activation.

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48

ERKOÇ, ŞAKIR, and KUNIO TAKAHASHI. "A COMPARATIVE STUDY OF EMPIRICAL POTENTIAL ENERGY FUNCTIONS: APPLICATIONS TO SILICON MICROCLUSTERS." International Journal of Modern Physics C 15, no. 03 (March 2004): 403–8. http://dx.doi.org/10.1142/s0129183104005814.

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A comparative study has been performed for silicon microclusters, Si 3 and Si 4, considering fifteen different empirical potential energy functions. It has been found that only two of the empirical potential energy functions give linear structure more stable for Si 3, the remaining potential functions give triangular structure as more stable. In the case of Si 4 microclusters eight potential functions give open tetrahedral structure as more stable, two functions give perfect tetrahedral as more stable, three functions give square structure as more stable, and two functions give linear structure as more stable.

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49

Rossenova, Boryana, Bryan Jackson, Michael Dustin, and Jay T. Groves. "Counting agonist in functional T cell receptor clusters using nanopatterned corrals (87.51)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S137—S138. http://dx.doi.org/10.4049/jimmunol.178.supp.87.51.

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Abstract T lymphocytes, the initiators of the adaptive immune response, are remarkable for their ability to recognize very few agonist peptides presented on APC, using their T cell receptors (TCR). Recent studies emphasize the role of spatial organization of TCR at the interface between the two cells in regulating T cell activation - a central cluster and peripheral microclusters. The microclusters are thought to initiate, amplify and maintain signaling, however their mechanism of function is largely unknown. Using nanopatterned square corrals, 1 micrometer in length, we can regulate the maximum number of agonist-MHC molecules per cluster presented by a fluid supported lipid bilayer containing MHC and ICAM-1 molecules. We find that at activating mean concentrations of agonist, T lymphocytes are unable to initiate signaling if the maximal number of agonist molecules per corral is 1–2. Surprisingly, agonist number as little as twice this amount per corral, results in full cell activation, as measured by the calcium flux inside the cell. These observations suggest that microclusters are not necessary to amplify signaling beyond what 3–4 agonist molecules are sufficient to do.

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50

Koylass, Nicholas Robert, Elizabeth A. DeRiso, Andrea L. Szymczak-Workman, Angela Montecalvo, Joanne M. Murphy, Maria Cristina Seminario, Lawrence P. Kane, and Stephen C. Bunnell. "Recruitment of NEMO/IKKγ to TCR microclusters during T cell activation." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 184.1. http://dx.doi.org/10.4049/jimmunol.202.supp.184.1.

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Abstract The IκB kinase (IKK) complex mediates the activation of canonical NFκB isoforms following T cell receptor (TCR) ligation. This complex consists of the kinases IKKα and IKKβ and an essential adaptor subunit, the NFκB essential modulator protein (NEMO). Most models suggest that the IKK complex is activated within oligomeric Carma1/Bcl10/Malt1 (CBM) signalosomes. However, we observed that NEMO enters TCR microclusters before CBM complexes are assembled, within ~70 seconds of TCR engagement. NEMO also entered mobile vesicles and in larger membrane-bounded structures (hereafter ‘macroclusters’). The recruitment of NEMO into TCR microclusters is prevented by Src kinase inhibitors and by the catalytic inactivation of ZAP-70, but occurs in the absence of either SLP-76 or Carma1. Further, NEMO fails to co-localize with TCR-induced CBM polymers. Thus, the recruitment of NEMO to the TCR occurs via a CBM-independent mechanism. The deletion the zinc-finger (ZnF) domain of NEMO disables NFκB signaling and eliminates NEMO from microclusters, while preserving NEMO macroclusters. Since the ZnF domain interacts with polyubiquitin chains, we generated point mutations impacting the ubiquitin-binding site in the ZnF domain and two independent sites within the NEMO ubiquitin-binding ‘NUB’ domain. These mutations impair the ability of NEMO to capture K63-linked and/or linear polymers, hinder NFκB signaling, and eliminate NEMO from microclusters without disrupting NEMO macroclusters. These findings suggest that NEMO is rapidly recruited to polyubiquitin chains associated with the TCR, rather than the CBM complex, and that the CBM complex augments IKK-dependent NFκB signaling via a distinct, recruitment-independent mechanism.

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