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Articoli di riviste sul tema "Sodium/calcium exchanger (NCX)"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 18 febbraio 2022

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1

Chovancova, Barbora, Veronika Liskova, Petr Babula, and Olga Krizanova. "Role of Sodium/Calcium Exchangers in Tumors." Biomolecules 10, no. 9 (August 31, 2020): 1257. http://dx.doi.org/10.3390/biom10091257.

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Abstract (sommario):

The sodium/calcium exchanger (NCX) is a unique calcium transport system, generally transporting calcium ions out of the cell in exchange for sodium ions. Nevertheless, under special conditions this transporter can also work in a reverse mode, in which direction of the ion transport is inverted—calcium ions are transported inside the cell and sodium ions are transported out of the cell. To date, three isoforms of the NCX have been identified and characterized in humans. Majority of information about the NCX function comes from isoform 1 (NCX1). Although knowledge about NCX function has evolved

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2

Chernysh, Olga, Madalina Condrescu, and John P. Reeves. "Sodium-dependent inactivation of sodium/calcium exchange in transfected Chinese hamster ovary cells." American Journal of Physiology-Cell Physiology 295, no. 4 (October 2008): C872—C882. http://dx.doi.org/10.1152/ajpcell.00221.2008.

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High concentrations of cytosolic Na+ ions induce the time-dependent formation of an inactive state of the Na+/Ca2+ exchanger (NCX), a process known as Na+-dependent inactivation. NCX activity was measured as Ca2+ uptake in fura 2-loaded Chinese hamster ovary (CHO) cells expressing the wild-type (WT) NCX or mutants that are hypersensitive (F223E) or resistant (K229Q) to Na+-dependent inactivation. As expected, 1) Na+-dependent inactivation was promoted by high cytosolic Na+ concentration, 2) the F223E mutant was more susceptible than the WT exchanger to inactivation, whereas the K229Q mutant wa

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3

Roome, Chris J., Emmet M. Power, and Ruth M. Empson. "Transient reversal of the sodium/calcium exchanger boosts presynaptic calcium and synaptic transmission at a cerebellar synapse." Journal of Neurophysiology 109, no. 6 (March 15, 2013): 1669–80. http://dx.doi.org/10.1152/jn.00854.2012.

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The sodium/calcium exchanger (NCX) is a widespread transporter that exchanges sodium and calcium ions across excitable membranes. Normally, NCX mainly operates in its “forward” mode, harnessing the electrochemical gradient of sodium ions to expel calcium. During membrane depolarization or elevated internal sodium levels, NCX can instead switch the direction of net flux to expel sodium and allow calcium entry. Such “reverse”-mode NCX operation is frequently implicated during pathological or artificially extended periods of depolarization, not during normal activity. We have used fast calcium im

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4

Smith, L., and J. B. Smith. "Activation of adenylyl cyclase downregulates sodium/calcium exchanger of arterial myocytes." American Journal of Physiology-Cell Physiology 269, no. 6 (December 1, 1995): C1379—C1384. http://dx.doi.org/10.1152/ajpcell.1995.269.6.c1379.

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Chronic elevation of adenosine 3',5'-cyclic monophosphate (cAMP) is known to inhibit the proliferation of cultured vascular smooth muscle cells. The present findings show that the activation of adenylyl cyclase with forskolin decreased Na+/Ca2+ exchanger (NCX) mRNA and activity. Fetal bovine serum restored NCX transcript and activity. The changes in NCX transcript preceded the changes in NCX activity. Incubation of low-passage immortalized myocytes with forskolin plus 3-isobutyl-1-methylxanthine (IBMX), which inhibits cAMP phosphodiesterase, decreased NCX mRNA by 60% in 6 h and 80% in 24 h. Af

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5

Münch, Götz, Kai Rosport, Christine Baumgartner, Zhongmin Li, Silvia Wagner, Andreas Bültmann, and Martin Ungerer. "Functional alterations after cardiac sodium-calcium exchanger overexpression in heart failure." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 2 (August 2006): H488—H495. http://dx.doi.org/10.1152/ajpheart.01324.2005.

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The sodium-calcium exchanger (NCX) is discussed as one of the key proteins involved in heart failure. However, the causal role and the extent to which NCX contributes to contractile dysfunction during heart failure are poorly understood. NCX overexpression was induced by infection with an adenovirus coding for NCX, which coexpressed green fluorescence protein (GFP) (AdNCX) by ex vivo gene transfer to nonfailing and failing rabbit cardiomyocytes. Myocardial gene transfer in rabbits in vivo was achieved by adenoviral delivery via aortic cross-clamping. Peak cell shortening of cardiomyocytes was

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6

Torrente, Angelo G., Rui Zhang, Audrey Zaini, Jorge F. Giani, Jeanney Kang, Scott T. Lamp, Kenneth D. Philipson, and Joshua I. Goldhaber. "Burst pacemaker activity of the sinoatrial node in sodium–calcium exchanger knockout mice." Proceedings of the National Academy of Sciences 112, no. 31 (July 20, 2015): 9769–74. http://dx.doi.org/10.1073/pnas.1505670112.

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In sinoatrial node (SAN) cells, electrogenic sodium–calcium exchange (NCX) is the dominant calcium (Ca) efflux mechanism. However, the role of NCX in the generation of SAN automaticity is controversial. To investigate the contribution of NCX to pacemaking in the SAN, we performed optical voltage mapping and high-speed 2D laser scanning confocal microscopy (LSCM) of Ca dynamics in an ex vivo intact SAN/atrial tissue preparation from atrial-specific NCX knockout (KO) mice. These mice lack P waves on electrocardiograms, and isolated NCX KO SAN cells are quiescent. Voltage mapping revealed disorga

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7

Haug-Collet, K., B. Pearson, R. Webel, R. T. Szerencsei, R. J. Winkfein, P. P. M. Schnetkamp, and N. J. Colley. "Cloning and Characterization of a Potassium-Dependent Sodium/Calcium Exchanger in Drosophila." Journal of Cell Biology 147, no. 3 (November 1, 1999): 659–70. http://dx.doi.org/10.1083/jcb.147.3.659.

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Sodium/calcium(-potassium) exchangers (NCX and NCKX) are critical for the rapid extrusion of calcium, which follows the stimulation of a variety of excitable cells. To further understand the mechanisms of calcium regulation in signaling, we have cloned a Drosophila sodium/calcium-potassium exchanger, Nckx30C. The overall deduced protein topology for NCKX30C is similar to that of mammalian NCKX, having five membrane-spanning domains in the NH2 terminus separated from six at the COOH-terminal end by a large intracellular loop. We show that NCKX30C functions as a potassium-dependent sodium/calciu

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8

de Ruijter, Wouter, Ger J. M. Stienen, Jan van Klarenbosch, and Jacob J. de Lange. "Negative and Positive Inotropic Effects of Propofol via L-type Calcium Channels and the Sodium-Calcium Exchanger in Rat Cardiac Trabeculae." Anesthesiology 97, no. 5 (November 1, 2002): 1146–55. http://dx.doi.org/10.1097/00000542-200211000-00019.

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Background Conflicting opinions are present in the literature regarding the origin of the negative inotropic effect of propofol on the myocardium. This study aims to resolve these discrepancies by investigating the inotropic effects of propofol the L-type calcium channels and the sodium-calcium exchanger (NCX). Methods The effect of 20 microg/ml propofol on force development was determined in rat cardiac trabeculae at different pacing frequencies and different extracellular calcium concentrations. Postrest potentiation, sodium withdrawal during quiescence, and the NCX inhibitor KB-R7943 were u

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9

Padín, Juan-Fernando, José-Carlos Fernández-Morales, Román Olivares, Stefan Vestring, Juan-Alberto Arranz-Tagarro, Enrique Calvo-Gallardo, Ricardo de Pascual, Luís Gandía, and Antonio G. García. "Plasmalemmal sodium-calcium exchanger shapes the calcium and exocytotic signals of chromaffin cells at physiological temperature." American Journal of Physiology-Cell Physiology 305, no. 2 (July 15, 2013): C160—C172. http://dx.doi.org/10.1152/ajpcell.00016.2013.

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The activity of the plasmalemmal Na+/Ca2+ exchanger (NCX) is highly sensitive to temperature. We took advantage of this fact to explore here the effects of the NCX blocker KB-R7943 (KBR) at 22 and 37°C on the kinetics of Ca2+ currents ( ICa), cytosolic Ca2+ ([Ca2+]c) transients, and catecholamine release from bovine chromaffin cells (BCCs) stimulated with high K+, caffeine, or histamine. At 22°C, the effects of KBR on those parameters were meager or nil. However, at 37°C whereby the NCX is moving Ca2+ at a rate fivefold higher than at 22°C, various of the effects of KBR were pronounced, namely

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10

Loffing, Johannes, Dominique Loffing-Cueni, Victor Valderrabano, Lea Kläusli, Steven C. Hebert, Bernard C. Rossier, Joost G. J. Hoenderop, René J. M. Bindels, and Brigitte Kaissling. "Distribution of transcellular calcium and sodium transport pathways along mouse distal nephron." American Journal of Physiology-Renal Physiology 281, no. 6 (December 1, 2001): F1021—F1027. http://dx.doi.org/10.1152/ajprenal.0085.2001.

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First published August 15, 2001; 10.1152/ajprenal. 00085.2001.—The organization of Na+ and Ca2+ transport pathways along the mouse distal nephron is incompletely known. We revealed by immunohistochemistry a set of Ca2+ and Na+transport proteins along the mouse distal convolution. The thiazide-sensitive Na+-Cl− cotransporter (NCC) characterized the distal convoluted tubule (DCT). The amiloride-sensitive epithelial Na+ channel (ENaC) colocalized with NCC in late DCT (DCT2) and extended to the downstream connecting tubule (CNT) and collecting duct (CD). In early DCT (DCT1), the basolateral Ca2+-e

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11

Linask, Kersti K., Ming-Da Han, Michael Artman, and Cheryl A. Ludwig. "Sodium-calcium exchanger (NCX-1) and calcium modulation: NCX protein expression patterns and regulation of early heart development." Developmental Dynamics 221, no. 3 (2001): 249–64. http://dx.doi.org/10.1002/dvdy.1131.

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12

Jha, Brajesh Kumar, and Amrita Jha. "Two dimensional finite element estimation of calcium ions in presence fo NCX and Buffers in Astrocytes." Boletim da Sociedade Paranaense de Matemática 36, no. 1 (January 1, 2018): 151. http://dx.doi.org/10.5269/bspm.v36i1.29137.

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Sodium calcium exchanger (NCX) plays effective role in signal transduction in most of the nerve cells like neuron, astrocytes. Sodium ion affects the cytosolic calcium concentration label in Astrocytes via various channels. This affects the movement of the nerve impulse from one cell to other cell. In this paper two dimensional model is developedin the form of diffusion equation to study the effect of NCX in presence and negligence of buffer in Astrocytes. Finite element method is employed to solve the problem and simulated in Matlab to estimate the affect of various parameter like flux, diffu

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13

Li, Sen, Anant Chopra, Wendy Keung, Camie W. Y. Chan, Kevin D. Costa, Chi-Wing Kong, Roger J. Hajjar, Christopher S. Chen, and Ronald A. Li. "Sarco/endoplasmic reticulum Ca2+-ATPase is a more effective calcium remover than sodium-calcium exchanger in human embryonic stem cell-derived cardiomyocytes." American Journal of Physiology-Heart and Circulatory Physiology 317, no. 5 (November 1, 2019): H1105—H1115. http://dx.doi.org/10.1152/ajpheart.00540.2018.

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Human pluripotent stem cell (hPSCs)-derived ventricular (V) cardiomyocytes (CMs) display immature Ca2+–handing properties with smaller transient amplitudes and slower kinetics due to such differences in crucial Ca2+-handling proteins as the poor sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) pump but robust Na+-Ca2+ exchanger (NCX) activities in human embryonic stem cell (ESC)-derived VCMs compared with adult. Despite their fundamental importance in excitation-contraction coupling, the relative contribution of SERCA and NCX to Ca2+-handling of hPSC-VCMs remains unexplored. We systematically a

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14

Kang, Beom Seok, Bo Young Choi, A. Ra Kho, Song Hee Lee, Dae Ki Hong, Jeong Hyun Jeong, Dong Hyeon Kang, Min Kyu Park, and Sang Won Suh. "An Inhibitor of the Sodium–Hydrogen Exchanger-1 (NHE-1), Amiloride, Reduced Zinc Accumulation and Hippocampal Neuronal Death after Ischemia." International Journal of Molecular Sciences 21, no. 12 (June 14, 2020): 4232. http://dx.doi.org/10.3390/ijms21124232.

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Acidosis in the brain plays an important role in neuronal injury and is a common feature of several neurological diseases. It has been reported that the sodium–hydrogen exchanger-1 (NHE-1) is a key mediator of acidosis-induced neuronal injury. It modulates the concentration of intra- and extra-cellular sodium and hydrogen ions. During the ischemic state, excessive sodium ions enter neurons and inappropriately activate the sodium–calcium exchanger (NCX). Zinc can also enter neurons through voltage-gated calcium channels and NCX. Here, we tested the hypothesis that zinc enters the intracellular

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15

Giladi, Moshe, Reut Shor, Michal Lisnyansky, and Daniel Khananshvili. "Structure-Functional Basis of Ion Transport in Sodium–Calcium Exchanger (NCX) Proteins." International Journal of Molecular Sciences 17, no. 11 (November 22, 2016): 1949. http://dx.doi.org/10.3390/ijms17111949.

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Giladi, Moshe, Reuben Hiller, Joel A. Hirsch, and Daniel Khananshvili. "Population Shift Underlies Ca2+-induced Regulatory Transitions in the Sodium-Calcium Exchanger (NCX)." Journal of Biological Chemistry 288, no. 32 (June 24, 2013): 23141–49. http://dx.doi.org/10.1074/jbc.m113.471698.

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17

Polo-Parada, Luis, and Amol A. Modgi. "Differences in Expression and Function in the Atrium versus Ventricle of the Sodium-Calcium Exchanger in the Embryonic Chicken Heart." ISRN Physiology 2013 (September 1, 2013): 1–12. http://dx.doi.org/10.1155/2013/921527.

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Heart function is well known to be dependent on intrinsic electrical activity. This electrical activity is primarily mediated by a combination of interactions among various ionic channels and transporters. In this study, we demonstrate that the Na+-Ca2+ exchanger (NCX) is equally present in both atrial and ventricular cells at early stages of development (st. 13). However, ventricular cells exhibit an increase in NCX messenger ribonucleic acid (mRNA) levels during later stages of development, while levels in atrial cells remain constant. We demonstrate that the current density of the NCX incre

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18

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 patte

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19

Boyman, Liron, George S. B. Williams, Daniel Khananshvili, Israel Sekler, and W. J. Lederer. "NCLX: The mitochondrial sodium calcium exchanger." Journal of Molecular and Cellular Cardiology 59 (June 2013): 205–13. http://dx.doi.org/10.1016/j.yjmcc.2013.03.012.

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Geramipour, Amir, Zsófia Kohajda, Claudia Corici, János Prorok, Zsolt Szakonyi, Kinga Oravecz, Zoltán Márton, et al. "The investigation of the cellular electrophysiological and antiarrhythmic effects of a novel selective sodium–calcium exchanger inhibitor, GYKB-6635, in canine and guinea-pig hearts." Canadian Journal of Physiology and Pharmacology 94, no. 10 (October 2016): 1090–101. http://dx.doi.org/10.1139/cjpp-2015-0566.

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The sodium–calcium exchanger (NCX) is considered as the major transmembrane transport mechanism that controls Ca2+ homeostasis. Its contribution to the cardiac repolarization has not yet been directly studied due to lack of specific inhibitors, so that an urgent need for more selective compounds. In this study, the electrophysiological effects of GYKB-6635, a novel NCX inhibitor, on the NCX, L-type calcium, and main repolarizing potassium currents as well as action potential (AP) parameters were investigated. Ion currents and AP recordings were investigated by applying the whole-cell patch cla

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Roberts, Diane E., Archibald McNicol, and Ratna Bose. "Mechanism of Collagen Activation in Human Platelets." Journal of Biological Chemistry 279, no. 19 (February 23, 2004): 19421–30. http://dx.doi.org/10.1074/jbc.m308864200.

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The mechanism of collagen-induced human platelet activation was examined using Ca2+, Na+, and the pH-sensitive fluorescent dyes calcium green/fura red, sodium-binding benzofuran isophthalate, and 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. Administration of a moderate dose of collagen (10 μg/ml) to human platelets resulted in an increase in [Ca2+]iand platelet aggregation. The majority of this increase in [Ca2+]iresulted from the influx of calcium from the extracellular milieu via the Na+/Ca2+exchanger (NCX) functioning in the reverse mode and was reduced in a dose-dependent manner by t

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22

Shlosman, Irina, Fabrizio Marinelli, José D. Faraldo-Gómez, and Joseph A. Mindell. "The prokaryotic Na+/Ca2+ exchanger NCX_Mj transports Na+ and Ca2+ in a 3:1 stoichiometry." Journal of General Physiology 150, no. 1 (December 13, 2017): 51–65. http://dx.doi.org/10.1085/jgp.201711897.

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Intracellular Ca2+ signals control a wide array of cellular processes. These signals require spatial and temporal regulation of the intracellular Ca2+ concentration, which is achieved in part by a class of ubiquitous membrane proteins known as sodium–calcium exchangers (NCXs). NCXs are secondary-active antiporters that power the translocation of Ca2+ across the cell membrane by coupling it to the flux of Na+ in the opposite direction, down an electrochemical gradient. Na+ and Ca2+ are translocated in separate steps of the antiport cycle, each of which is thought to entail a mechanism whereby i

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23

Newton, Jamila, Luli Rebecca Akinfiresoye, and Prosper N’Gouemo. "Inhibition of the Sodium Calcium Exchanger Suppresses Alcohol Withdrawal-Induced Seizure Susceptibility." Brain Sciences 11, no. 2 (February 23, 2021): 279. http://dx.doi.org/10.3390/brainsci11020279.

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Calcium influx plays important roles in the pathophysiology of seizures, including acoustically evoked alcohol withdrawal-induced seizures (AWSs). One Ca2+ influx route of interest is the Na+/Ca2+ exchanger (NCX) that, when operating in its reverse mode (NCXrev) activity, can facilitate Ca2+ entry into neurons, possibly increasing neuronal excitability that leads to enhanced seizure susceptibility. Here, we probed the involvement of NCXrev activity on AWS susceptibility by quantifying the effects of SN-6 and KB-R7943, potent blockers of isoform type 1 (NCX1rev) and 3 (NCX3rev), respectively. M

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Ibáñez, Ignacio, David Bartolomé-Martín, Dolores Piniella, Cecilio Giménez, and Francisco Zafra. "Activity dependent internalization of the glutamate transporter GLT-1 requires calcium entry through the NCX sodium/calcium exchanger." Neurochemistry International 123 (February 2019): 125–32. http://dx.doi.org/10.1016/j.neuint.2018.03.012.

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Limbu, Bijay, Kushal Shah, Seth H. Weinberg, and Makarand Deo. "Role of Cytosolic Calcium Diffusion in Murine Cardiac Purkinje Cells." Clinical Medicine Insights: Cardiology 10s1 (January 2016): CMC.S39705. http://dx.doi.org/10.4137/cmc.s39705.

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Cardiac Purkinje cells (PCs) are morphologically and electrophysiologically different from ventricular myocytes and, importantly, exhibit distinct calcium (Ca2+) homeostasis. Recent studies suggest that PCs are more susceptible to action potential (AP) abnormalities than ventricular myocytes; however, the exact mechanisms are poorly understood. In this study, we utilized a detailed biophysical mathematical model of a murine PC to systematically examine the role of cytosolic Ca2+ diffusion in shaping the AP in PCs. A biphasic spatiotemporal Ca2+ diffusion process, as recorded experimentally, wa

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Oceandy, D., P. J. Stanley, E. J. Cartwright, and L. Neyses. "The regulatory function of plasma-membrane Ca2+-ATPase (PMCA) in the heart." Biochemical Society Transactions 35, no. 5 (October 25, 2007): 927–30. http://dx.doi.org/10.1042/bst0350927.

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The PMCA (plasma-membrane Ca2+-ATPase) is a ubiquitously expressed calcium-extruding enzymatic pump important in the control of intracellular calcium concentration. Unlike in non-excitable cells, where PMCA is the only system for calcium extrusion, in excitable cells, such as cardiomyocytes, PMCA has been shown to play only a minor role in calcium homoeostasis compared with the NCX (sodium/calcium exchanger), another system of calcium extrusion. However, increasing evidence points to an important role for PMCA in signal transduction; of particular interest in cardiac physiology is the modulati

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TEWARI, SHIVENDRA G., and K. R. PARDASANI. "MODELING EFFECT OF SODIUM PUMP ON CALCIUM OSCILLATIONS IN NEURON CELLS." Journal of Multiscale Modelling 04, no. 03 (September 2012): 1250010. http://dx.doi.org/10.1142/s1756973712500102.

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Calcium plays a significant role in a number of processes like muscle contraction, gene expression, synaptic plasticity, signal transduction etc. but the significance of calcium oscillation is not yet completely understood in most of the cell types. A number of investigators have reported the oscillatory behavior of calcium due to intracellular concentration of inositol 1,4,5-trisphosphate (IP3). In this paper, an attempt has been made to study the oscillations induced in calcium due to dynamically changing membrane potential with special relevance to sodium pump. A mathematical model is devel

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Amran, M. S., N. Homma, and K. Hashimoto. "Effects of SEA0400 on Ouabain-induced Arrhythmias in Guinea Pigs." Journal of Scientific Research 4, no. 1 (December 26, 2011): 213. http://dx.doi.org/10.3329/jsr.v4i1.7722.

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The sodium-calcium exchange (NCX) is one of the major regulators of intracellular Ca2+ concentration in cardiac myocytes. The effects of NCX blockers as antiarrhythmic agents are still controversial. We investigated antiarrhythmic effects of SEA0400 (SEA), a novel NCX inhibitor, on ouabain-induced arrhythmias in guinea pigs. In the whole animal arrhythmia model, we observed effects of SEA on the ouabain-induced arrhythmia using ECG recordings. In the isolated myocyte, we observed action potential configurations and oscillations due to calcium overload using the current clamp method. In the who

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Barthmes, Maria, Jun Liao, Youxing Jiang, Andrea Brüggemann, and Christian Wahl-Schott. "Electrophysiological characterization of the archaeal transporter NCX_Mj using solid supported membrane technology." Journal of General Physiology 147, no. 6 (May 30, 2016): 485–96. http://dx.doi.org/10.1085/jgp.201611587.

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Sodium–calcium exchangers (NCXs) are membrane transporters that play an important role in Ca2+ homeostasis and Ca2+ signaling. The recent crystal structure of NCX_Mj, a member of the NCX family from the archaebacterium Methanococcus jannaschii, provided insight into the atomistic details of sodium–calcium exchange. Here, we extend these findings by providing detailed functional data on purified NCX_Mj using solid supported membrane (SSM)–based electrophysiology, a powerful but unexploited tool for functional studies of electrogenic transporter proteins. We show that NCX_Mj is highly selective

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Estacion, M., B. P. S. Vohra, S. Liu, J. Hoeijmakers, C. G. Faber, I. S. J. Merkies, G. Lauria, J. A. Black, and S. G. Waxman. "Ca2+ toxicity due to reverse Na+/Ca2+ exchange contributes to degeneration of neurites of DRG neurons induced by a neuropathy-associated Nav1.7 mutation." Journal of Neurophysiology 114, no. 3 (September 2015): 1554–64. http://dx.doi.org/10.1152/jn.00195.2015.

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Gain-of-function missense mutations in voltage-gated sodium channel Nav1.7 have been linked to small-fiber neuropathy, which is characterized by burning pain, dysautonomia and a loss of intraepidermal nerve fibers. However, the mechanistic cascades linking Nav1.7 mutations to axonal degeneration are incompletely understood. The G856D mutation in Nav1.7 produces robust changes in channel biophysical properties, including hyperpolarized activation, depolarized inactivation, and enhanced ramp and persistent currents, which contribute to the hyperexcitability exhibited by neurons containing Nav1.8

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Moonga, Baljit S., Robert Davidson, Li Sun, Olugbenga A. Adebanjo, James Moser, Mohammad Abedin, Neeha Zaidi, Christopher L. H. Huang, and Mone Zaidi. "Identification and Characterization of a Sodium/Calcium Exchanger, NCX-1, in Osteoclasts and Its Role in Bone Resorption." Biochemical and Biophysical Research Communications 283, no. 4 (May 2001): 770–75. http://dx.doi.org/10.1006/bbrc.2001.4870.

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Khananshvili, Daniel. "Sodium-calcium exchangers (NCX): molecular hallmarks underlying the tissue-specific and systemic functions." Pflügers Archiv - European Journal of Physiology 466, no. 1 (November 27, 2013): 43–60. http://dx.doi.org/10.1007/s00424-013-1405-y.

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Moon, H. S., E. Choi, and C. Hyun. "The Cardiac Sodium-Calcium Exchanger Gene (NCX-1) is a Potential Canine Cardiac Biomarker of Chronic Mitral Valvular Insufficiency." Journal of Veterinary Internal Medicine 22, no. 6 (November 2008): 1360–65. http://dx.doi.org/10.1111/j.1939-1676.2008.0209.x.

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Hassan, Mohamed Tarek, and Jonathan Lytton. "Potassium-dependent sodium-calcium exchanger (NCKX) isoforms and neuronal function." Cell Calcium 86 (March 2020): 102135. http://dx.doi.org/10.1016/j.ceca.2019.102135.

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35

Manunta, Paolo, Bruce P. Hamilton, and John M. Hamlyn. "Salt intake and depletion increase circulating levels of endogenous ouabain in normal men." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290, no. 3 (March 2006): R553—R559. http://dx.doi.org/10.1152/ajpregu.00648.2005.

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Abstract (sommario):

High-salt diets elevate circulating Na+ pump inhibitors, vascular resistance, and blood pressure. Ouabain induces a form of hypertension mediated via the α2-Na+ pump isoform and the calcium influx mode of the vascular sodium calcium exchanger (NCX). Whereas elevated levels of an endogenous ouabain (EO) and NCX have been implicated in salt-sensitive hypertension, acute changes in sodium balance do not affect plasma EO. This study investigated the impact of longer-term alterations in sodium balance on the circulating levels and renal clearance of EO in normal humans. Thirteen normal men consumed

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36

Pallafacchina, Giorgia, Sofia Zanin, and Rosario Rizzuto. "Recent advances in the molecular mechanism of mitochondrial calcium uptake." F1000Research 7 (November 28, 2018): 1858. http://dx.doi.org/10.12688/f1000research.15723.1.

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Abstract (sommario):

In the last few decades, a large body of experimental evidence has highlighted the complex role for mitochondria in eukaryotic cells: they are not only the site of aerobic metabolism (thus providing most of the ATP supply for endergonic processes) but also a crucial checkpoint of cell death processes (both necrosis and apoptosis) and autophagy. For this purpose, mitochondria must receive and decode the wide variety of physiological and pathological stimuli impacting on the cell. The “old” notion that mitochondria possess a sophisticated machinery for accumulating and releasing Ca2+, the most c

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37

Zhang, Weihua, Changqing Xu, Guangdong Yang, Lingyun Wu, and Rui Wang. "Interaction of H2S with Calcium Permeable Channels and Transporters." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/323269.

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Abstract (sommario):

A growing amount of evidence has suggested that hydrogen sulfide (H2S), as a gasotransmitter, is involved in intensive physiological and pathological processes. More and more research groups have found that H2S mediates diverse cellular biological functions related to regulating intracellular calcium concentration. These groups have demonstrated the reciprocal interaction between H2S and calcium ion channels and transporters, such as L-type calcium channels (LTCC), T-type calcium channels (TTCC), sodium/calcium exchangers (NCX), transient receptor potential (TRP) channels,β-adrenergic receptor

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38

Lariccia, Vincenzo, Silvia Piccirillo, Alessandra Preziuso, Salvatore Amoroso, and Simona Magi. "Cracking the code of sodium/calcium exchanger (NCX) gating: Old and new complexities surfacing from the deep web of secondary regulations." Cell Calcium 87 (May 2020): 102169. http://dx.doi.org/10.1016/j.ceca.2020.102169.

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39

Smith, L., H. Porzig, H. W. Lee, and J. B. Smith. "Phorbol esters downregulate expression of the sodium/calcium exchanger in renal epithelial cells." American Journal of Physiology-Cell Physiology 269, no. 2 (August 1, 1995): C457—C463. http://dx.doi.org/10.1152/ajpcell.1995.269.2.c457.

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Abstract (sommario):

The Na+/Ca2+ exchanger (NCE) contributes to Ca2+ reabsorption by connecting tubules of the nephron. A line of renal epithelial cells from monkey kidney (LLC-MK2) was used to investigate the regulation of NCE expression. After the activation of protein kinase C (PKC) by phorbol myristate acetate (PMA), NCE activity decreased exponentially by 75% in 48 h (half time approximately 19 h). PMA decreased NCE mRNA by 85% in 24 h. The decrease in NCE transcript preceded the downregulation of NCE activity. NCE protein was quantified with a monoclonal antibody to cardiac NCE. PMA decreased the binding of

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40

Groenke, Sabine, Eric D. Larson, Haruko Nakano, Atsushi Nakano, Catherine Proenza, Kenneth D. Philipson, and Joshua I. Goldhaber. "Atrial-Specific NCX KO Mice Reveal Dependence of Sinoatrial Node Pacemaker Activity on Sodium-Calcium Exchange." Biophysical Journal 102, no. 3 (January 2012): 663a. http://dx.doi.org/10.1016/j.bpj.2011.11.3612.

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41

Cantero-Recasens, Gerard, Cristian M. Butnaru, Nathalie Brouwers, Sandra Mitrovic, Miguel A. Valverde, and Vivek Malhotra. "Sodium channel TRPM4 and sodium/calcium exchangers (NCX) cooperate in the control of Ca2+-induced mucin secretion from goblet cells." Journal of Biological Chemistry 294, no. 3 (November 27, 2018): 816–26. http://dx.doi.org/10.1074/jbc.ra117.000848.

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42

Khananshvili, Daniel. "The SLC8 gene family of sodium–calcium exchangers (NCX) – Structure, function, and regulation in health and disease." Molecular Aspects of Medicine 34, no. 2-3 (April 2013): 220–35. http://dx.doi.org/10.1016/j.mam.2012.07.003.

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43

Nam, S. J., S. H. Han, H. W. Kim, and C. Hyun. "The Cardiac Biomarker Sodium-Calcium Exchanger (NCX-1) Can Differentiate between Heart Failure and Renal Failure: A Comparative Study of NCX-1 Expression in Dogs with Chronic Mitral Valvular Insufficiency and Azotemia." Journal of Veterinary Internal Medicine 24, no. 6 (November 2010): 1383–87. http://dx.doi.org/10.1111/j.1939-1676.2010.0628.x.

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44

Liu, Cuiping, Guoli Shao, Yirong Lu, Minmin Xue, Fenfen Liang, Zhenshu Zhang та Lan Bai. "Parathyroid Hormone-Related Protein (1-40) Enhances Calcium Uptake in Rat Enterocytes Through PTHR1 Receptor and Protein Kinase Cα/β Signaling". Cellular Physiology and Biochemistry 51, № 4 (2018): 1695–709. http://dx.doi.org/10.1159/000495674.

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Abstract (sommario):

Background/Aims: Parathyroid hormone-related protein (PTHrP) is implicated in regulating calcium homeostasis in vertebrates, including sea bream, chick, and mammals. However, the molecular mechanism underlying the function of PTHrP in regulating calcium transport is still not fully investigated. This study aimed to investigate the effect of PTHrP on the calcium uptake and its underlying molecular mechanism in rat enterocytes. Methods: The rat intestinal epithelial cell line (IEC-6) was used. Calcium uptake was determined by using the fluo-4 acetoxymethyl ester fluorescence method. The expressi

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45

Morales, Danna, Tamara Hermosilla та Diego Varela. "Calcium-dependent inactivation controls cardiac L-type Ca2+ currents under β-adrenergic stimulation". Journal of General Physiology 151, № 6 (27 лютого 2019): 786–97. http://dx.doi.org/10.1085/jgp.201812236.

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Abstract (sommario):

The activity of L-type calcium channels is associated with the duration of the plateau phase of the cardiac action potential (AP) and it is controlled by voltage- and calcium-dependent inactivation (VDI and CDI, respectively). During β-adrenergic stimulation, an increase in the L-type current and parallel changes in VDI and CDI are observed during square pulses stimulation; however, how these modifications impact calcium currents during an AP remains controversial. Here, we examined the role of both inactivation processes on the L-type calcium current activity in newborn rat cardiomyocytes in

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46

Kohajda, Zsófia, Nikolett Farkas-Morvay, Norbert Jost, Norbert Nagy, Amir Geramipour, András Horváth, Richárd S. Varga, et al. "The Effect of a Novel Highly Selective Inhibitor of the Sodium/Calcium Exchanger (NCX) on Cardiac Arrhythmias in In Vitro and In Vivo Experiments." PLOS ONE 11, no. 11 (November 10, 2016): e0166041. http://dx.doi.org/10.1371/journal.pone.0166041.

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47

Dave, Vijay, and Rohit Manchanda. "A computational model of the Ca2+ transients and influence of buffering in guinea pig urinary bladder smooth muscle cells." Journal of Bioinformatics and Computational Biology 15, no. 03 (April 20, 2017): 1750011. http://dx.doi.org/10.1142/s0219720017500111.

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Abstract (sommario):

Many cellular events including electrical activity and muscle contraction are regulated and coordinated by intracellular [Formula: see text] concentration ([[Formula: see text]][Formula: see text]. In detrusor smooth muscle (DSM) cells, [[Formula: see text]]i is normally maintained at very low levels and rises transiently during signalling processes as a result of (i) influx from the extracellular space (mainly via L-type and T-type [Formula: see text] channels) and (ii) [Formula: see text] release from sarcoplasmic reticulum (SR) into the cytoplasm. Intracellular [Formula: see text] buffers,

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48

Sobrinho, Cleyton R., Christopher M. Gonçalves, Ana C. Takakura, Daniel K. Mulkey, and Thiago S. Moreira. "Fluorocitrate-mediated depolarization of astrocytes in the retrotrapezoid nucleus stimulates breathing." Journal of Neurophysiology 118, no. 3 (September 1, 2017): 1690–97. http://dx.doi.org/10.1152/jn.00032.2017.

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Abstract (sommario):

Evidence indicates that CO2/H+-evoked ATP released from retrotrapezoid nucleus (RTN) astrocytes modulates the activity of CO2-sensitive neurons. RTN astrocytes also sense H+ by inhibition of Kir4.1 channels; however, the relevance of this pH-sensitive current remains unclear since ATP release appears to involve CO2-dependent gating of connexin 26 hemichannels. Considering that depolarization mediated by H+ inhibition of Kir4.1 channels is expected to increase sodium bicarbonate cotransporter (NBC) conductance and favor Ca2+ influx via the sodium calcium exchanger (NCX), we hypothesize that dep

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49

Schoenmakers, T. J., and G. Flik. "Sodium-extruding and calcium-extruding sodium/calcium exchangers display similar calcium affinities." Journal of Experimental Biology 168, no. 1 (July 1, 1992): 151–59. http://dx.doi.org/10.1242/jeb.168.1.151.

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Abstract (sommario):

Na+/Ca2+ exchange activities in purely inside-out and mixed inside-out and right-side-out fish enterocyte basolateral plasma membrane vesicle preparations display equal affinities for Ca2+, showing that only the intracellular Ca2+ transport site of the Na+/Ca2+ exchanger is detected in experiments on vesicle preparations with mixed orientation. Therefore, Ca2+ pump and Na+/Ca2+ exchange activity may be compared directly without correction for vesicle orientation. The Na+/Ca2+ exchange activity in fish enterocyte vesicles is compared to the activity found in dog erythrocyte vesicles. The calciu

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50

Pittner, János, Kristie Rhinehart, and Thomas L. Pallone. "Ouabain modulation of endothelial calcium signaling in descending vasa recta." American Journal of Physiology-Renal Physiology 291, no. 4 (October 2006): F761—F769. http://dx.doi.org/10.1152/ajprenal.00326.2005.

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Abstract (sommario):

Using fura 2-loaded vessels, we tested whether ouabain modulates endothelial cytoplasmic calcium concentration ([Ca2+]CYT) in rat descending vasa recta (DVR). Over a broad range between 10−10 and 10−4 M, ouabain elicited biphasic peak and plateau [Ca2+]CYT elevations. Blockade of voltage-gated Ca2+ entry with nifedipine did not affect the response to ouabain mitigating against a role for myo-endothelial gap junctions. Reduction of extracellular Na+ concentration ([Na+]o) or Na+/Ca2+ exchanger (NCX) inhibition with SEA-0400 (10−6 M) elevated [Ca2+]CYT, supporting a role for NCX in the setting o

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