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Mutations in ATP1A1 cause the excessive autonomous aldosterone secretion of Aldosterone-producing Adenomas.
Cardiotonic steroids activate NF-kappaB (show NFKB1 Proteins) leading to proinflammatory cytokine production in primary macrophages through a signaling complex, including CD36 (show CD36 Proteins), TLR4 (show TLR4 Proteins), and Na/K-ATPase.
This study reports molecular dynamic simulations of the human NaK-ATPase alpha1 beta 1 isoform embedded into 1,2-oleoylphosphatidylcholine bilayer.
Data show that the expression of aquaporin (AQP) 1, AQP3, AQP5, epithelial Na+ channel (ENaC) and sodium potassium ATPase (Na-K-ATPase) are altered in patients with acute respiratory failure (ARF) due to diffuse alveolar damage (DAD), and the cause of DAD does not seem to influence the level of impairment of these channels.
Ouabain stimulates NKA (show TAC1 Proteins) in renal proximal tubule cells through an angiotensin/AT1R (show AGTR1 Proteins)-dependent mechanism and that this pathway contributes to cardiac glycoside associated hypertension.
Reduction in ATP1A1 expression levels is related to major depressive disorder anxiety score.
Our current findings demonstrate that Arctigenin is an antagonist of MR and effectively decreases the Na/K-ATPase 1 gene expression. Our work provides a hint for the drug discovery against cardiovascular disease
Data suggest that targeting Na(+)/K(+) ATPase alpha-1 subunit (ATP1A1) is a approach to the treatment of hepatocellular carcinoma (HCC (show FAM126A Proteins)).
Mutations in ATP1A1 gene is associated with aldosterone-producing adenomas.
Gal-3 (show LGALS3 Proteins) interacts with ATP1A1 and induces the phosphorylation of MDR1, mediating multidrug resistance.
The findings are consistent with previous studies that indicate a link between Na,K-ATPase activity and SFK signaling.
Uroguanylin (show GUCA2B Proteins) modulates (Na++K+)ATPase in a proximal tubule cells via cGMP/protein kinase (show CDK7 Proteins) G, cAMP/protein kinase A, and mTOR (show FRAP1 Proteins) pathways.
Data indicate that magnesium fluoride, magnesium fluoride and Na,K-ATPase form a very stable complex in the E2 conformation.
Data indicate that Rb(+) can be occluded through Na(+)/K(+)-ATPase cycling mode that takes place in the absence of Na(+) ions.
Expression of mutant alpha1 Na/K-ATPase defective in conformational transition attenuates Src (show SRC Proteins)-mediated signal transduction
re-arrangements of the Na+,K+-ATPase stabilized by cardiotonic steroids may affect protein-protein interactions within the intracellular signal transduction networks
Data indicate that the transmembrane domain of the Na+/K+ -ATPase in the E1 state is less exposed to the lipids than in E2.
The plasma membrane Na/K-ATPase-caveolin-1 (show CAV1 Proteins) interaction may represent an important sensing mechanism by which the cells regulate the sterol regulatory element-binding protein (show CNBP Proteins) pathway.
Investigations of K(+)-occlusion by the phosphoenzyme of Na(+),K(+)-ATPase from shark rectal gland and pig kidney by stopped-flow fluorimetry reveal major differences in the kinetics of the two enzymes.
The results indicate that PKC (show FYN Proteins) could be the final target and an integrator molecule of different signaling pathways triggered by angiotensin II (Ang II), which could explain the sustained activation of Na(+)-ATPase by Ang II (show AGT Proteins).
Suggest ATP1A1 has a central role in the osmoregulatory response of nucleus pulposus cells.
The ATP1A1 gene polymorphism has potential as a marker for mastitis resistance in dairy cattle.
The polymorphisms within the coding region of bovine ATP1A1 gene, were analyzed.
ATP1A1 gene polymorphism has a role in heat tolerance traits in dairy cattle
The C-terminal contacts of Xenopus Na,K-ATPase alpha-1 provide important stabilization of the occluded E1P(Na3) pump conformation, regardless of the route of Na ion entry into the binding pocket.
Na,K-ATPase interaction with magnesium ions
Altered localization of Na-K-ATPase as a result of transcriptional down-regulation of ankyrin-G mediates the down-regulation of Na-K-ATPase activity during chronic intestinal inflammation.
Pb(2+) ions are able to confine the Na(+),K(+)-ATPase into a phosphorylated E(2) state.
Study identified the Na+/K+-ATPase alpha 1 and 3 subunits as receptors for the extracellular fragment of GPNMB that mediates activation of cellular signaling pathways and subsequent neuroprotective effects.
effects of endogenous acetylcholine on alveolar fluid clearance are likely mediated by Na,K-ATPase function through activation of muscarinic acetylcholine receptors on alveolar epithelia
Oxidized LDL-bound CD36 (show CD36 Proteins) recruits an Na/K-ATPase-Lyn (show LYN Proteins) complex in macrophages that promotes atherosclerosis.
TGFbeta1 (show TGFB1 Proteins) is a powerful regulator of megakaryocytic Na+/K+ ATPase activity.
Inhibition of the Na+/K+-ATPase pathway in astrocytes leads to rearrangement of cytoskeleton.
Reduction of Na/K-ATPase affects cardiac remodeling and increases c-kit cell abundance in partial nephrectomized mice.
Enhanced Na+ entry did not alter Na,K-ATPase a1 mRNA level in tranfected mCDD cells. Post-transcriptional control of Na,K-ATPase abundance is effected by lysosomal degradation.
This coupling of astrocytic A2ARs to the regulation of glutamate (show GRIN1 Proteins) transport through modulation of NKA (show TAC1 Proteins)-alpha2 activity provides a novel mechanism linking neuronal activity to ion homeostasis controlling glutamatergic activity.
Concurrent impairment of Na(+)+K(+)-ATPase function in multi-organ may serve as one of the molecular pathways participating in and contributing to the mechanism of type-1 diabetes-induced complications in NOD mice.
Data identify the K+-independent, ouabain-insensitive Na+-ATPase as a unique P-type ATPase (show ATP7A Proteins).
The protein encoded by this gene belongs to the family of P-type cation transport ATPases, and to the subfamily of Na+/K+ -ATPases. Na+/K+ -ATPase is an integral membrane protein responsible for establishing and maintaining the electrochemical gradients of Na and K ions across the plasma membrane. These gradients are essential for osmoregulation, for sodium-coupled transport of a variety of organic and inorganic molecules, and for electrical excitability of nerve and muscle. This enzyme is composed of two subunits, a large catalytic subunit (alpha) and a smaller glycoprotein subunit (beta). The catalytic subunit of Na+/K+ -ATPase is encoded by multiple genes. This gene encodes an alpha 1 subunit. Multiple transcript variants encoding different isoforms have been found for this gene.
, (Na+ + K+)-ATPase
, Na(+)/K(+) ATPase alpha-1 subunit
, sodium pump subunit alpha-1
, sodium/potassium-transporting ATPase subunit alpha-1
, Na+, K+ ATPase alpha subunit
, Na+/K+ ATPase 1
, Na, K-ATPase, alpha-A catalytic polypeptide
, Na,K-ATPase alpha-1 subunit
, Na,K-ATPase catalytic subunit alpha-A protein
, sodium pump 1
, sodium-potassium ATPase catalytic subunit alpha-1
, sodium-potassium-ATPase, alpha 1 polypeptide
, ATPase, Na+K+ transporting, alpha 1
, (Na+, K+)-ATPase alpha-subunit
, Na+/K+ transporting alpha 1 polypeptide
, sodium/potassium-transporting ATPase alpha-1 chain
, Na+-K+-ATPase alpha 1 subunit
, Na+/K+ ATPase
, Na+K+ ATPase
, Na+/K+ -ATPase alpha 1 subunit
, Na/K ATPase alpha 1 subunit
, sodium/potassium-ATPase alpha-subunit 1
, alpha1 subunit of equine Na/K ATPase
, horse alpha-1 subunit of Na,K-ATPase