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Structure-Dynamic Coupling Through Ca(2+)-Binding Regulatory Domains of Mammalian NCX Isoform/Splice Variants
The results show that estrogen upregulates cardiac L-type Ca(2+) and sodium-calcium exchange in women through genomic mechanisms that account for sex differences in Ca(2+) handling and spatial heterogeneities of repolarization due to base-apex heterogeneities of Cav1.2alpha and NCX1. By analogy with rabbit studies, these effects account for human sex-difference in arrhythmia risk.
Diacylglycerol generation downstream of VEGF receptors activatesTRPC3 causing Na(+) influx with subsequent reversal of NCX1, ERK1/2 activation and ultimately contributes to enhanced angiogenesis.
NCX1 expression correlates with the smoking status of esophageal squamous cell carcinoma patients, and NNK activates the Ca2+ entry mode of NCX1 in ESCC cells, leading to cell proliferation and migration
We also observed that acetylcholine attenuated the formation of NCX1-TRPC3-IP3R1 complexes and maintained calcium homeostasis in cells treated with TNF-alpha.
SLC8A1 polymorphisms alter calcium flux in cells that mediate coronary artery damage in Kawasaki disease.
CaSR exerts a suppressive function in pancreatic tumorigenesis through a novel NCX1/Ca(2+)/beta-catenin signaling pathway.
Palmitoylation of cardiac NCX1 can modify its function, physical interactions, and removal from the sarcolemma by domain-dependent endocytosis.
NCX1 and the calcium binding protein calretinin cooperate within the striatum to confer tolerance against cerebral ischemia.
ADD2 and NCX1 variants influence the risk and the clinical features of systemic lupus erythematosus and lupus nephritis.
NCX1 operating in reverse mode plays a prominent role in calcium cytosolic regulation in highly metastatic melanoma cells.
The expression of miR-206 by HUVECs reduced exosome production by regulating ADP-Ribosylation Factor 6 (ARF6) and sodium/calcium exchanger 1 (NCX1).
interaction of NHE1, NCX1 and CaM mediates the effects of IL6 on human hepatocellular carcinoma
NCX1.3 is the predominant NCX variant in the distal convoluted and connecting tubules tubules
results demonstrate that CaM senses changes in [Ca2+]i and binds to the cytoplasmic loop of NCX1 to regulate exchange activity.
The expressions of NCX1 and NCKX4 were significantly higher in the patent ductus arteriosus group at both the protein and mRNA levels.
Down-regulation of the SLC8A1 gene, most likely mediated by its regulator miR-223, can lead to decreased calcium in penile carcinoma and consequently to suppressed apoptosis and increased tumor cell proliferation
These data confirm the role of NCX1 activity in regulating renal epithelial cell migration.
Three novel loci were identified in East Asians with cardiac arrhythmias: rs2483280 (PRDM16 locus) and rs335206 (PRDM6 locus) were associated with QRS duration; and rs17026156 (SLC8A1 locus) correlated with PR interval.
There is a functional role of sodium-calcium exchanger SLC8A1 in human atrial and atrioventricular nodal conduction as suggested by genetically modified mouse models.
the increased CaMKII activity and consequent c-Fos expression likely account for the dysregulation of amygdala-dependent cued fear memory in NCX1(+/-) mice.
These findings indicate that NCX1 may play a role in maintaining patent DA not only by preventing DA functional closure through reducing cytosolic Ca(2+) level in DASMC but also by delaying the anatomical closure process.
present study highlights the significant role of NCX in the evolution of neonatal brain injury and in the learning and memory processes that are impaired in mice injured in the neonatal period
Pin1 serves as a modulator of SERCA2a and Na(2+)/Ca(2+) exchanger 1 Ca(2+) handling proteins, with loss of function resulting in impaired cardiomyocyte relaxation
NCX1 (and NCX2) are expressed in neurons that regulate the motility of the gastric fundus.
Induced overexpression of NCX1 attenuated pressure overload-induced pathological cardiac remodelling
The heterogeneous expression of multiple types of Na(+)/Ca(2+) exchangers and the quantitative differences found in calcium concentration, together with other risk factors specific to dopaminergic neurons such as dopamine oxidation resulting in oxidative stress, may drive these cells to undergo selective degeneration.
NCX1 is dispensable for osteoclast differentiation.
the functional role of NCX on gastrointestinal motility
These results suggested that NCX1 may play an important role in the proper spatial distribution of LTCC and JP2 in T-tubules in the context of pressure-overloading.
In this study, authors demonstrate that NCX1 regulates gastric fundus motility.
NCX1 and NCX2 play important roles in ileal motility and suggest that NCX1 and NCX2 regulate the motility in the ileum by controlling the sensitivity of smooth muscles to ACh and SP.
Data show that transforming growth factor beta1 (TGFbeta1) is a powerful stimulator of both, store operated Ca2+ entry (SOCE) and Na+/Ca2+-exchanger activity in megakaryocytes.
dobutamine upregulates of voltage-gated Na+ channel function and Na+ influx-induced activation of the reverse mode of NCX
JAK3 deficiency is followed by down-regulation of cytosolic Ca(2+) release, receptor and store operated Ca(2+) entry and Na(+)/Ca(2+) exchanger activity in dendritic cells.
Results suggested that down-regulation of hippocampal NCX1 expression is associated with pentylenetetrazole-induced kindling seizure development
TRPC3-NCX micro/nanodomain communication as determinant of cardiac contractility and susceptibility to arrhythmogenic stimuli.
cellular Ca accumulation hinders spontaneous depolarization in the NCX knockout sinoatrial node, possibly by inhibiting L-type Ca currents.
thrombin-induced ERK1/2 activation required NADPH oxidase 2-mediated reactive oxygen species (ROS) production, and reverse-mode NCX inhibitors and NCX1 siRNA suppressed thrombin-induced ROS production
NCX1 plays an important role in smooth muscle motility in the mouse distal colon.
These results indicate that, for a proper MgATP up-regulation of NCX1, the enzyme responsible for PtdIns-4,5P2 synthesis must be (i) functionally competent and (ii) set in the NCX1 microenvironment closely associated to the exchanger.
The cleavage of NCX1 by m-calpain in the caveolae vesicles may be interpreted as an important mechanism of Ca(2+) overload
a novel mechanism for the regulation of NCX1 activity
Na/Ca exchanger's (NCX1) associates specifically with caveolin-3(NCX1)(caveolin-3)
the regulation of phosphatidylinositol-4,5-biphosphate binding to the bovine cardiac Na+/Ca2+ exchanger(NCX1)
Data suggest that peroxynitrite leads to calcium (Ca2+) uptake through stimulation of Ca2+-ATPase, but inhibits Ca2+ uptake through inhibition of the sodium-Ca2+ exchanger, resulting in decreased overall Ca2+ uptake in smooth muscle microsomes.
These data suggest a role for the reverse mode of the NCX in refilling the sarcoplasmic reticulum in airway smooth muscle following Ca(2+) mobilization.
Cleavage of NCX may be interpreted as the main cause of Ca(2+) overload and could lay a key role in activation of apoptotic processes in pulmonary smooth muscle.
The SOCE/Cl(Ca) interaction does not require reverse-mode Na+/Ca2+ exchange in our conditions.
There were substantial transmural gradients in Cav1.2, KChIP2, ERG, KvLQT1, Kir2.1, NCX1, SERCA2a and RyR2 at the mRNA and, in some cases, protein level-in every case the mRNA or protein was more abundant in the epicardium than the endocardium.
NCX is an important determinant for premature ventricular activity in a drug-induced model of Andersen-Tawil syndrome.
In cardiac myocytes, Ca(2+) concentrations alternate between high levels during contraction and low levels during relaxation. The increase in Ca(2+) concentration during contraction is primarily due to release of Ca(2+) from intracellular stores. However, some Ca(2+) also enters the cell through the sarcolemma (plasma membrane). During relaxation, Ca(2+) is sequestered within the intracellular stores. To prevent overloading of intracellular stores, the Ca(2+) that entered across the sarcolemma must be extruded from the cell. The Na(+)-Ca(2+) exchanger is the primary mechanism by which the Ca(2+) is extruded from the cell during relaxation. In the heart, the exchanger may play a key role in digitalis action. The exchanger is the dominant mechanism in returning the cardiac myocyte to its resting state following excitation.
Na(+)/Ca(2+)-exchange protein 1
, Na+/Ca++ exchanger
, Na+/Ca2+ exchanger
, sodium/calcium exchanger 1
, Na/Ca exchanger
, sodium/calcium exchanger isoform NaCa7
, Na-Ca exchanger
, solute carrier family 8, member 1
, sodium-calcium exchanger
, solute carrier family 8 (sodium/calcium exchanger), member 1
, sodium calcium exchanger 1n
, sodium/calcium exchanger
, sodium/calcium exchanger 1-like
, sodium/calcium exchanger isoform NaCa13
, sodium/calcium exchanger isoform NaCa3
, sodium/calcium exchanger isoform NaCa9
, solute carrier family 8 member 1