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Academic literature on the topic 'Sequential Link Activation'
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Journal articles on the topic "Sequential Link Activation"
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Martinuzzi, Emanuela, Georgia Afonso, Marie-Claude Gagnerault, Gaetano Naselli, Diana Mittag, Béhazine Combadière, Christian Boitard, et al. "acDCs enhance human antigen–specific T-cell responses." Blood 118, no. 8 (August 25, 2011): 2128–37. http://dx.doi.org/10.1182/blood-2010-12-326231.
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Abstract Detection of human Ag-specific T cells is limited by sensitivity and blood requirements. As dendritic cells (DCs) can potently stimulate T cells, we hypothesized that their induction in PBMCs in situ could link Ag processing and presentation to Ag-specific T-cell activation. To this end, unfractionated PBMCs (fresh or frozen) or whole blood were incubated for 48 hours with protein or peptide Ag together with different DC-activating agents to rapidly and sequentially induce, pulse, and mature DCs. DC activation was therefore lined up with Ag recognition by neighboring T cells, thus telescoping the sequential steps of T-cell activation. Efficient processing of protein Ags made prior knowledge of epitopes and HLA restrictions dispensable. While reducing stimulation time, manipulation and blood requirements, in situ DC induction specifically amplified Ag-specific T-cell responses (cytokine secretion, proliferation, CD137/CD154 up-regulation, and binding of peptide-HLA multimers). IL-1β, although released by DCs, was also secreted in an Ag-specific fashion, thus providing an indirect biomarker of T-cell responses. These accelerated cocultured DC (acDC) assays offered a sensitive means with which to evaluate T-cell responses to viral and melanoma Ag vaccination, and may therefore find application for immune monitoring in viral, tumor, autoimmune, and transplantation settings.
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Vachharajani, Vidula T., Tiefu Liu, Xianfeng Wang, Jason J. Hoth, Barbara K. Yoza, and Charles E. McCall. "Sirtuins Link Inflammation and Metabolism." Journal of Immunology Research 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/8167273.
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Sirtuins (SIRT), first discovered in yeast as NAD+ dependent epigenetic and metabolic regulators, have comparable activities in human physiology and disease. Mounting evidence supports that the seven-member mammalian sirtuin family (SIRT1–7) guard homeostasis by sensing bioenergy needs and responding by making alterations in the cell nutrients. Sirtuins play a critical role in restoring homeostasis during stress responses. Inflammation is designed to “defend and mend” against the invading organisms. Emerging evidence supports that metabolism and bioenergy reprogramming direct the sequential course of inflammation; failure of homeostasis retrieval results in many chronic and acute inflammatory diseases. Anabolic glycolysis quickly induced (compared to oxidative phosphorylation) for ROS and ATP generation is needed for immune activation to “defend” against invading microorganisms. Lipolysis/fatty acid oxidation, essential for cellular protection/hibernation and cell survival in order to “mend,” leads to immune repression. Acute/chronic inflammations are linked to altered glycolysis and fatty acid oxidation, at least in part, by NAD+ dependent function of sirtuins. Therapeutically targeting sirtuins may provide a new class of inflammation and immune regulators. This review discusses how sirtuins integrate metabolism, bioenergetics, and immunity during inflammation and how sirtuin-directed treatment improves outcome in chronic inflammatory diseases and in the extreme stress response of sepsis.
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Bogatcheva, Natalia V., Peiyi Wang, Anna A. Birukova, Alexander D. Verin, and Joe G. N. Garcia. "Mechanism of fluoride-induced MAP kinase activation in pulmonary artery endothelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 290, no. 6 (June 2006): L1139—L1145. http://dx.doi.org/10.1152/ajplung.00161.2005.
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In this study, we demonstrate that challenge of endothelial cells (EC) with NaF, a recognized G protein activator and protein phosphatase inhibitor, leads to a significant Erk activation, with increased phosphorylation of the well-known Erk substrate caldesmon. Inhibition of the Erk MAPK, MEK, by U0126 produces a marked decrease in NaF-induced caldesmon phosphorylation. NaF transiently increases the activity of the MEK kinase known as Raf-1 (∼3- to 4-fold increase over basal level), followed by a sustained Raf-1 inhibition (∼3- to 4-fold decrease). Selective Raf-1 inhibitors (ZM-336372 and Raf-1 inhibitor 1) significantly attenuate NaF-induced Erk and caldesmon phosphorylation. Because we have previously shown that Ca2+/calmodulin-dependent protein kinase II (CaMKII) participates in Erk activation in thrombin-challenged cells, we next explored if CaMKII is involved in NaF-induced EC responses. We found that in NaF-treated EC, CaMKII activity increases in a time-dependent manner with maximal activity at 10 min (∼4-fold increase over a basal level). Pretreatment with KN93, a specific CaMKII inhibitor, attenuates NaF-induced barrier dysfunction and Erk phosphorylation. The Rho inhibitor C3 exotoxin completely abolishes NaF-induced CaMKII activation. Collectively, these data suggest that sequential activation of Raf-1, MEK, and Erk is modulated by Rho-dependent CaMKII activation and represents important NaF-induced signaling response. Caldesmon phosphorylation occurring by an Erk-dependent mechanism in NaF-treated pulmonary EC may represent a link between NaF stimulation and contractile responses of endothelium.
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Jeschke, Andreas, and Albert Haas. "Sequential actions of phosphatidylinositol phosphates regulate phagosome-lysosome fusion." Molecular Biology of the Cell 29, no. 4 (February 15, 2018): 452–65. http://dx.doi.org/10.1091/mbc.e17-07-0464.
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Phagosomes mature into phagolysosomes by sequential fusion with early endosomes, late endosomes, and lysosomes. Phagosome-with-lysosome fusion (PLF) results in the delivery of lysosomal hydrolases into phagosomes and in digestion of the cargo. The machinery that drives PLF has been little investigated. Using a cell-free system, we recently identified the phosphoinositide lipids (PIPs) phosphatidylinositol 3-phosphate (PI(3)P) and phosphatidylinositol 4-phosphate (PI(4)P) as regulators of PLF. We now report the identification and the PIP requirements of four distinct subreactions of PLF. Our data show that (i) PI(3)P and PI(4)P are dispensable for the disassembly and activation of (phago)lysosomal soluble N-ethylmaleimide-sensitive factor attachment protein receptors, that (ii) PI(3)P is required only after the tethering step, and that (iii) PI(4)P is required during and after tethering. Moreover, our data indicate that PI(4)P is needed to anchor Arl8 (Arf-like GTPase 8) and its effector homotypic fusion/vacuole protein sorting complex (HOPS) to (phago)lysosome membranes, whereas PI(3)P is required for membrane association of HOPS only. Our study provides a first link between PIPs and established regulators of membrane fusion in late endocytic trafficking.
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Okamoto, Isamu, Yoshiaki Kawano, Daizo Murakami, Takashi Sasayama, Norie Araki, Toru Miki, Albert J. Wong, and Hideyuki Saya. "Proteolytic release of CD44 intracellular domain and its role in the CD44 signaling pathway." Journal of Cell Biology 155, no. 5 (November 19, 2001): 755–62. http://dx.doi.org/10.1083/jcb.200108159.
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CD44 is a widely distributed cell surface adhesion molecule and is implicated in diverse biological processes. However, the nature of intracellular signaling triggered by CD44 remains to be elucidated. Here, we show that CD44 undergoes sequential proteolytic cleavage in the ectodomain and intracellular domain, resulting in the release of a CD44 intracellular domain (ICD) fragment. Consequently, CD44ICD acts as a signal transduction molecule, where it translocates to the nucleus and activates transcription mediated through the 12-O-tetradecanoylphorbol 13-acetate–responsive element, which is found in numerous genes involved in diverse cellular processes. Expression of an uncleavable CD44 mutant as well as metalloprotease inhibitor treatment blocks CD44-mediated transcriptional activation. In search of the underlying mechanism, we have found that CD44ICD potentiates transactivation mediated by the transcriptional coactivator CBP/p300. Furthermore, we show that cells expressing CD44ICD produce high levels of CD44 messenger RNA, suggesting that the CD44 gene is one of the potential targets for transcriptional activation by CD44ICD. These observations establish a novel CD44 signaling pathway and shed new light on the functional link between proteolytic processing of an adhesion molecule at the cell surface and transcriptional activation in the nucleus.
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Romanelli, Angela, Kathleen A. Martin, Alex Toker, and John Blenis. "p70 S6 Kinase Is Regulated by Protein Kinase Cζ and Participates in a Phosphoinositide 3-Kinase-Regulated Signalling Complex." Molecular and Cellular Biology 19, no. 4 (April 1, 1999): 2921–28. http://dx.doi.org/10.1128/mcb.19.4.2921.
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ABSTRACT p70 S6 kinase (p70S6K) is an important regulator of cell proliferation. Its activation by growth factor requires phosphorylation by various inputs on multiple sites. Data accumulated thus far support a model whereby p70S6K activation requires sequential phosphorylations at proline-directed residues in the putative autoinhibitory pseudosubstrate domain, as well as threonine 389. Threonine 229, a site in the catalytic loop is phosphorylated by phosphoinositide-dependent kinase 1 (PDK-1). Experimental evidence suggests that p70S6K activation requires a phosphoinositide 3-kinase (PI3-K)-dependent signal(s). However, the intermediates between PI3-K and p70S6K remain unclear. Here, we have identified PI3-K-regulated atypical protein kinase C (PKC) isoform PKCζ as an upstream regulator of p70S6K. In coexpression experiments, we found that a kinase-inactive PKCζ mutant antagonized activation of p70S6K by epidermal growth factor, PDK-1, and activated Cdc42 and PI3-K. While overexpression of a constitutively active PKCζ mutant (myristoylated PKCζ [myr-PKCζ]) only modestly activated p70S6K, this mutant cooperated with PDK-1 activation of p70S6K. PDK-1-induced activation of a C-terminal truncation mutant of p70S6K was also enhanced by myr-PKCζ. Moreover, we have found that p70S6K can associate with both PDK-1 and PKCζ in vivo in a growth factor-independent manner, while PDK-1 and PKCζ can also associate with each other, suggesting the existence of a multimeric PI3-K signalling complex. This work provides evidence for a link between a phorbol ester-insensitive PKC isoform and p70S6K. The existence of a PI3-K-dependent signalling complex may enable efficient activation of p70S6K in cells.
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Lacanà, E., J. K. Ganjei, P. Vito, and L. D'Adamio. "Dissociation of apoptosis and activation of IL-1beta-converting enzyme/Ced-3 proteases by ALG-2 and the truncated Alzheimer's gene ALG-3." Journal of Immunology 158, no. 11 (June 1, 1997): 5129–35. http://dx.doi.org/10.4049/jimmunol.158.11.5129.
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Abstract Recent attention has been focused on the members of the IL-1beta-converting enzyme (ICE)/Ced-3 family of cysteine protease as the key components of programmed cell death. However, the molecular events that lead to protease activation and link it to the final apoptotic processes remain poorly characterized. We have shown recently that ALG-2 is a Ca2+-binding protein required for apoptosis. ALG-2 depletion protects the mouse T cell hybridoma 3DO from programmed cell death induced by several stimuli, such as synthetic glucocorticoids, TCR, and Fas triggering. In this work, we show that in the ALG-2-depleted clones the ICE/Ced-3 proteases are normally activated upon TCR, Fas, and dexamethasone stimulation, as determined by cleavage of the endogenous substrate poly(ADP-ribose) polymerase and of a fluorogenic substrate. ALG-3, a truncated form of the familial Alzheimer's disease gene PS2, confers resistance to TCR- and Fas-induced apoptosis. Of interest, it also reduces protease activity and inhibits poly(ADP-ribose) polymerase cleavage upon Fas triggering. Our results suggest that, during apoptosis, ALG-2 functions downstream of, and that ALG-3 interferes with the sequential activation of members of the ICE family proteases.
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Würtz, R. P., and C. von der Malsburg. "A Hierarchical Dynamic Link Network to Solve the Visual Correspondence Problem." Perception 25, no. 1_suppl (August 1996): 183. http://dx.doi.org/10.1068/v96l0702.
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Conventional neural networks try to solve the problem of object recognition in a single step by building a stimulus — response system that codes its result as cell activities. We take a different approach assuming that recognition is an active process with temporal dynamics and results in an ordered state. We present a structure of neuronal layers, interconnected by dynamic links (von der Malsburg, 1985 Berichte der Bunsengesellschaft für Physikalische Chemie89 703 – 710) that solves the correspondence problem between two images and thus constitutes an important building block for a model of recognition. Images as well as stored models are represented as Gabor pyramids. This allows the dynamics to proceed from coarse to fine scale and reduces the sequential processing time inherent in the concept. Invariance under background changes is also made possible. On the lowest frequency level, a single blob of activity moves across the image and model layer, respectively. Dynamic links between these layers are initialised to the (highly ambiguous) feature similarities. Links grow or decline according to a combination of feature similarity and correlated activation. This enforces correct neighbourhood relationships in addition to feature similarity. On the higher levels the established correspondences are refined by several blobs in parallel. We present an improved version of the dynamical system proposed by Würtz [1995 Multilayer Dynamic Link Networks for Establishing Image Point Correspondences and Visual Object Recognition (Thun, Frankfurt a.M.: Harri Deutsch)] and show, with examples of human faces, that it evolves from an unordered link distribution to any ordered state where only corresponding point pairs are connected by strong links. Correspondences between sample points are population-coded by a set of neighbouring links.
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Rescan, Claude, Alexandre Coutant, Hélène Talarmin, Nathalie Theret, Denise Glaise, Christiane Guguen-Guillouzo, and Georges Baffet. "Mechanism in the Sequential Control of Cell Morphology and S Phase Entry by Epidermal Growth Factor Involves Distinct MEK/ERK Activations." Molecular Biology of the Cell 12, no. 3 (March 2001): 725–38. http://dx.doi.org/10.1091/mbc.12.3.725.
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Cell shape plays a role in cell growth, differentiation, and death. Herein, we used the hepatocyte, a normal, highly differentiated cell characterized by a long G1 phase, to understand the mechanisms that link cell shape to growth. First, evidence was provided that the mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) cascade is a key transduction pathway controlling the hepatocyte morphology. MEK2/ERK2 activation in early G1 phase did not lead to cell proliferation but induced cell shape spreading and demonstration was provided that this MAPK-dependent spreading was required for reaching G1/S transition and DNA replication. Moreover, epidermal growth factor (EGF) was found to control this morphogenic signal in addition to its mitogenic effect. Thus, blockade of cell spreading by cytochalasin D or PD98059 treatment resulted in inhibition of EGF-dependent DNA replication. Our data led us to assess the first third of G1, is exclusively devoted to the growth factor-dependent morphogenic events, whereas the mitogenic signal occured at only approximately mid-G1 phase. Moreover, these two growth factor-related sequential signaling events involved successively activation of MEK2-ERK2 and then MEK1/2-ERK1/2 isoforms. In addition, we demonstrated that inhibition of extracellular matrix receptor, such as integrin β1 subunit, leads to cell arrest in G1, whereas EGF was found to up-regulated integrin β1 and fibronectin in a MEK-ERK–dependent manner. This process in relation to cytoskeletal reorganization could induce hepatocyte spreading, making them permissive for DNA replication. Our results provide new insight into the mechanisms by which a growth factor can temporally control dual morphogenic and mitogenic signals during the G1 phase.
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Wei, Xiumei, Yu Zhang, Cheng Li, Kete Ai, Kang Li, Huiying Li, and Jialong Yang. "The evolutionarily conserved MAPK/Erk signaling promotes ancestral T-cell immunity in fish via c-Myc–mediated glycolysis." Journal of Biological Chemistry 295, no. 10 (January 29, 2020): 3000–3016. http://dx.doi.org/10.1074/jbc.ra119.012231.
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The mitogen-activated protein kinase (MAPK) cascade is an ancient and evolutionarily conserved signaling pathway involved in numerous physiological processes. Despite great advances in understanding MAPK-mediated regulation of adaptive immune responses in mammals, its contribution to T-cell immunity in early vertebrates remains unclear. Herein, we used Nile tilapia (Oreochromis niloticus) to investigate the regulatory roles of MAPK/extracellular signal–regulated kinase (Erk) signaling in ancestral T-cell immunity of jawed fish. We found that Nile tilapia possesses an evolutionarily conserved MAPK/Erk axis that is activated through a classical three-tier kinase cascade, involving sequential phosphorylation of RAF proto-oncogene serine/threonine-protein kinase (Raf), MAPK/Erk kinase 1/2 (Mek1/2), and Erk1/2. In Nile tilapia, MAPK/Erk signaling participates in adaptive immune responses during bacterial infection. Upon T-cell activation, the MAPK/Erk axis is robustly activated, and MAPK/Erk blockade by specific inhibitors severely impairs T-cell activation. Furthermore, signals from MAPK/Erk were indispensable for primordial T cells to proliferate and exert their effector functions. Mechanistically, activation of the MAPK/Erk axis promoted glycolysis via induction of the transcriptional regulator proto-oncogene c-Myc (c-Myc), to ensure the proper activation and proliferation of fish T cells. Our results reveal the regulatory mechanisms of MAPK/Erk signaling in T-cell immunity in fish and highlight a close link between immune signals and metabolic programs. We propose that regulation of T-cell immunity by MAPK/Erk is a basic and sophisticated strategy that evolved before the emergence of the tetrapod lineage. These findings shed light on the evolution of the adaptive immune system.
Conference papers on the topic "Sequential Link Activation"
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Badimon, J. J., L. Badimon, A. Galvez, J. Camunas, and V. Fuster. "DYNAMICS AND LOCALIZATION OF PLATELET DEPOSITION ON A SYNTHETIC VASCULAR GRAFT: CONTINUOUS IMAGING." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643954.
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The in vivo dynamics of thrombus formation have not been extensively studied, mainly due to technical limitations. We assessed the dynamics and localization of platelet deposition on a prosthetic vascular graft for the first 24 hours after implantation in swine, with continuous monitoring during the initial 6 hours, and the effect of heparin. Polytetrafluoro-ethylene (PTFE) grafts (5cm. L × 0.5 cm. ID) were inplanted in one of the common carotids of 13 normal pigs; 8 received iv heparin (150uAg) perioperatively. 111 In-labelled autologous platelets were injected 5 min before reperfusion of the graft. From 10 min to 24 hrs after unclamping the vessel sequential gamma camera images of the neck were taken and stored in an on-line computer. Pinpoint analysis of the platelet deposition was performed by creating seven regions of interest of 5 × 5 pixels over both graft and contralateral carotid territories. We obtained the ratio of the 111 In-activity in each region of the graft, including both anastomoses, with respect to its contralateral homologous region. The ratios differed along the graft in both groups of animals, with maximal values at the anastomosis. Peak ratios were reached within 1 to 3 hrs, and were significatively lower in heparinized pigs (anastomosis: 1.95±0.36; graft: 1.3±0.66) than in rion-heparinized-pigs (anastomosis: 3.23±0.66; graft: 2.16±0.41; p<0.05). Heparinized pigs showed a progressive decrease of the ratios up to 24 hrs. In contrast, platelet deposition in non-heparinized-pigs continued up to 6 hrs. Patency at 24 hrs was 88% in heparinized-pigs versus 20% in non-heparinized-pigs. We conclude that computer assisted pinpoint analysis of platelet deposition may help to a better understanding of the thrombotic process differentiating platelet-graft interaction from platelet anastomosis interaction. The deposition of platelets and graft patency is strongly influenced by the stabilizing effect of procoagulant moieties, and the presence of the anastomosis (release of vessel wall procoagulant and platelet activating products and induction of blood flow disturbances) induces localized activation and deposition of platelets.
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Murchie, Stuart William, Bård Martin Tinnen, Arne Motland, Bjarte Bore, and Peter Gaballa. "Highly Instrumented Electric Line Deployed Intervention Technology Platform Provides Precise, Controlled High Expansion Completion Manipulation Capabilities." In SPE/ICoTA Well Intervention Conference and Exhibition. SPE, 2022. http://dx.doi.org/10.2118/208987-ms.
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Abstract Manipulation of downhole completion components such as formation isolation valves, inflow control valves and sliding sleeves has become a regular phase of both new well initiation and existing well production optimisation scope. This often occurs in deviated and extended reach well trajectories frequently involving mono-bore completions. Although primarily done by pressure activation, electric line deployment of linear actuators that engage with associated shifting profiles of such valves and sleeves offers a secondary means of manipulation, one that is often relied upon. Deployment of these devices through smaller ID restrictions located higher up in the completion string necessitates in-situ activated high expansion anchoring and shifting capabilities. The electric line powered tractor-stroker-shifting device toolstrings capable of high deviation conveyance coupled with precise and real-time controlled completion component manipulation are desired, providing visibility throughout the operation. Furthermore, sufficient force to cover not only the shifting specification of the valve or sleeve design but also to overcome sleeve seizing commonly encountered downhole from scale or debris infringement is necessary to maximise the certainty of these operations. The technology platform presented in this paper has been designed to provide conveyance, positioning, anchoring, and high bi-directional force and stroke generation in a slim tool architecture offering high expansion shifting capability. Its downhole logic for optimised electric and hydraulic power distribution and a high degree of instrumentation and sensors has brought reliable target search, device engagement and real-time operational visibility and control to completion manipulation operations. Extensive system integration tests done on replica valve sleeves using the full tractor-stroker-shifting device toolstring to confirm the functionality and effectiveness will be described in the paper. This has been done within a reconstructed horizontal completion configuration to confirm successful string conveyance, shifting dog engagement and stroker shifting action, collaborating toolstring sensor measurements with those incorporated in the test jig configuration. A single run multi-sleeve shifting operation carried out in the North Sea will also be described, with real-time surface readout information which allowed the engineer to better understand the in-situ situation and take immediate and controlled corrective actions, circumventing a false shift scenario due to sleeve seizing and delivering an efficient operation. The seamless integration and interaction between the tractor, stroker and shifting device that make up the full manipulation toolstring assembly presented in this paper are transformative. Tractor wheels are kept in an extended mode whilst setting the stroker anchors, aiding optimal centralisation of the toolstring throughout the stroker anchoring and manipulation sequence. This reduces the risk of the shifting dogs unlatching from the profile of the completion component being manipulated as is often the case with a sequential tool operation scenario—the intervention technology platform providing a true convey-position-inspect-act-verify ethos.