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Journal articles on the topic 'Link activation'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

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1

Jamshidiha, Saeed, Vahid Pourahmadi, Abbas Mohammadi, and Mehdi Bennis. "Link Activation Using Variational Graph Autoencoders." IEEE Communications Letters 25, no. 7 (2021): 2358–61. http://dx.doi.org/10.1109/lcomm.2021.3076190.

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2

Roy, Joyashree, and Shamik Pal. "Lifestyles and climate change: link awaiting activation." Current Opinion in Environmental Sustainability 1, no. 2 (2009): 192–200. http://dx.doi.org/10.1016/j.cosust.2009.10.009.

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3

Chen, Dan, Jian-dong Li, and Chang-le Li. "Topology-transparent Link Activation MAC Protocol for MIMO Link Ad hoc Networks." Journal of Electronics & Information Technology 32, no. 11 (2010): 2593–98. http://dx.doi.org/10.3724/sp.j.1146.2009.01513.

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4

BERTINA, ROGIER M., NICO H. TILBURG, NANNEKE J. FOUW, and FRITS HAVERKATE. "Thrombin, a Link between Coagulation Activation and Fibrinolysis." Annals of the New York Academy of Sciences 667, no. 1 Plasminogen A (1992): 239–48. http://dx.doi.org/10.1111/j.1749-6632.1992.tb51621.x.

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5

Chaggar, Parminder S., Melanie Greaves, and Simon G. Williams. "Aortic dissection and cytomegalovirus activation: a possible link?" British Journal of Hospital Medicine 72, no. 1 (2011): 50–51. http://dx.doi.org/10.12968/hmed.2011.72.1.50.

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6

Aizawa, Hideyuki, Hiroyuki Kawahara, Keiji Tanaka, and Hideyoshi Yokosawa. "Activation of the Proteasome duringXenopusEgg Activation Implies a Link between Proteasome Activation and Intracellular Calcium Release." Biochemical and Biophysical Research Communications 218, no. 1 (1996): 224–28. http://dx.doi.org/10.1006/bbrc.1996.0039.

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7

Shiva, Sruti. "The Mitochondrion: A Link Between Hemolysis and Platelet Activation." Blood 134, Supplement_1 (2019): SCI—39—SCI—39. http://dx.doi.org/10.1182/blood-2019-121112.

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Patients with Sickle Cell Disease (SCD) demonstrate characteristics of chronic hemostatic activation including elevated baseline platelet activation. While it is well established that platelet activation is positively correlated with the magnitude of erythrocytic hemolysis in these patients, the mechanisms linking hemolysis to platelet activation remain unclear. In this study, we investigate the role of the platelet mitochondrion as the molecular link between hemolysis and downstream platelet activation. Using extracellular flux analysis, we demonstrate that platelets isolated from patients wi

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8

Kalra, P. "Sympathetic activation and malignant ventricular arrhythmias: a molecular link?" European Heart Journal 23, no. 14 (2002): 1078–80. http://dx.doi.org/10.1053/euhj.2001.3183.

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9

Hogquist, Kristin. "RasGRP: the missing link for Ras activation in thymocytes." Trends in Immunology 22, no. 2 (2001): 69. http://dx.doi.org/10.1016/s1471-4906(00)01845-7.

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10

Gil, Jesús, Maria Angel García, Paulino Gomez-Puertas та ін. "TRAF Family Proteins Link PKR with NF-κB Activation". Molecular and Cellular Biology 24, № 10 (2004): 4502–12. http://dx.doi.org/10.1128/mcb.24.10.4502-4512.2004.

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ABSTRACT The double-stranded RNA (dsRNA)-dependent protein kinase PKR activates NF-κB via the IκB kinase (IKK) complex, but little is known about additional molecules that may be involved in this pathway. Analysis of the PKR sequence enabled us to identify two putative TRAF-interacting motifs. The viability of such an interaction was further suggested by computer modeling. Here, we present evidence of the colocalization and physical interaction between PKR and TRAF family proteins in vivo, as shown by immunoprecipitation and confocal microscopy experiments. This interaction is induced upon PKR

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11

Golomb, Lior, and Moshe Oren. "DePICTing p53 Activation: A New Nucleolar Link to Cancer." Cancer Cell 20, no. 3 (2011): 283–84. http://dx.doi.org/10.1016/j.ccr.2011.08.017.

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12

Huang, Huifang, Scott R. Rajski, Robert M. Williams, and Paul B. Hopkins. "FR66979 requires reductive activation to cross-link DNA efficiently." Tetrahedron Letters 35, no. 52 (1994): 9669–72. http://dx.doi.org/10.1016/0040-4039(94)88355-6.

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13

Boccaccio, Carla, and Paolo M. Comoglio. "Genetic Link Between Cancer and Thrombosis." Journal of Clinical Oncology 27, no. 29 (2009): 4827–33. http://dx.doi.org/10.1200/jco.2009.22.7199.

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From the beginning of their lives, cancer cells exert a procoagulant activity in their microenvironment, which can extend systemically and become clinically evident as Trousseau's syndrome, the well-known association between tumor and thrombosis. It is becoming clear that the genetic mechanisms responsible for neoplastic transformation (activation of oncogenes such as RAS or MET, and inactivation of tumor suppressor genes such as p53 or PTEN) directly induce the expression of genes controlling hemostasis. Activation of blood coagulation results in a selective advantage for cancer cells, as fib

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14

Kerrigan, Steven W., Meenakshi Gaur, Ronan P. Murphy, Sanford J. Shattil та Andrew D. Leavitt. "Caspase-12: a developmental link between G-protein–coupled receptors and integrin αIIbβ3 activation". Blood 104, № 5 (2004): 1327–34. http://dx.doi.org/10.1182/blood-2003-10-3633.

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Abstract Fibrinogen binding by integrin αIIbβ3 is promoted by platelet agonists that increase the affinity and avidity of αIIbβ3 for fibrinogen through a process called “inside-out” signaling. Having previously demonstrated that inside-out activation of αIIbβ3 is defective in murine megakaryocytes that lack the transcription factor NF-E2, we screened for NF-E2–regulated genes that affect αIIbβ3 activation. Caspase-12 is the most down-regulated gene we identified in NF-E2–/– megakaryocytes. Therefore, the role of this protein in αIIbβ3 activation was determined using platelets from caspase-12–/

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15

Herbig, Eric, Linda Warfield, Lisa Fish, et al. "Mechanism of Mediator Recruitment by Tandem Gcn4 Activation Domains and Three Gal11 Activator-Binding Domains." Molecular and Cellular Biology 30, no. 10 (2010): 2376–90. http://dx.doi.org/10.1128/mcb.01046-09.

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ABSTRACT Targets of the tandem Gcn4 acidic activation domains in transcription preinitiation complexes were identified by site-specific cross-linking. The individual Gcn4 activation domains cross-link to three common targets, Gal11/Med15, Taf12, and Tra1, which are subunits of four conserved coactivator complexes, Mediator, SAGA, TFIID, and NuA4. The Gcn4 N-terminal activation domain also cross-links to the Mediator subunit Sin4/Med16. The contribution of the two Gcn4 activation domains to transcription was gene specific and varied from synergistic to less than additive. Gcn4-dependent genes h

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16

Vuckovic, Biljana, and Mirjana Djeric. "Lipoprotein (a): A link between thrombogenesis and atherogenesis." Medical review 60, no. 1-2 (2007): 37–41. http://dx.doi.org/10.2298/mpns0702037v.

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Introduction It is well known that numerous mechanisms of thrombogenesis can participate in every stage of atherosclerotic disease. The discovery of Lp(a) lipoprotein and its structural similarity with plasminogen suggests another pathogenic link between atherogenesis and thrombogenesis. Some characteristics of Lp(a) lipoprotein This lipoprotein is present in the whole human population in a wide range of plasma concentrations. It has numerous different isoforms. Its synthesis occurs in the liver, but it is practically metabolically independent from other lipoproteins. Today, Lp(a) lipoprotein

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17

van der Meijden, Paola EJ, and Johan WM Heemskerk. "Polyphosphates: a link between platelet activation, intrinsic coagulation and inflammation?" Expert Review of Hematology 3, no. 3 (2010): 269–72. http://dx.doi.org/10.1586/ehm.10.26.

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18

O'Leary, M. E., L. Q. Chen, R. G. Kallen, and R. Horn. "A molecular link between activation and inactivation of sodium channels." Journal of General Physiology 106, no. 4 (1995): 641–58. http://dx.doi.org/10.1085/jgp.106.4.641.

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A pair of tyrosine residues, located on the cytoplasmic linker between the third and fourth domains of human heart sodium channels, plays a critical role in the kinetics and voltage dependence of inactivation. Substitution of these residues by glutamine (Y1494Y1495/QQ), but not phenylalanine, nearly eliminates the voltage dependence of the inactivation time constant measured from the decay of macroscopic current after a depolarization. The voltage dependence of steady state inactivation and recovery from inactivation is also decreased in YY/QQ channels. A characteristic feature of the coupling

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19

Yuan, Di, Vangelis Angelakis, Lei Chen, Eleftherios Karipidis, and Erik G. Larsson. "On Optimal Link Activation With Interference Cancelation in Wireless Networking." IEEE Transactions on Vehicular Technology 62, no. 2 (2013): 939–45. http://dx.doi.org/10.1109/tvt.2012.2222683.

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20

Humphries, Martin J. "Integrin activation: the link between ligand binding and signal transduction." Current Opinion in Cell Biology 8, no. 5 (1996): 632–40. http://dx.doi.org/10.1016/s0955-0674(96)80104-9.

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21

Wilson, Paul P. H., and Douglass L. Henderson. "ALARA: The Next Link in a Chain of Activation Codes." Fusion Technology 30, no. 3P2A (1996): 1053–57. http://dx.doi.org/10.13182/fst96-a11963076.

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22

Chlamtac, I., and A. Lerner. "Fair Algorithms for Maximal Link Activation in Multihop Radio Networks." IEEE Transactions on Communications 35, no. 7 (1987): 739–46. http://dx.doi.org/10.1109/tcom.1987.1096847.

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23

Kim, Kyung-Ah, Jingsong Zhao, Susan Andarmani, et al. "R-Spondin Proteins: A Novel Link to β-catenin Activation." Cell Cycle 5, no. 1 (2005): 23–26. http://dx.doi.org/10.4161/cc.5.1.2305.

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24

Kissler, Stephan, Steve M. Anderton, and David C. Wraith. "Antigen-presenting Cell Activation: a Link Between Infection and Autoimmunity?" Journal of Autoimmunity 16, no. 3 (2001): 303–8. http://dx.doi.org/10.1006/jaut.2000.0498.

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25

Porzionato, Andrea, Aron Emmi, Silvia Barbon, et al. "Sympathetic activation: a potential link between comorbidities and COVID‐19." FEBS Journal 287, no. 17 (2020): 3681–88. http://dx.doi.org/10.1111/febs.15481.

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26

Zeisler, R., R. M. Lindstrom, and R. R. Greenberg. "Instrumental neutron activation analysis: A valuable link in chemical metrology." Journal of Radioanalytical and Nuclear Chemistry 263, no. 2 (2005): 315–19. http://dx.doi.org/10.1007/s10967-005-0056-7.

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27

Rueda, Daniel, та Margot Thome. "Phosphorylation of CARMA1: The Link(er) to NF-κB Activation". Immunity 23, № 6 (2005): 551–53. http://dx.doi.org/10.1016/j.immuni.2005.11.007.

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28

Yang, Wen, Chao Yang, Hongbo Shi, Ling Shi, and Guanrong Chen. "Stochastic link activation for distributed filtering under sensor power constraint." Automatica 75 (January 2017): 109–18. http://dx.doi.org/10.1016/j.automatica.2016.09.009.

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29

Franzini, Carlo. "Sleep, dreaming, and brain activation." Behavioral and Brain Sciences 23, no. 6 (2000): 939–40. http://dx.doi.org/10.1017/s0140525x00414020.

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Both Solms and Nielsen acknowledge the difficulty of accounting for the similarities between REM and NREM sleep mentation with a two-generator model, and each link dreams, either explicitly (Solms) or implicitly (Nielsen), to brain activation. At present, however, no data indicate that brain activation can be demonstrated whenever vivid dream reports are obtained.[Nielsen; Solms]

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30

Steiger, Howard, and Linda Booij. "Eating Disorders, Heredity and Environmental Activation: Getting Epigenetic Concepts into Practice." Journal of Clinical Medicine 9, no. 5 (2020): 1332. http://dx.doi.org/10.3390/jcm9051332.

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Epigenetic mechanisms are believed to link environmental exposures to alterations in gene expression, and in so doing, to provide a physical substrate for the activation of hereditary potentials by life experiences. In keeping with this idea, accumulating data suggest that epigenetic processes are implicated in eating-disorder (ED) etiology. This paper reviews literature on putative links between epigenetic factors and EDs, and examines ways in which epigenetic programming of gene expression could account for gene-environment interactions acting in the EDs. The paper also presents evidence sug

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31

Muñoz, Yorka, Carlos M. Carrasco, Joaquín D. Campos, Pabla Aguirre, and Marco T. Núñez. "Parkinson’s Disease: The Mitochondria-Iron Link." Parkinson's Disease 2016 (2016): 1–21. http://dx.doi.org/10.1155/2016/7049108.

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Mitochondrial dysfunction, iron accumulation, and oxidative damage are conditions often found in damaged brain areas of Parkinson’s disease. We propose that a causal link exists between these three events. Mitochondrial dysfunction results not only in increased reactive oxygen species production but also in decreased iron-sulfur cluster synthesis and unorthodox activation of Iron Regulatory Protein 1 (IRP1), a key regulator of cell iron homeostasis. In turn, IRP1 activation results in iron accumulation and hydroxyl radical-mediated damage. These three occurrences—mitochondrial dysfunction, iro

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32

Lindenberg, Siegwart. "The Third Speed: Flexible Activation and Its Link to Self-Regulation." Review of Behavioral Economics 2, no. 1-2 (2015): 147–60. http://dx.doi.org/10.1561/105.00000024.

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33

Simko, Myrtill. "EMF and the redox homeostasis: The link to cell activation processes." Toxicology Letters 280 (October 2017): S32. http://dx.doi.org/10.1016/j.toxlet.2017.07.077.

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34

Tepe, Jetze J., Christi Kosogof, and Robert M. Williams. "DNA interstrand cross-link formation by reductive activation of dehydropyrrolizidine progenitors." Tetrahedron 58, no. 18 (2002): 3553–59. http://dx.doi.org/10.1016/s0040-4020(02)00311-3.

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35

Sekutowicz, Maria, Katharina Schmack, Rosa Steimke, et al. "Striatal activation as a neural link between cognitive and perceptual flexibility." NeuroImage 141 (November 2016): 393–98. http://dx.doi.org/10.1016/j.neuroimage.2016.07.046.

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36

Mannon, R. B. "Necroptosis in Solid Organ Transplantation: A Missing Link to Immune Activation?" American Journal of Transplantation 13, no. 11 (2013): 2785–86. http://dx.doi.org/10.1111/ajt.12450.

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37

Aliahmad, Parinaz, Emmett O'Flaherty, Peggy Han, et al. "TOX Provides a Link Between Calcineurin Activation and CD8 Lineage Commitment." Journal of Experimental Medicine 199, no. 8 (2004): 1089–99. http://dx.doi.org/10.1084/jem.20040051.

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T cell development is dependent on the integration of multiple signaling pathways, although few links between signaling cascades and downstream nuclear factors that play a role in thymocyte differentiation have been identified. We show here that expression of the HMG box protein TOX is sufficient to induce changes in coreceptor gene expression associated with β-selection, including CD8 gene demethylation. TOX expression is also sufficient to initiate positive selection to the CD8 lineage in the absence of MHC–TCR interactions. TOX-mediated positive selection is associated with up-regulation of

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38

Chlamtac, I., A. Farago, and Hye Yeon Ahn. "A topology transparent link activation protocol for mobile CDMA radio networks." IEEE Journal on Selected Areas in Communications 12, no. 8 (1994): 1426–33. http://dx.doi.org/10.1109/49.329334.

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39

Carney, Ellen F. "A link between mitochondrial dysfunction and innate immune activation in FSGS." Nature Reviews Nephrology 14, no. 12 (2018): 721. http://dx.doi.org/10.1038/s41581-018-0075-6.

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40

Passeron, Thierry, and Jean-Paul Ortonne. "Activation of the Unfolded Protein Response in Vitiligo: The Missing Link?" Journal of Investigative Dermatology 132, no. 11 (2012): 2502–4. http://dx.doi.org/10.1038/jid.2012.328.

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41

Mochizuki, G., T. Hoque, R. Mraz, et al. "Challenging the brain: Exploring the link between effort and cortical activation." Brain Research 1301 (November 2009): 9–19. http://dx.doi.org/10.1016/j.brainres.2009.09.005.

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42

Hardy, John, and Dervis Salih. "TREM2-mediated activation of microglia breaks link between amyloid and tau." Lancet Neurology 20, no. 6 (2021): 416–17. http://dx.doi.org/10.1016/s1474-4422(21)00133-2.

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43

Haling, Jacob R., Susan J. Monkley, David R. Critchley, and Brian G. Petrich. "Talin-dependent integrin activation is required for fibrin clot retraction by platelets." Blood 117, no. 5 (2011): 1719–22. http://dx.doi.org/10.1182/blood-2010-09-305433.

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Abstract Talin functions both as a regulator of integrin affinity and as an important mechanical link between integrins and the cytoskeleton. Using genetic deletion of talin, we show for the first time that the capacity of talin to activate integrins is required for fibrin clot retraction by platelets. To further dissect which talin functions are required for this process, we tested clot retraction in platelets expressing a talin1(L325R) mutant that binds to integrins, but exhibits impaired integrin activation ascribable to disruption of the interaction between talin and the membrane-proximal

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44

Morganti, Alessio G., Lino Pasquarelli, Francesco Deodato, et al. "Videoconferencing to Enhance the Integration between Clinical Medicine and Teaching: A Feasibility Study." Tumori Journal 94, no. 6 (2008): 822–29. http://dx.doi.org/10.1177/030089160809400608.

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Aims and Background The aim of the study was to analyze the feasibility of a setting up of a radiotherapy department using videoconferencing technology. Material and Methods A videoconferencing network was started to link an academic center of radiotherapy to a peripheral center of research at the start of its activity. Two years of data of involved professionals, subjects of links, audio, video link problems and running costs were recorded. Results A total of 418 links was established for an overall duration of 458 hours. The participants included all departmental staff. Videoconferencing inv

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45

Guo, Yuan Hua, and Chun Lun Huang. "Functional Link Artificial Neural Networks Filter for Gaussian Noise." Applied Mechanics and Materials 347-350 (August 2013): 2580–85. http://dx.doi.org/10.4028/www.scientific.net/amm.347-350.2580.

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In this paper, FLANN(functional link ANN) filter is presented for Gaussian noise. FLANN is a singer layer with expanded input vectors and has lower computational cost than MLP(multilayer perceptron). Three types of functional expansion are discussed. BP(back propagation algorithm) for nonlinear activation function and matrix calculation for identical activation function are exploited for training FLANN. Simulation shows that convergence is not guaranteed in BP and related to the initial weight matrix and training images, and that linear FLANN trained by matrix calculation performs better than

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46

Wachowicz, Katarzyna, та Gottfried Baier. "Protein kinase Cθ: the pleiotropic T-cell signalling intermediate". Biochemical Society Transactions 42, № 6 (2014): 1512–18. http://dx.doi.org/10.1042/bst20140179.

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Activating as well as inhibitory circuits tightly regulate T-cell activation thresholds and effector differentiation processes enabling proper immune response outcomes. Recently, an additional molecular link between T-cell receptor signalling and CD4+ Th17 cell skewing has been reported, namely that protein kinase C (PKC) θ critically regulates Th17/Th1 phenotypic differentiation and plasticity in CD4+ T-cells by selectively acting as a ‘reprogramming element’ that suppresses Th1-typical genes during Th17-mediated immune activation in order to stabilize a Th17 cell phenotype.

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47

Ramadan, Nabih M. "The Link Between Glutamate and Migraine." CNS Spectrums 8, no. 6 (2003): 446–49. http://dx.doi.org/10.1017/s1092852900018757.

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ABSTRACTMigraine pain-relay centers, including the trigeminal ganglion, trigeminal nucleus caudalis, and thalamus, contain glutamate-positive neurons, and glutamate activates the trigeminal nucleus caudalis. Glutamate is implicated in cortical spreading depression, trigeminovascular activation, and central sensitization. Glutamate receptor-subtype antagonists are effective in preclinical models of migraine, and in the clinic. These preclinical and clinical observations argue for a strong link between migraine and the glutamatergic system, a link that is important to further characterize in an

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48

Leonard, Brian E. "Inflammation and depression: a causal or coincidental link to the pathophysiology?" Acta Neuropsychiatrica 30, no. 1 (2017): 1–16. http://dx.doi.org/10.1017/neu.2016.69.

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This review summarises the evidence that chronic low grade inflammation triggers changes that contribute to the mental and physical ill health of patients with major depression. Inflammation, and the activation of the hypothalamic pituitary axis by stress, are normal components of the stress response but when stress is prolonged and the endocrine and immune system become chronic resulting in the activation of the peripheral macrophages, the central microglia and hypercortisolemia, the neuronal networks are damaged and become dysfunctional. The proinflammatory cytokines, in addition to activati

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49

Wong, Sok Kuan, Kok-Yong Chin, and Soelaiman Ima-Nirwana. "Toll-like Receptor as a Molecular Link between Metabolic Syndrome and Inflammation: A Review." Current Drug Targets 20, no. 12 (2019): 1264–80. http://dx.doi.org/10.2174/1389450120666190405172524.

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Metabolic Syndrome (MetS) involves a cluster of five conditions, i.e. obesity, hyperglycaemia, hypertension, hypertriglyceridemia and low High-Density Lipoprotein (HDL) cholesterol. All components of MetS share an underlying chronic inflammatory aetiology, manifested by increased levels of pro-inflammatory cytokines. The pathogenic role of inflammation in the development of MetS suggested that toll-like receptor (TLR) activation may trigger MetS. This review summarises the supporting evidence on the interactions between MetS and TLR activation, bridged by the elevation of TLR ligands during Me

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50

Gangopadhyay, Jaya P., and Noriaki Ikemoto. "Aberrant interaction of calmodulin with the ryanodine receptor develops hypertrophy in the neonatal cardiomyocyte." Biochemical Journal 438, no. 2 (2011): 379–87. http://dx.doi.org/10.1042/bj20110203.

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We have shown previously that the inter-domain interaction between the two domains of RyR (ryanodine receptor), CaMBD [CaM (calmodulin)-binding domain] and CaMLD (CaM-like domain), activates the Ca2+ channel, and this process is called activation-link formation [Gangopadhyay and Ikemoto (2008) Biochem. J. 411, 415–423]. Thus CaM that is bound to CaMBD is expected to interfere the activation-link formation, thereby stabilizing the closed state of the channel under normal conditions. In the present paper, we report that, upon stimulation of neonatal cardiomyocytes with the pro-hypertrophy agonis

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