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Academic literature on the topic 'NCX3'

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Published: 4 June 2021
Last updated: 3 February 2022

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Journal articles on the topic "NCX3"

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Iwamoto, Takahiro, and Munekazu Shigekawa. "Differential inhibition of Na+/Ca2+exchanger isoforms by divalent cations and isothiourea derivative." American Journal of Physiology-Cell Physiology 275, no. 2 (August 1, 1998): C423—C430. http://dx.doi.org/10.1152/ajpcell.1998.275.2.c423.

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We compared the properties of three mammalian Na+/Ca2+exchanger isoforms, NCX1, NCX2, and NCX3, by analyzing the effects of Ni2+ and other cations as well as the recently identified inhibitor isothiourea derivatives on intracellular Na+-dependent45Ca2+uptake into CCL-39 (Dede) fibroblasts stably expressing each isoform. All these NCX isoforms had similar affinities for the extracellular transport substrates Ca2+ and Na+. Ni2+ inhibited45Ca2+uptake by competing with Ca2+ for the external transport site, with 10-fold less affinity in NCX3 than in NCX1 or NCX2. Ni2+ and Co2+ were most efficient in such discrimination of NCX isoforms, although their inhibitory potencies were less than those of La3+ and Cd2+. The monovalent cation Li+ stimulated45Ca2+uptake rate by all NCX isoforms similarly with low affinity, although the extent of stimulation was somewhat smaller in NCX1. On the other hand, the isothiourea derivative KB-R7943 was threefold more inhibitory to NCX3 than to NCX1 or NCX2. Thus distinct differences in the kinetic and pharmacological properties were detected between NCX3 and the other two isoforms.
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Boscia, Francesca, Rosaria Gala, Giuseppe Pignataro, Andrea de Bartolomeis, Maria Cicale, Alberto Ambesi-Impiombato, Gianfranco Di Renzo, and Lucio Annunziato. "Permanent Focal Brain Ischemia Induces Isoform-Dependent Changes in the Pattern of Na+/Ca2+ Exchanger Gene Expression in the Ischemic Core, Periinfarct Area, and Intact Brain Regions." Journal of Cerebral Blood Flow & Metabolism 26, no. 4 (August 17, 2005): 502–17. http://dx.doi.org/10.1038/sj.jcbfm.9600207.

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Dysregulation of sodium [Na+]i and calcium [Ca2+]i homeostasis plays a pivotal role in the pathophysiology of cerebral ischemia. Three gene products of the sodium–calcium exchanger family NCX1, NCX2, and NCX3 couple, in a bidirectional way, the movement of these ions across the cell membrane during cerebral ischemia. Each isoform displays a selective distribution in the rat brain. To determine whether NCX gene expression can be regulated after cerebral ischemia, we used NCX isoform-specific antisense radiolabeled probes to analyze, by radioactive in situ hybridization histochemistry, the pattern of NCX1, NCX2, and NCX3 transcripts in the ischemic core, periinfarct area, as well as in nonischemic brain regions, after 6 and 24 h of permanent middle cerebral artery occlusion (pMCAO) in rats. We found that in the focal region, comprising divisions of the prefrontal, somatosensory, and insular cortices, all three NCX transcripts were downregulated. In the periinfarct area, comprising part of the motor cortex and the lateral compartments of the caudate-putamen, NCX2 messenger ribonucleic acid (mRNA) was downregulated, whereas NCX3 mRNA was significantly upregulated. In remote nonischemic brain regions such as the prelimbic and infralimbic cortices, and tenia tecta, both NCX1 and NCX3 transcripts were upregulated, whereas in the medial caudate-putamen only NCX3 transcripts increased. In all these intact regions, NCX2 signal strongly decreased. These results indicate that NCX gene expression is regulated after pMCAO in a differential manner, depending on the exchanger isoform and region involved in the insult. These data may provide a better understanding of each NCX subtype's pathophysiologic role and may allow researchers to design appropriate pharmacological strategies to treat brain ischemia.
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Marshall, Christian R., Joanne A. Fox, Stefanie L. Butland, B. F. Francis Ouellette, Fiona S. L. Brinkman, and Glen F. Tibbits. "Phylogeny of Na+/Ca2+ exchanger (NCX) genes from genomic data identifies new gene duplications and a new family member in fish species." Physiological Genomics 21, no. 2 (April 14, 2005): 161–73. http://dx.doi.org/10.1152/physiolgenomics.00286.2004.

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The Na+/Ca2+ exchanger (NCX) is a member of the cation/Ca2+ antiporter (CaCA) family and plays a key role in maintaining cellular Ca2+ homeostasis in a variety of cell types. NCX is present in a diverse group of organisms and exhibits high overall identity across species. To date, three separate genes, i.e., NCX1, NCX2, and NCX3, have been identified in mammals. However, phylogenetic analysis of the exchanger has been hindered by the lack of nonmammalian NCX sequences. In this study, we expand and diversify the list of NCX sequences by identifying NCX homologs from whole-genome sequences accessible through the Ensembl Genome Browser. We identified and annotated 13 new NCX sequences, including 4 from zebrafish, 4 from Japanese pufferfish, 2 from chicken, and 1 each from honeybee, mosquito, and chimpanzee. Examination of NCX gene structure, together with construction of phylogenetic trees, provided novel insights into the molecular evolution of NCX and allowed us to more accurately annotate NCX gene names. For the first time, we report the existence of NCX2 and NCX3 in organisms other than mammals, yielding the hypothesis that two serial NCX gene duplications occurred around the time vertebrates and invertebrates diverged. In addition, we have found a putative new NCX protein, named NCX4, that is related to NCX1 but has been observed only in fish species genomes. These findings present a stronger foundation for our understanding of the molecular evolution of the NCX gene family and provide a framework for further NCX phylogenetic and molecular studies.
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Pignataro, Giuseppe, Elga Esposito, Ornella Cuomo, Rossana Sirabella, Francesca Boscia, Natascia Guida, Gianfranco Di Renzo, and Lucio Annunziato. "The NCX3 Isoform of the Na+/Ca2+ Exchanger Contributes to Neuroprotection Elicited by Ischemic Postconditioning." Journal of Cerebral Blood Flow & Metabolism 31, no. 1 (July 14, 2010): 362–70. http://dx.doi.org/10.1038/jcbfm.2010.100.

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It has been recently shown that a short sublethal brain ischemia subsequent to a prolonged harmful ischemic episode may confer ischemic neuroprotection, a phenomenon termed ischemic postconditioning. Na+/Ca2+ exchanger (NCX) isoforms, NCX1, NCX2, and NCX3, are plasma membrane ionic transporters widely distributed in the brain and involved in the control of Na+ and Ca2+ homeostasis and in the progression of stroke damage. The objective of this study was to evaluate the role of these three proteins in the postconditioning-induced neuroprotection. The NCX protein and mRNA expression was evaluated at different time points in the ischemic temporoparietal cortex of rats subjected to tMCAO alone or to tMCAO plus ischemic postconditioning. The results of this study showed that NCX3 protein and ncx3 mRNA were upregulated in those brain regions protected by postconditioning treatment. These changes in NCX3 expression were mediated by the phosphorylated form of the ubiquitously expressed serine/threonine protein kinase p-AKT, as the p-AKT inhibition prevented NCX3 upregulation. The relevant role of NCX3 during postconditioning was further confirmed by results showing that NCX3 silencing, induced by intracerebroventricular infusion of small interfering RNA (siRNA), partially reverted the postconditioning-induced neuroprotection. The results of this study support the idea that the enhancement of NCX3 expression and activity might represent a reasonable strategy to reduce the infarct extension after stroke.
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Quednau, B. D., D. A. Nicoll, and K. D. Philipson. "Tissue specificity and alternative splicing of the Na+/Ca2+ exchanger isoforms NCX1, NCX2, and NCX3 in rat." American Journal of Physiology-Cell Physiology 272, no. 4 (April 1, 1997): C1250—C1261. http://dx.doi.org/10.1152/ajpcell.1997.272.4.c1250.

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The gene coding for the Na+/Ca2+ exchanger NCX1 is characterized by a cluster of six exons (A, B, C, D, E, and F) coding for a variable region in the COOH terminus of the large intracellular loop of the protein. Alternative splicing of these exons generates multiple tissue-specific variants of NCX1. Using reverse transcriptase-polymerase chain reaction, we analyzed eight previously described and four new splicing isoforms of NCX1 in a wide variety of tissues and cells. Exons A and B are mutually exclusive, as shown in earlier studies, and splicing isoforms containing exon A are preferentially expressed in heart, brain, and skeletal muscle, whereas splicing variants with exon B are found in all rat tissues except heart. The second and third isoforms of the Na+/Ca2+ exchanger, NCX2 and NCX3, show a deletion of 37 amino acids in the intracellular loop corresponding to parts of the variable region of NCX1. We identified three splicing isoforms of NCX3 in brain and skeletal muscle by reverse transcriptase-polymerase chain reaction. These splice variants are generated by including either of two alternative exons equivalent to the NCX1 exon A or B and by including or excluding a sequence equivalent to the NCX1 exon C. We did not detect any alternative splicing of NCX2. We examined selected tissues from neonatal and adult rats and found developmental regulation for NCX1 and NCX3 splicing isoforms in skeletal muscle. Specific isoform patterns were also detected for NCX1 and NCX3 in cultured cortical neurons, astrocytes, and oligodendrocytes. We suggest a new terminology to distinguish the different splice variants of individual NCX isoforms.
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Molinaro, Pasquale, Rossana Sirabella, Giuseppe Pignataro, Tiziana Petrozziello, Agnese Secondo, Francesca Boscia, Antonio Vinciguerra, et al. "Neuronal NCX1 overexpression induces stroke resistance while knockout induces vulnerability via Akt." Journal of Cerebral Blood Flow & Metabolism 36, no. 10 (July 22, 2016): 1790–803. http://dx.doi.org/10.1177/0271678x15611913.

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Three different Na+/Ca2+ exchanger (NCX) isoforms, NCX1, NCX2, and NCX3, are expressed in brain where they play a relevant role in maintaining Na+ and Ca2+ homeostasis. Although the neuroprotective roles of NCX2 and NCX3 in stroke have been elucidated, the relevance of NCX1 is still unknown because of embryonic lethality of its knocking-out, heart dysfunctions when it is overexpressed, and the lack of selectivity in currently available drugs. To overcome these limitations we generated two conditional genetically modified mice that upon tamoxifen administration showed a selective decrease or increase of NCX1 in cortical and hippocampal neurons. Interestingly, in cortex and hippocampus NCX1 overexpression increased, where NCX1 knock-out reduced, both exchanger activity and Akt1 phosphorylation, a neuronal survival signaling. More important, mice overexpressing NCX1 showed a reduced ischemic volume and an amelioration of focal and general deficits when subjected to transient middle cerebral artery occlusion. Conversely, NCX1-knock-out mice displayed a worsening of brain damage, focal and neurological deficits with a decrease in Akt phosphorylation. These results support the idea that NCX1 overexpression/activation may represent a feasible therapeutic opportunity in stroke intervention.
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Fraysse, Bodvaël, Thierry Rouaud, Marie Millour, Josiane Fontaine-Pérus, Marie-France Gardahaut, and Dmitri O. Levitsky. "Expression of the Na+/Ca2+exchanger in skeletal muscle." American Journal of Physiology-Cell Physiology 280, no. 1 (January 1, 2001): C146—C154. http://dx.doi.org/10.1152/ajpcell.2001.280.1.c146.

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The expression of the Na+/Ca2+ exchanger was studied in differentiating muscle fibers in rats. NCX1 and NCX3 isoform (Na+/Ca2+ exchanger isoform) expression was found to be developmentally regulated. NCX1 mRNA and protein levels peaked shortly after birth. Conversely, NCX3 isoform expression was very low in muscles of newborn rats but increased dramatically during the first 2 wk of postnatal life. Immunocytochemical analysis showed that NCX1 was uniformly distributed along the sarcolemmal membrane of undifferentiated rat muscle fibers but formed clusters in T-tubular membranes and sarcolemma of adult muscle. NCX3 appeared to be more uniformly distributed along the sarcolemma and inside myoplasm. In the adult, NCX1 was predominantly expressed in oxidative (type 1 and 2A) fibers of both slow- and fast-twitch muscles, whereas NCX3 was highly expressed in fast glycolytic (2B) fibers. NCX2 was expressed in rat brain but not in skeletal muscle. Developmental changes in NCX1 and NCX3 as well as the distribution of these isoforms at the cellular level and in different fiber types suggest that they may have different physiological roles.
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Linck, Bettina, Zhiyong Qiu, Zhaoping He, Qiusheng Tong, Donald W. Hilgemann, and Kenneth D. Philipson. "Functional comparison of the three isoforms of the Na+/Ca2+ exchanger (NCX1, NCX2, NCX3)." American Journal of Physiology-Cell Physiology 274, no. 2 (February 1, 1998): C415—C423. http://dx.doi.org/10.1152/ajpcell.1998.274.2.c415.

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Three distinct mammalian Na+/Ca2+exchangers have been cloned: NCX1, NCX2, and NCX3. We have undertaken a detailed functional comparison of these three exchangers. Each exchanger was stably expressed at high levels in the plasma membranes of BHK cells. Na+/Ca2+exchange activity was assessed using three different complementary techniques: Na+ gradient-dependent45Ca2+uptake into intact cells, Na+gradient-dependent45Ca2+uptake into membrane vesicles isolated from the transfected cells, and exchange currents measured using giant patches of excised cell membrane. Apparent affinities for the transported ions Na+ and Ca2+ were markedly similar for the three exchangers at both membrane surfaces. Likewise, generally similar responses to changes in pH, chymotrypsin treatment, and application of various inhibitors were obtained. Depletion of cellular ATP inhibited NCX1 and NCX2 but did not affect the activity of NCX3. Exchange activities of NCX1 and NCX3 were modestly increased by agents that activate protein kinases A and C. All exchangers were regulated by intracellular Ca2+. NCX1-induced exchange currents were especially large in excised patches and, like the native myocardial exchanger, were stimulated by ATP. Results may be influenced by our choice of expression system and specific splice variants, but, overall, the three exchangers appear to have very similar properties.
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Iwamoto, Takahiro, Tomoe Nishitani, and Munekazu Shigekawa. "Pharmacological characterization of Na+/Ca2+ exchanger isoforms (NCX1, NCX2, NCX3)." Japanese Journal of Pharmacology 76 (1998): 110. http://dx.doi.org/10.1016/s0021-5198(19)40559-3.

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POLUMURI, S. K., A. RUKNUDIN, MARGARET M. McCARTHY, TARA S. PERROT-SINAL, and D. H. SCHULZE. "Sodium-Calcium Exchanger NCX1, NCX2, and NCX3 Transcripts in Developing Rat Brain." Annals of the New York Academy of Sciences 976, no. 1 (January 24, 2006): 60–63. http://dx.doi.org/10.1111/j.1749-6632.2002.tb04714.x.

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Dissertations / Theses on the topic "NCX3"

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Sokolow, Sophie. "Les souris déficientes pour les échangeurs sodium-calcium (NCX1 et NCX3): deux modèles murins pour l'étude de leurs rôles pysiologiques in vivo ;Implication de NCX3 dans la fonction neuromusculaire." Doctoral thesis, Universite Libre de Bruxelles, 2004. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/211196.

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Nous avons généré des souris déficientes pour les gènes codant pour les échangeurs Na/Ca de type I (NCX1) et de type III (NCX3) afin d'étudier, in vivo, le rôle de ces deux protéines.

L‘analyse phénotypique des souris adultes totalement déficientes pour le gène Ncx1 (Ncx1-/-) n'a pu être menée étant donné que ces souris décèdent au cours du développement embryonnaire.

Les souris déficientes pour le gène Ncx3 (Ncx3-/-) sont viables et fertiles. Nous avons analysé l'effet de l'inactivation du gène Ncx3 dans le muscle squelettique et plus particulièrement au niveau de la jonction neuromusculaire.

L'analyse histologique des muscles squelettiques de souris Ncx3-/- a révélé des altérations des fibres musculaires caractérisées par la présence de foyers de fibres nécrotiques et d'infiltrats de cellules mononuclées.

L'analyse électromyographique classique a montré un électromyogramme anormal du muscle gastrocnémien de souris Ncx3-/-, révélant une affection neuromusculaire pré- et post-synaptique caractérisée par (i) la petitesse de l'amplitude de la réponse M au repos, (ii) le décrément après stimulation répétitive à basse fréquence, (iii) l'incrément après stimulation répétitive à haute fréquence et (iv) la facilitation post-exercice. L'électromyographie à fibre unique a révélé une MCD élevée et des blocages anormaux de la transmission neuromusculaire, reflétant une atteinte post-synaptique de la jonction neuromusculaire chez les souris Ncx3-/-. L'ensemble de ces anomalies électromyographiques sont les caractéristiques du syndrome myasthénique de Lambert-Eaton.

Finalement, pour déterminer les conséquences de l'inactivation du gène Ncx3 sur l'activité physique des souris Ncx3-/-, nous avons réalisé des tests comportementaux sur ces souris. Ces tests ont permis de détecter un épuisement et une faiblesse musculaire accrus à l'effort chez ces souris.

En conclusion, nos observations montrent que les souris Ncx3-/- présentent des anomalies électromyographiques similaires à celles du syndrome myasthénique de Lambert-Eaton. Ces résultats suggèrent que l'échangeur NCX3 est peut-être impliqué dans la pathogenèse de certaines formes de cette maladie.

Des études supplémentaires afin de confirmer notre hypothèse devront donc être réalisées.

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We produced and analyzed mice deficient for Na/Ca exchanger 3 (NCX3), a protein which mediates cellular Ca2+ efflux (forward mode) or Ca2+ influx (reverse mode) and thus controls intracellular Ca2+ concentration. NCX3-deficient mice (Ncx3-/-) present a skeletal muscle fiber necrosis and a defective neuromuscular transmission, reflecting the absence of NCX3 in the sarcolemma of the muscle fibers and at the neuromuscular junction. The defective neuromuscular transmission is characterized by the presence of electromyographic abnormalities including low compound muscle action potential amplitude, a decremental response at low frequency nerve stimulation, an incremental response and a prominent post-exercise facilitation at high frequency nerve stimulation as well as neuromuscular blocks. The analysis of quantal transmitter release in Ncx3-/- neuromuscular junctions revealed an important facilitation superimposed on the depression of synaptic responses and an elevated delayed release during high frequency nerve stimulation. It is suggested that Ca2+ entering nerve terminals is cleared relatively slowly in the absence of NCX3, thereby enhancing residual Ca2+ and evoked and delayed quantal transmitter release during repetitive nerve stimulation. Our findings indicate that NCX3 plays an important role in vivo in the control of Ca2+ concentrations in the skeletal muscle fibers and at the neuromuscular junction.


Doctorat en sciences biomédicales
info:eu-repo/semantics/nonPublished

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Jeffs, Graham J. "The effect of sodium/calcium exchanger 3 (NCX3) knockout on neuronal survival following global cerebral ischaemia in mice." University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2007. http://theses.library.uwa.edu.au/adt-WU2008.0063.

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Cerebral ischaemia is a leading cause of disability and death world-wide. The only effective treatments are thrombolytic therapy (plasminogen activator; tPA) and hypothermia (33?C). However, tPA has limited clinical application due to its short therapeutic time window and its specific application in thrombo-embolic stroke. Moderate hypothermia (33?C) is only being used following cardiac arrest in comatose survivors. Hence more treatments are urgently required. The first step in developing new treatments is the identification and characterisation of a potential therapeutic target. Since brain damage following cerebral ischaemia is associated with disturbances in intracellular calcium homeostasis, the sodium-calcium exchanger (NCX) is a potential therapeutic target due to its ability to regulate intracellular calcium. Currently, however there is uncertainty as to whether the plasma membrane NCX has a neuroprotective or neurodamaging role following cerebral ischemia. To address this issue I compared hippocampal neuronal injury in NCX3 knockout mice (Ncx3-/-) and wild-type mice (Ncx3+/+) following global cerebral ischaemia. In order to perform this study I first established a bilateral common carotid occlusion (BCCAO) model of global ischaemia in wild-type C57/BlHsnD mice using controlled ventilation. After trials of several ischaemic time points, 17 minutes was established as the optimum duration of ischaemia to produce selective hippocampal CA1 neuronal loss in the wild-type mice. I then subjected NCX3 knockout and wild-type mice to 17 minutes of ischaemia. Following the 17 minute period of ischaemia, wild-type mice exhibited 80% CA1 neuronal loss and 40% CA2 neuronal loss. In contrast, NCX3 knockout mice displayed > 95% CA1 neuronal loss and 95% CA2 neuronal loss. Following experiments using a 17 minute duration of global ischaemia, a 15 minute duration of ischaemia was also evaluated. Wild-type mice exposed to a 15 minute period of ischaemia, did not exhibit any significant hippocampal neuronal loss. In contrast, NCX3 knockout mice displayed 45% CA1 neuronal loss and 25% CA2 neuronal loss. The results clearly demonstrate that mice deficient for the NCX3 protein are more susceptible to global cerebral ischaemia than wild-type mice. My findings showing a neuroprotective role for NCX3 following ischaemia, suggest that the exchanger has a positive role in maintaining neuronal intracellular calcium homeostasis. When this function is disrupted, neurons are more susceptible to calcium deregulation, with resultant cell death via calcium mediated pathways. Therefore, improving NCX activity following cerebral ischaemia may provide a therapeutic strategy to reduce neuronal death.
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Bauer, Klemens Verfasser], and Christian [Akademischer Betreuer] [Pott. "Einfluss des Natrium-Kalzium-Austauscher (NCX1)-Antagonisten SEA0400 auf Kalzium-Handling und Arrhythmogenese in Abhängigkeit vom NCX1-Expressionsniveau / Klemens Bauer ; Betreuer: Christian Pott." Münster : Universitäts- und Landesbibliothek Münster, 2016. http://d-nb.info/1141577461/34.

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Sieber, Matthias. "Modulatoren des Calcineurin-NFATc-Signalweges in humanen TH-Zellen." Phd thesis, Universität Potsdam, 2010. http://opus.kobv.de/ubp/volltexte/2010/4467/.

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Die Ca2+/Calmodulin-aktivierte Serin/Threonin-Phosphatase Calcineurin ist ein Schlüsselmolekül des T-Zell-Rezeptorabhängigen Signalnetzwerkes. Calcineurin aktiviert die Transkriptionsfaktoren der NFATc-Familie durch Dephosphorylierung und reguliert darüber die Expression wichtiger Zytokine und Oberflächenproteine. Die Aktivität von Calcineurin wird durch zahlreiche endogene Proteine moduliert und ist Angriffspunkt der immunsuppressiven Substanzen Cyclosporin A und FK506. In dieser Arbeit wurde der alternative niedermolekulare Calcineurin-NFATc-Inhibitor NCI3 hinsichtlich seiner Effekte auf T-Zell-Rezeptor-abhängige Signalwege charakterisiert. Die Ergebnisse zeigen, daß das Pyrazolopyrimidinderivat NCI3 nichttoxisch und zellmembranpermeabel ist. In T-Zell-Rezeptor-stimulierten primären humanen TH-Zellen unterdrückt NCI3 die Proliferation und IL-2-Produktion (IC50-Wert ~4 µM), da die Dephosphorylierung von NFATc und die anschließende nukleäre Translokation gehemmt wird. NCI3 inhibiert die calcineurinabhängige NFAT- und NF-κB-, aber nicht die AP-1-kontrollierte Reprtergenexpression, in mikromolaren Konzentrationen (IC50-Werte 2 bzw. 7 µM). Im Gegensatz zu Cyclosporin A stört NCI3 nicht die Phosphataseaktivität von Calcineurin, sondern interferiert mit der Calcineurin-NFATc-Bindung. Ein wichtiges endogenes Modulatorprotein für die Calcineurinaktivität ist RCAN1, das vermutlich den Calcineurin-NFATc-Signalweg über einen negativen Rückkopplungsmechanismus reguliert. Hier wurde gezeigt, daß RCAN1 in humanen TH-Zellen exprimiert wird. Die Spleißvariante RCAN1-1 ist in ruhenden T-Zellen basal exprimiert und wird nicht durch T-Zell-Rezeptor-Stimulierung in seiner Expression verändert. RCAN1-4 dagegen ist in ruhenden Zellen kaum zu detektieren und wird stimulierungsabhängig induziert. Durch die Verwendung Calcineurin-NFATc-spezifischer Inhibitoren wie NCI3 wurde gezeigt, daß die RCAN1-4-Induktion durch diesen Signalweg limitiert ist. Die in dieser Arbeit gewonnenen Daten und Erkenntnisse tragen dazu bei, das Verständnis der Funktion und Regulation von Calcineurin in T-Zellen zu vertiefen.
The Ca2+/calmodulin dependent serine/threonine phosphatase calcineurin is a key molecule in the T cell receptor dependent signalling network. Calcineurin dephosphorylates and thereby activates the transcription factors of the NFATc family that, among others, control the expression of important cytokines and cell surface molecules. The activity of Calcineurin is modulated by several endogenous proteins and is inhibited by the immunosuppressants cyclosporine A and FK506. Here, the novel low molecular weight inhibitor NCI3 was characterized in respect to its effects on T cell receptor dependent signalling. The results of this work show, that the pyrazolopyrimidine derivate NCI3 is nontoxic and permeates the cell membrane. Upon TCR stimulation NCI3 suppresses T cell proliferation and IL-2 production of primary human TH cells with IC50 values of ~4 µM by blocking the dephosphorylation and subsequent nuclear translocation of NFATc. NCI3 conse-quently inhibits calcineurin dependent NFAT- and NF-κB-, but not AP-1-controlled reporter gene expression, in micromolar concentrations (IC50 values 2 and 7 µM, respectively). In opposite to cyclosporine A and FK506, NCI3 does not interfere with the phosphatase activity of calcineurin but rather disturbs the calcineurin-NFATc interaction. A major endogenous modulator of calcineurin is the protein RCAN1, which is supposed to regulate calcineurin-NFATc signalling in a negative feedback loop. The presented data show that RCAN1 is expressed in human TH cells. The splice variant RCAN1-1 is basally expressed in resting T cells, and its expression levels are not changed by T cell receptor stimulation. Expression of RCAN1-4, on the other hand, is nearly undetectable in resting TH cells and is induced upon cell stimulation. By using calcineurin-NFATc specific inhibitors such as NCI3 it could be shown that RCAN1-4 induction is limited by this pathway. This work provides a comprehensive characterization of the novel inhibitor NCI3 and insights into the regulation of calcineurin by RCAN1 in human TH cells.
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Germaud, Nathalie. "Polymorphisme du gène NCR3/NKp30 et variabilité de la fonction des cellules Natural Killer humaines." Phd thesis, Université René Descartes - Paris V, 2012. http://tel.archives-ouvertes.fr/tel-00789417.

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Les cellules Natural Killer (NK) sont non, seulement de précieux effecteurs cytotoxiques de la réponse immunitaire innée dirigée contre les tumeurs et les infections, mais aussi d'importants immunorégulateurs. Leur activation dépend d'une balance complexe entre des signaux émanant de multiples récepteurs, tantôt inhibiteurs, tantôt activateurs. Parmi les récepteurs activateurs, NCR3 représente un acteur important de la lyse tumorale et de l'interaction avec les cellules dendritiques. Dans le but de caractériser la variabilité interindividuelle de la réponse NK et d'établir une référence pour des études ultérieures dans un contexte pathologique, nous avons examiné, dans un échantillon de 43 donneurs sains, les corrélations entre la variabilité fonctionnelle des cellules NK en réponse à la stimulation de leur récepteur NKp30 et le niveau d'expression des transcrits de NCR3 ainsi que celui de la protéine correspondante, au regard du polymorphisme génomique. Nous avons mis en évidence une étroite corrélation entre l'expression membranaire de NKp30 et NKp46 et la fonction cytotoxique NK, mais pas avec la sécrétion de cytokines. Nous avons retrouvé l'effet déjà connu du variant rs986475 sur l'expression de l'un des transcrits alternatifs de NCR3, T3. Nous avons également identifié un autre variant, rs11575836, influençant le niveau de transcrits T1, en relation avec la cytotoxicité induite par la signalisation NKp30. Cette étude pointe le doigt sur la spécificité des voies de signalisation des fonctions NK et le réseau complexe de gènes impliqués dans leur régulation. Nous avons par ailleurs évalué la variabilité génétique de NCR3 dans la myasthénie auto-immune où les cellules NK pourraient jouer un rôle. Le re-séquençage du gène NCR3 n'a pas révélé d'association avec un polymorphisme commun mais a permis d'identifier deux mutations rares, " faux-sens ", retrouvées uniquement chez des patients myasthéniques. L'une d'elle, L19R, est non-conservative et représente un candidat particulièrement intéressant à examiner en détail du fait de sa localisation dans une région très conservée dans la phylogénie. Même si de nombreux points restent à élucider, ces résultats indiquent qu'il devrait être possible de relier de façon globale et intégrative le polymorphisme de l'ADN, ainsi que l'expression des transcrits et des protéines, à la réponse fonctionnelle des cellules NK
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Baaklini, Sabrina. "Compréhension de la résistance humaine au paludisme : des études génétiques aux approches fonctionnelles." Thesis, Aix-Marseille, 2017. http://www.theses.fr/2017AIXM0384/document.

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La sévérité du paludisme est influencée par des interactions complexes entre de nombreux facteurs dont la génétique de l’hôte. Plusieurs études de liaison génétique menées dans différentes ethnies africaines ont montré une liaison entre le locus 6p21 et le paludisme simple. De plus, différents variants au sein des gènes TNF et NCR3, retrouvés dans ce locus, ont été indépendamment associés à ce phénotype au Burkina Faso.Ainsi, nous nous sommes tout d’abord intéressés aux polymorphismes du TNF. Nos résultats montrent que les variants TNF-308, TNF-244, et TNF-238 sont associés à la parasitémie maximale ou aux accès simples au Congo. Les approches moléculaires indiquent que le TNF-244 a un effet cis-régulateur avec une activité promotrice réduite en présence du variant A ainsi qu’une fixation altérée de protéines nucléaires en présence de ce même variant. Enfin, nos analyses bio-informatiques suggèrent que le TNF-244 et le TNF-238 agissent en synergie pour modifier le site de fixation d’au moins un facteur de transcription.Nous avons ensuite confirmé l’association du NCR3-412 avec le paludisme simple et le nombre d’accès fébrile au Congo. Les analyses fonctionnelles montrent que ce SNP a aussi un effet cis-régulateur avec une activité promotrice accrue en présence de l’allèle G et une liaison altérée de deux complexes protéiques en présence de l’allèle C. Les approches in silico et in vitro indiquent que les facteurs STAT4 et RUNX3 sont ceux dont la fixation est altérée.NCR3-412 altérant la résistance à la forme simple du paludisme, nous avons souhaité déterminer s’il est aussi impliqué dans la résistance au paludisme sévère mais nous n’avons détecté aucune association
The severity of malaria is influenced by complex interactions between many factors including host genetics. Numerous genetic studies conducted in different African ethnic groups have shown a significant linkage between the 6p21 locus and mild malaria attack. In addition to their linkage, several polymorphisms found under the linkage peak, and more precisely within TNF and NCR3, were also independently associated with different sub-phenotypes of mild malaria in Burkina Faso.Thus, we first focused on TNF polymorphisms. Among the 4 polymorphisms analyzed, we found associations between TNF-238, TNF-244, TNF-308 and either mild malaria attack or maximum parasitemia. Molecular approaches showed that TNF-244 has a cis-regulatory effect. Indeed, we observe a decreased promoter activity and an altered binding of nuclear proteins in the presence of the A variant. In addition, our bioinformatics analyses suggested a cooperative effect of TNF-244 and TNF-238 in modifying the binding of at least one transcription factor.We then confirmed the association of NCR3-412 with both mild malaria and the number of febrile episodes in Congo. Functional analyses have shown that this SNP has also a cis-regulatory effect with a decreased promoter activity and an altered binding of two nuclear protein complexes in the presence of the C allele. Finally, in silico and in vitro approaches indicated that STAT4 and RUNX3 are the two transcription factors affected.As NCR3-412 is associated with resistance to mild malaria, we therefore investigated whether this SNP is also involved in severe malaria resistance, but we did not detect any association neither with severe anemia nor with cerebral malaria
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Semeraro, Michaela. "Neuroblastoma and gastrointestinal stromal tumor as a target for natural killer lymphocytes : the role of ncr3/nkp30." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T045/document.

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Depuis la formulation de la théorie de l’immuno-surveillance en 1957 par Burnet et Thomas, le monde scientifique s’est efforcé d’identifier les cellules immunitaires impliquées dans ce processus. Les lymphocytes Natural Killer (NK) constituent une composant majeure de l’immuno-surveillance innée dans plusieurs cancers hématologiques et solides. L’activité des lymphocytes NK passe principalement par une grande variété de récepteurs avec un rôle activateur ou inhibiteur. Parmi les récepteurs activateurs présents à la surface des lymphocytes NK, le récepteur NCR3/NKp30 a un rôle majeur dans la toxicité directe contre la cellule cible et dans l’activation des cellules dendritiques.Les tumeurs stromales gastrointestinales (GIST) et le Neuroblastome (NB) sont deux tumeurs sensibles à l’immuno-surveillance par les lymphocytes NK. Dans une étude récente notre équipe a démontré que l’épissage alternatif du gène NCR3/NKp30 peut être déterminant dans la fonction NK et dans la survie des patients atteints de GIST.Afin de caractériser les lymphocytes infiltrant le GIST, nous avons effectué une recherche visant à analyser l’infiltrat des lymphocytes CD3+, des lymphocytes T régulateurs (Treg) et des lymphocytes NK dans des tumeurs GIST localisés, et corréler ces résultats à la survie des patients. Nous avons mis en évidence que, avant traitement, les lymphocytes NK sont surtout localisés au niveau des fibres trabéculaires qui entourent la tumeur, alors que les lymphocytes T sont localisé à l’intérieur de la tumeur en contact avec les cellules tumorales qui expriment HLA-I.Nous avons aussi observé que les cellules NK ont un phénotype plutôt CD56bright et migrent à l’intérieur de la tumeur après traitement par Imatinib. L’analyse de survie a mis en évidence que les lymphocytes NK et T peuvent prédire la survie sans progression (PFS). Ces résultats mettent en évidence l’importance de l’infiltrat immunitaire dans la prédiction du risque de rechute dans le GIST et surlignent l’importance de viser une réponse immunitaire dans les protocoles thérapeutiques.Nous avons ensuite déterminé la proportion de lymphocytes NK dans le sang périphérique et dans la moelle dans une cohorte de Neuroblastome (NB) localisé et métastatique : une infiltration plus important par les NK CD56bright a été observé chez les patients présentant une maladie métastatique et chez les patients avec une réponse mineure au traitement d’induction. De plus, les NK présents dans les échantillons de moelle osseuse infiltrés par les neuroblastes, présentaient une expression plus basse du récepteur NKp30. L’expression du ligand de NKp30, B7-H6, a été mise en évidence sur les neuroblastes infiltrant la moelle osseuse, et sa forme soluble, sB7-H6, a été retrouvée être positivement corrélée à l’extension de maladie et inversement à la réponse au traitement d’induction. L’analyse de l’épissage alternatif du gène NCR3/NKp30 a permis de mettre en évidence l’impact des isoformes NKp30 sur la survie sans progression chez les patients atteints de NB de haut risque en maladie minimale résiduelle après chimiothérapie d’induction. En particulier, les patients présentant un taux élevé de l’isoforme pro-inflammatoire (NKp30b) par rapport à l’isoforme immunosuppressive (NKp30c), présentent une meilleure survie sans évènement. Nous avons aussi démontré le rôle des monocytes dans l’amplification de la réponse NKp30 dépendant. Les résultats de notre recherche dans le GIST et dans le NB, deux maladies différentes mais toutes les deux sensibles aux lymphocytes NK, surlignent l’importance d’intégrer de nouvelles options thérapeutiques aptes à cibler le système immunitaire
Since Burnet and Thomas formulated in 1957 the cancer immunosurveillance theory, the scientific world has made tremendous progress to identify the immune cells involved in this process. Natural Killer (NK) cells have emerged as a major component of the innate immunosurveillance of several hematological and solid malignancies. The activity of NK-cells is mainly mediated through their wide variety of receptors with activating and inhibitory functions. Among the versatile receptors present on NK cells, the activating receptor NCR3/NKp30 is a major receptor involved in both direct killing of target cells and mutual NK and dendritic cell activation.Gastrointestinal stromal tumors (GIST) and Neuroblastoma (NB) are known to be tumors sensitive to NK immunosurveillance. In a recent study we showed that alternative splicing of NCR3/NKp30 gene can affect NK cell function and GIST patient’s outcome.In order to better characterize the GIST tumor-infiltrating lymphocytes, we analyzed the CD3+, T regulatory (Treg) and NK lymphocytes infiltration within primary localized GIST tumors and we determined their prognostic value. We described that, before treatment, NK cells are mainly localized in fibrous trabeculae while T lymphocytes are in the tumor nests in HLA-I positive tumor cells contact. Moreover infiltrating NK cells displayed a secreting CD56bright phenotype, and accumulate in tumor nests after Imatinib (IM) treatment. Importantly CD3+ and NK lymphocytes independently predicted progression free survival (PFS). These results highlight the importance of the immune infiltrate in re-define the GIST risk stratification and allow enhancing the immune response in the therapeutic decisions.We next investigated the proportions of NK cells in blood and bone marrow (BM) in a cohort of localized and metastatic NB; a high proportion of CD56bright NK cells was associated with metastatic NB and with poor response to induction treatment within the metastatic NB. Moreover, infiltrated BM presented NKp30 down regulation. The expression of the NKp30 ligand, B7-H6, was found on BM neuroblasts, while the soluble protein, sB7-H6 correlated with resistance to treatment. Furthermore the transcriptional status of NKp30/NCR3 dictated the event-free survival rates of HR-NBs with minimal residual disease post-induction chemotherapy: in particular patients presenting a high proportion of the immunosuppressive isoform (NKp30c) compared to the pro-inflammatory isoform (NKp30b), presented a worse outcome. We further demonstrated the significant role of monocytes to amplify the NKp30 activation response.These researches in GIST and NB, two different but at the meantime NK-sensitive diseases support the effort to define new immunological therapeutic approaches and to determine their optimal use
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Yoo, Edwin. "Inflammatory cytokines induce human bronchial smooth muscle cell proliferation via an NCX-1 dependent mechanism." Diss., [La Jolla] : University of California, San Diego, 2010. http://wwwlib.umi.com/cr/fullcit?p1477952.

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Thesis (M.S.)--University of California, San Diego, 2010.
Title from first page of PDF file (viewed July 16, 2010). Available via ProQuest Digital Dissertations. Includes bibliographical references (leaves 36-40).
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Burr, Adam R. "Sodium dysregulation coupled with calcium entry leads to muscular dystrophy in mice." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1414750156.

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Choudhury, Moinuddin Hasan. "Biopacemaking : new targets and new mechanisms." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/biopacemaking-new-targets-and-new-mechanisms(b35ec222-29eb-432f-9b6d-238f3cbcd72d).html.

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Background: Biopacemaking is the attempt to replicate sinoatrial node (SAN)-like pacemaker activity in other areas of the heart by manipulating genes involved in pacemaking. Application of this could emulate the electronic pacemaker without the need for implantation of permanent hardware, or directly repair dysfunctional SAN tissue in human disease. We upregulated the transcription factors Tbx18, Tbx3 and the membrane ion exchanger NCX1 in bradycardic subsidiary atrial pacemaker (SAP) tissue which we used as a model of SAN dysfunction. We aimed to show that one or more of these gene targets could improve pacemaker function and alter the molecular character of SAP tissue and thus could potentially be used for the repair of dysfunctional SAN tissue. Methods: SAP tissue was isolated from the right atria of rats and kept beating in culture at 37°C for 48 hours. Recombinant adenoviruses were injected into SAP preparations to upregulate Tbx18, Tbx3 and NCX1 individually. Beating rate, overdrive suppression and pharmacological response to If blockade and β-adrenergic stimulation were measured along with molecular changes in pacemaker and atrial genes and proteins using RT-qPCR and immunohistochemistry. Results: Tbx18 upregulation significantly increased SAP beating rate after 48 hours of culture (a final rate of 141 ± 9 bpm in uninfected SAP tissue versus 215 ± 16 bpm in Ad-Tbx18 infected SAP tissue, p<0.01). It induced upregulation of HCN2 (p<0.01) and RYR2 (p<0.05), downregulation of HCN4 (p<0.05) and no change HCN1, Tbx3, Kv1.5, Kir2.1, Nav1.5, NCX1, Cx43, Cx45, Cav1.2 or Cav3.1. There was also no change in overdrive suppression and no change in response to pharmacology. No increase in beating rate was seen with either Tbx3 or NCX1 upregulation. Tbx3 preparations induced downregulation of the atrial genes Kir2.1 (p<0.01) and Nav1.5 (p<0.05), along with HCN1 (p<0.05), HCN4 (p<0.01), Tbx18 (p<0.05) and NCX1 (p<0.01), upregulated Cx43 (p<0.05) and showed no change in Cx45, RYR2, Kv1.5. NCX1 preparations demonstrated reduced overdrive suppression (p<0.05). Conclusion: Tbx18 showed the most potential for biopacemaking in SAP tissue, however both Tbx3 and NCX1 could be applied as secondary targets to fine tune biopacemaker function. Future work would focus on applying these targets to dysfunctional SAN tissue in larger animals.
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Books on the topic "NCX3"

1

Psakhis, Lev. French defence 3 Nc3 Bb4. London: B.T. Batsford, 2003.

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Singer, Kenneth D. "Poling of microwave electro-optic devices": Final technical report : contract # NCC3-431. [Washington, DC: National Aeronautics and Space Administration, 1997.

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Beckermann, Christoph. Transport phenomena during equiaxed solidification of alloys: Final technical report, NCC3-290. [Washington, DC: National Aeronautics and Space Administration, 1997.

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Rigby, David L. Internal passage heat transfer prediction using multiblock grids and a [kappa-omega] turbulence model: Under cooperative agreement NCC3-370. [Washington, DC: National Aeronautics and Space Administration, 1996.

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International Conference on the Structure of Non-Crystalline Materials (3rd 1985 Grenoble). NCM3: Third International Conference onthe Structure of Non-Crystalline Materials, July 8-12, 1985, Institut v. Laue-Langevin, Grenoble, France. Les Ulis: Les Editions de Physique, 1985.

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Li, Ben Q. Final report on numerical study of magnetic damping during unidirectional solidification (NASA grant #: NCC3-435), duration: October 1, 1995 - September 30, 1997. [Washington, DC: National Aeronautics and Space Administration, 1997.

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Selig, Michael S. The effects of the critical ice accretion on airfoil and wing performance: NASA contract # NCC3-408 : January 24, 1995-November 30, 1996 : final report. [Washington, DC: National Aeronautics and Space Administration, 1998.

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Chalifman, Aleksandr. Opening for white according to Anand 1.e4: 1.e4 c5 2. Nf3 Nc6 3.d4 cxd4 4. Nxd4 Nf6 5. Nc3, Chelyabinsk variation / [transl. from the Russian by Evgeny Ermenkov]. Sofia: Chess stars, 2007.

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Clacy, Girad A. NCX: A Trilogy. Writers Club Press, 2003.

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1.Nc3 Dunst Opening. Chess Enterprises, 1995.

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Book chapters on the topic "NCX3"

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Lane, J. D., C. J. Pickett, and D. R. Stanley. "From NCI3." In Inorganic Reactions and Methods, 99. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2007. http://dx.doi.org/10.1002/9780470145227.ch71.

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Ottolia, Michela, and Kenneth D. Philipson. "NCX1: Mechanism of Transport." In Advances in Experimental Medicine and Biology, 49–54. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4756-6_5.

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Clausen, Torben, José Luis Trejo, Mark P. Mattson, Alexis M. Stranahan, Joanna Erion, Rosa Maria Bruno, Stefano Taddei, and Melinda M. Manore. "Na+/Ca2+ Exchanger (NCX)." In Encyclopedia of Exercise Medicine in Health and Disease, 632. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2738.

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Valsecchi, Valeria, Giuseppe Pignataro, Rossana Sirabella, Carmela Matrone, Francesca Boscia, Antonella Scorziello, Maria Josè Sisalli, et al. "Transcriptional Regulation of ncx1 Gene in the Brain." In Advances in Experimental Medicine and Biology, 137–45. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4756-6_12.

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Tóth, András, and András Varró. "Role of NCX1 and NHE1 in Ventricular Arrhythmia." In Heart Rate and Rhythm, 543–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-17575-6_30.

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Fiorucci, Stefano, Elisabetta Antonelli, and Antonio Morelli. "NCX-1000: a liver-specific NO donor." In Portal Hypertension in the 21st Century, 105–10. Dordrecht: Springer Netherlands, 2004. http://dx.doi.org/10.1007/978-94-007-1042-9_12.

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Nicoll, Debora A., Michela Ottolia, Joshua I. Goldhaber, and Kenneth D. Philipson. "20 Years from NCX Purification and Cloning: Milestones." In Advances in Experimental Medicine and Biology, 17–23. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4756-6_2.

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Giladi, Moshe, and Daniel Khananshvili. "Molecular Determinants of Allosteric Regulation in NCX Proteins." In Advances in Experimental Medicine and Biology, 35–48. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4756-6_4.

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Rahamimoff, Hannah, Benayahu Elbaz, Michael Valitsky, Mahdi Khatib, Marina Eskin-Schwartz, and Daniela Elmaz. "Immunosuppressive Drugs, Immunophilins, and Functional Expression of NCX Isoforms." In Advances in Experimental Medicine and Biology, 275–87. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4756-6_23.

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Noda, Mami, Masataka Ifuku, Yuki Mori, and Alexei Verkhratsky. "Calcium Influx Through Reversed NCX Controls Migration of Microglia." In Advances in Experimental Medicine and Biology, 289–94. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4756-6_24.

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Conference papers on the topic "NCX3"

1

McDermott, William, Robert Coombe, Julanna Gilbert, Boris Nizamov, and Zane Lambert. "Kinetic Experiments for an NCl3 Fueled Iodine Laser." In 36th AIAA Plasmadynamics and Lasers Conference. Reston, Virigina: American Institute of Aeronautics and Astronautics, 2005. http://dx.doi.org/10.2514/6.2005-5038.

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Han, Jiande, and Michael Heaven. "Kinetics of Singlet NCl Following the Photodissociation of NCl3." In 36th AIAA Plasmadynamics and Lasers Conference. Reston, Virigina: American Institute of Aeronautics and Astronautics, 2005. http://dx.doi.org/10.2514/6.2005-5039.

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Shahlol, A., and A. Manani. "Seismic Inversion and Reservoir Characterization, NC73, Sirt Basin, Libya." In 1st EAGE North African/Mediterranean Petroleum & Geosciences Conference & Exhibition. European Association of Geoscientists & Engineers, 2003. http://dx.doi.org/10.3997/2214-4609-pdb.8.p041.

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Gok, Caglar, Alan D. Robertson, and William Fuller. "BS27 Harnessing the power of palmitoylation to tune NCX1 Physiology." In British Cardiovascular Society Virtual Annual Conference, ‘Cardiology and the Environment’, 7–10 June 2021. BMJ Publishing Group Ltd and British Cardiovascular Society, 2021. http://dx.doi.org/10.1136/heartjnl-2021-bcs.225.

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Schwartz, R. N., and R. A. McFarlane. "Room Temperature Upconversion Spectral Studies of CsCdBr3:Er." In Advanced Solid State Lasers. Washington, D.C.: OSA, 1992. http://dx.doi.org/10.1364/assl.1992.nc13.

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Yoo, Edwin, Lan Tang, Rongrong Wu, Tyson Torres, Dana Balitzer, Hui Dong, and Timothy D. Bigby. "Cytokines Induce Human Bronchial Smooth Muscle Cell Growth Via An NCX1-Dependent Mechanism." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3604.

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Malysheva, Lyuba. "First-principle DFT modeling of IR spectra of oriented helical HS(CH2CH2O)nCH3 molecules." In MOLECULAR NANOSTRUCTURES: XVII International Winterschool Euroconference on Electronic Properties of Novel Materials. AIP, 2003. http://dx.doi.org/10.1063/1.1628077.

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Verisokin, Andrey Y., Darya V. Verveyko, Varvara V. Kucherenko, Dmitry E. Postnov, and Alexey R. Brazhe. "Modulatory effect of NCX on IP3-dependent Ca2+ oscillations in astrocytes." In Computations and Data Analysis: from Molecular Processes to Brain Functions, edited by Dmitry E. Postnov. SPIE, 2021. http://dx.doi.org/10.1117/12.2590417.

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McCarthy, M. J., and D. C. Hanna. "CW Mode-Locked Singly Resonant Optical Parametric Oscillator Synchronously Pumped by a Laser Diode-Pumped Nd:YLF Laser." In Advanced Solid State Lasers. Washington, D.C.: OSA, 1992. http://dx.doi.org/10.1364/assl.1992.nc3.

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Rahman, Mozibur, and Luke J. Janssen. "NCX In Airway Smooth Muscle: Electrophysiological Properties And Altered Expression During Allergen-Induced Airway Hyperresponsiveness." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1266.

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Reports on the topic "NCX3"

1

Frese, Hans. Network Communication Executive (NCX) Programmer's Guide. Office of Scientific and Technical Information (OSTI), June 2018. http://dx.doi.org/10.2172/1454022.

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Dye, Robert Craig. Update on the Status of Modernizing NC3. Office of Scientific and Technical Information (OSTI), July 2019. http://dx.doi.org/10.2172/1544646.

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