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The results show that estrogen upregulates cardiac L-type Ca(2 (Montrer CA2 Protéines)+) and sodium-calcium exchange in women through genomic mechanisms that account for sex differences in Ca(2 (Montrer CA2 Protéines)+) handling and spatial heterogeneities of repolarization due to base-apex (Montrer APEX1 Protéines) 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.
The results show that estrogen upregulates cardiac ICa,L and sodium-calcium exchange (INCX) in women through genomic mechanisms that account for sex differences in Ca(2 (Montrer CA2 Protéines)+) handling and spatial heterogeneities of repolarization due to base-apex (Montrer APEX1 Protéines) heterogeneities of Cav1.2alpha and NCX1.
NCX1 expression correlates with the smoking status of esophageal squamous cell carcinoma patients, and NNK activates the Ca2 (Montrer CA2 Protéines)+ entry mode of NCX1 in ESCC cells, leading to cell proliferation and migration
We also observed that acetylcholine attenuated the formation of NCX1-TRPC3 (Montrer TRPC3 Protéines)-IP3R1 (Montrer ITPR1 Protéines) complexes and maintained calcium homeostasis in cells treated with TNF-alpha (Montrer TNF Protéines).
SLC8A1 polymorphisms alter calcium flux in cells that mediate coronary artery damage in Kawasaki disease.
CaSR (Montrer CASR Protéines) exerts a suppressive function in pancreatic tumorigenesis through a novel NCX1/Ca(2 (Montrer CA2 Protéines)+)/beta-catenin (Montrer CTNNB1 Protéines) 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 (Montrer CETN1 Protéines) calretinin (Montrer CALB2 Protéines) cooperate within the striatum to confer tolerance against cerebral ischemia.
ADD2 (Montrer ADD2 Protéines) and NCX1 variants influence the risk and the clinical features of systemic lupus erythematosus and lupus nephritis.
Pin1 (Montrer PIN1 Protéines) serves as a modulator of SERCA2a (Montrer ATP2A2 Protéines) and Na(2+)/Ca(2 (Montrer CA2 Protéines)+) exchanger 1 Ca(2 (Montrer CA2 Protéines)+) 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 (Montrer CA2 Protéines)+) 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 (Montrer JPH2 Protéines) 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 (Montrer FGFR3 Protéines) and SP.
Data show that transforming growth factor beta1 (TGFbeta1 (Montrer TGFB1 Protéines)) is a powerful stimulator of both, store operated Ca2 (Montrer CA2 Protéines)+ entry (SOCE) and Na+/Ca2+-exchanger activity in megakaryocytes.
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 (Montrer CAPN2 Protéines) in the caveolae vesicles may be interpreted as an important mechanism of Ca(2 (Montrer CA2 Protéines)+) overload
a novel mechanism for the regulation of NCX1 activity
Na/Ca exchanger's (NCX1) associates specifically with caveolin-3 (Montrer CAV3 Protéines)(NCX1)(caveolin-3 (Montrer CAV3 Protéines))
the regulation of phosphatidylinositol-4,5-biphosphate binding to the bovine cardiac Na+/Ca2+ exchanger(NCX1)
Data suggest that peroxynitrite leads to calcium (Ca2 (Montrer CA2 Protéines)+) uptake through stimulation of Ca2+-ATPase, but inhibits Ca2 (Montrer CA2 Protéines)+ uptake through inhibition of the sodium-Ca2 (Montrer CA2 Protéines)+ exchanger, resulting in decreased overall Ca2 (Montrer CA2 Protéines)+ 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 (Montrer CA2 Protéines)+) mobilization.
Cleavage of NCX may be interpreted as the main cause of Ca(2 (Montrer CA2 Protéines)+) 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 (Montrer CA2 Protéines)+ 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