Relevant bibliographies by topics / NCX3 knockout mouse

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'NCX3 knockout mouse'

Author: Grafiati
Published: 4 June 2021
Last updated: 3 February 2022

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Journal articles on the topic "NCX3 knockout mouse"

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Zhang, Jin, Chongyu Ren, Ling Chen, Manuel F. Navedo, Laura K. Antos, Stephen P. Kinsey, Takahiro Iwamoto, et al. "Knockout of Na+/Ca2+ exchanger in smooth muscle attenuates vasoconstriction and L-type Ca2+ channel current and lowers blood pressure." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 5 (May 2010): H1472—H1483. http://dx.doi.org/10.1152/ajpheart.00964.2009.

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Mice with smooth muscle (SM)-specific knockout of Na+/Ca2+ exchanger type-1 (NCX1SM−/−) and the NCX inhibitor, SEA0400, were used to study the physiological role of NCX1 in mouse mesenteric arteries. NCX1 protein expression was greatly reduced in arteries from NCX1SM−/− mice generated with Cre recombinase. Mean blood pressure (BP) was 6–10 mmHg lower in NCX1SM−/− mice than in wild-type (WT) controls. Vasoconstriction was studied in isolated, pressurized mesenteric small arteries from WT and NCX1SM−/− mice and in heterozygotes with a global null mutation (NCX1Fx/−). Reduced NCX1 activity was ma
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Koo, T. H., and E. B. Jeung. "148 DIFFERENTIAL REGULATION OF CALCIUM TRANSPORT GENES, I.E., Na+/Ca2+ EXCHANGERS, TRANSIENT RECEPTOR POTENTIAL CATION CHANNEL 6 AND CALBINDINS, IN THE DIVERSE PLACENTAL TISSUES OF CALBINDIN-D9k AND -28k KNOCKOUT MICE VIA PUTATIVE STEROIDS." Reproduction, Fertility and Development 24, no. 1 (2012): 186. http://dx.doi.org/10.1071/rdv24n1ab148.

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During pregnancy, the placenta represents the establishment of an intimate connection between mother and fetus that is specific to mammals. Calbindins [Calbindin-D9k (CaBP-9k) and -D28k (CaBP-28k)] are proteins possessing EF-hand motifs that have a high affinity for Ca2+ ions and play an important role in the regulation and buffering of Ca2+ in the various tissues. Many types of calcium channels, intracellular calcium binding proteins, Na+/Ca2+ exchangers (NCX) and transient receptor potential cation channels (TRPV) have been found in the placenta. In this study, the calcium channel in materna
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Pott, Christian, Xiaoyan Ren, Diana X. Tran, Ming-Jim Yang, Scott Henderson, Maria C. Jordan, Kenneth P. Roos, Alan Garfinkel, Kenneth D. Philipson, and Joshua I. Goldhaber. "Mechanism of shortened action potential duration in Na+-Ca2+ exchanger knockout mice." American Journal of Physiology-Cell Physiology 292, no. 2 (February 2007): C968—C973. http://dx.doi.org/10.1152/ajpcell.00177.2006.

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In cardiac-specific Na+-Ca2+ exchanger (NCX) knockout (KO) mice, the ventricular action potential (AP) is shortened. The shortening of the AP, as well as a decrease of the L-type Ca2+ current ( ICa), provides a critical mechanism for the maintenance of Ca2+ homeostasis and contractility in the absence of NCX (Pott C, Philipson KD, Goldhaber JI. Excitation-contraction coupling in Na+-Ca2+ exchanger knockout mice: reduced transsarcolemmal Ca2+ flux. Circ Res 97: 1288–1295, 2005). To investigate the mechanism that underlies the accelerated AP repolarization, we recorded the transient outward curr
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Bai, Yan, Eric E. Morgan, David R. Giovannucci, Sandrine V. Pierre, Kenneth D. Philipson, Amir Askari, and Lijun Liu. "Different roles of the cardiac Na+/Ca2+-exchanger in ouabain-induced inotropy, cell signaling, and hypertrophy." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 3 (February 1, 2013): H427—H435. http://dx.doi.org/10.1152/ajpheart.00462.2012.

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Previous studies have shown that digitalis drugs, acting as specific inhibitors of cardiac Na+/K+-ATPase, not only cause positive inotropic effects, but also activate cell signaling pathways that lead to cardiac myocyte hypertrophy. A major aim of this work was to assess the role of Na+/Ca2+-exchanger, NCX1, in the above two seemingly related drug effects. Using a mouse with ventricular-specific knockout (KO) of NCX1, ouabain-induced positive inotropy that was evident in isolated wild-type (Wt) hearts was clearly reduced in KO hearts. Ouabain also increased Ca2+ transient amplitudes in Wt myoc
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Song, Jianliang, Xue-Qian Zhang, JuFang Wang, Ellina Cheskis, Tung O. Chan, Arthur M. Feldman, Amy L. Tucker, and Joseph Y. Cheung. "Regulation of cardiac myocyte contractility by phospholemman: Na+/Ca2+ exchange versus Na+-K+-ATPase." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 4 (October 2008): H1615—H1625. http://dx.doi.org/10.1152/ajpheart.00287.2008.

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Phospholemman (PLM) regulates cardiac Na+/Ca2+ exchanger (NCX1) and Na+-K+-ATPase in cardiac myocytes. PLM, when phosphorylated at Ser68, disinhibits Na+-K+-ATPase but inhibits NCX1. PLM regulates cardiac contractility by modulating Na+-K+-ATPase and/or NCX1. In this study, we first demonstrated that adult mouse cardiac myocytes cultured for 48 h had normal surface membrane areas, t-tubules, and NCX1 and sarco(endo)plasmic reticulum Ca2+-ATPase levels, and retained near normal contractility, but α1-subunit of Na+-K+-ATPase was slightly decreased. Differences in contractility between myocytes i
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Lux, Christopher, Kathleen McGrath, Simon Conway, James Palis, and Mervin C. Yoder. "Circulation Plays an Essential Role in Distributing Mammalian Yolk Sac Definitive Hematopoietic Progenitor Cells to the Embryo Proper; Using the Ncx1 Knockout Mouse Model To Prevent Circulation." Blood 106, no. 11 (November 16, 2005): 517. http://dx.doi.org/10.1182/blood.v106.11.517.517.

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Abstract The yolk sac is the lone site of primitive hematopoiesis. The role of the yolk sac in generating definitive hematopoietic progenitors, however, has remained controversial. One complicating factor preventing an accurate investigation of this subject has been the onset of early circulation which alters the localization of hematopoietic progenitors. An Ncx1 knockout mouse (which fails to initiate a heartbeat) is used here to investigate the temporal and spatial distribution of definitive hematopoietic progenitor cells (HPCs: adult type BFU-E, CFU-GM, CFU-GEMM) in an environment lacking c
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Rhodes, Katrin E., Christos Gekas, Yanling Wang, Christopher T. Lux, Cameron S. Francis, Simon Conway, Stuart H. Orkin, Mervin C. Yoder, and Hanna K. A. Mikkola. "Hematopoietic Stem Cells Emerge in the Placental Vasculature in the Absence of Circulation." Blood 110, no. 11 (November 16, 2007): 1258. http://dx.doi.org/10.1182/blood.v110.11.1258.1258.

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Abstract The placenta was recently unveiled as an important hematopoietic organ, harboring a large pool of HSCs during midgestation. Yet, it has not been defined whether the placenta can generate HSCs de novo. By using the Runx1-LacZ and Ncx1 knockout mouse models we show that the placenta is a site of HSC generation and identify the cellular niches in which placental HSCs reside. Runx1 is essential for the emergence of definitive HSCs and remains expressed in HSCs throughout fetal development and adult life. Analysis of Runx1LacZ/+ and Runx1LacZ/LacZ placental sections nominated the large ves
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Myeong, Go Seon, Donglin Yi, Jae-Hwan Lee, Yeong-Min Yoo, and Eui-Bae Jeung. "Gene expression of claudins in NCKX3 knockout mouse." Endocrine Abstracts, August 21, 2020. http://dx.doi.org/10.1530/endoabs.70.aep214.

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Lotteau, Sabine, Rui Zhang, Adina Hazan, Christina Grabar, Devina Gonzalez, Stephan Aynaszyan, Kenneth D. Philipson, Michela Ottolia, and Joshua I. Goldhaber. "Acute Genetic Ablation of Cardiac Sodium/Calcium Exchange in Adult Mice: Implications for Cardiomyocyte Calcium Regulation, Cardioprotection, and Arrhythmia." Journal of the American Heart Association 10, no. 17 (September 7, 2021). http://dx.doi.org/10.1161/jaha.120.019273.

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Background Sodium‐calcium (Ca 2+ ) exchanger isoform 1 (NCX1) is the dominant Ca 2+ efflux mechanism in cardiomyocytes and is critical to maintaining Ca 2+ homeostasis during excitation‐contraction coupling. NCX1 activity has been implicated in the pathogenesis of cardiovascular diseases, but a lack of specific NCX1 blockers complicates experimental interpretation. Our aim was to develop a tamoxifen‐inducible NCX1 knockout (KO) mouse to investigate compensatory adaptations of acute ablation of NCX1 on excitation‐contraction coupling and intracellular Ca 2+ regulation, and to examine whether ac
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Boegeholz, N., V. Knappe, P. Pauls, G. Nickenig, L. Eckardt, J. W. Schrickel, and T. B. Beiert. "P1595Increased in vivo perpetuation of whole-heart ventricular arrhythmia in heterozygous Na+/Ca2+-exchanger knockout mice." European Heart Journal 40, Supplement_1 (October 1, 2019). http://dx.doi.org/10.1093/eurheartj/ehz748.0354.

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Abstract Background Commonly, innovative antiarrhythmic strategies are derived from single cell studies that frequently yield promising in vitro findings. However, these results may differ on the whole-heart level, since multicellular electrophysiology is characterized by several emergent features. In previous cellular studies, we have identified the Na+/Ca2+-exchanger (NCX) as a promising target for an innovative antiarrhythmic strategy, as NCX upregulation is present in major cardiac diseases (e.g. heart failure) and promotes independently cellular early and late afterdepolarizations (EADs a
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Dissertations / Theses on the topic "NCX3 knockout mouse"

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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 d
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