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anti-Human ATP1A1 Antibodies:
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Cow (Bovine) Monoclonal ATP1A1 Primary Antibody for FACS, ICC - ABIN152492
Burgess, Parkinson, Racke, Hirsch-Reinshagen, Fan, Wong, Stukas, Theroux, Chan, Donkin, Wilkinson, Balik, Christie, Poirier, Lütjohann, Demattos, Wellington: ABCG1 influences the brain cholesterol biosynthetic pathway but does not affect amyloid precursor protein or apolipoprotein E metabolism in vivo. in Journal of lipid research 2008
Show all 85 Pubmed References
Human Polyclonal ATP1A1 Primary Antibody for IF, IHC - ABIN6711994
Xie, Zhang, Li, Fan, Zhang, Mu, Li, Xu, Zhao, Jin, Li: Sodium tanshinone iia sulfonate attenuates seawater aspiration-induced acute pulmonary edema by up-regulating Na(+),K(+)-ATPase activity. in Experimental lung research 2012
Show all 3 Pubmed References
Rat (Rattus) Polyclonal ATP1A1 Primary Antibody for WB - ABIN1882162
Hara, Urayama, Kawakami, Nojima, Nagamune, Kojima, Ohta, Nagano, Nakao: Primary structures of two types of alpha-subunit of rat brain Na+,K+,-ATPase deduced from cDNA sequences. in Journal of biochemistry 1987
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Human Polyclonal ATP1A1 Primary Antibody for WB - ABIN6674053
Li, Liu, Yang, Fu, Zhao, Shen, Miao, Rayner, Chavanas, Zhu, Britt, Tang, McVoy, Luo: Human Cytomegalovirus Infection Dysregulates the Localization and Stability of NICD1 and Jag1 in Neural Progenitor Cells. in Journal of virology 2015
Human Polyclonal ATP1A1 Primary Antibody for IF, IHC - ABIN6713019
Xu, Hu, Zhao, Gao, Jiang, Liu, Liu, Huang: Quercetin differently regulates insulin-mediated glucose transporter 4 translocation under basal and inflammatory conditions in adipocytes. in Molecular nutrition & food research 2014
Human Polyclonal ATP1A1 Primary Antibody for WB - ABIN6676925
Wang, Niu, Liu, Yuan, Liu, Fu: Exercise improves glucose uptake in murine myotubes through the AMPKα2-mediated induction of Sestrins. in Biochimica et biophysica acta. Molecular basis of disease 2018
mutations in ATP1A1, which encodes the alpha1 subunit of the Na(+),K(+)-ATPase, are identified as a cause of autosomal-dominant CMT2.
Low ATP1A1 expression is associated with renal cell carcinoma.
These data suggest the role of beta-amyloid as a novel physiological regulator of Na,K-ATPase.
induction of a novel pathway (alpha1-AMPK-ULK1) induces autophagy as a host-directed strategy for HCMV inhibition.IMPORTANCE
An antibody against the extracellular DR region (897-911) of Na(+)-K(+)-ATPase subunit alpha 1 disrupted the Na+-K+-ATPase/ROS amplifier and protected cultured cardiomyocytes from ROS-induced injury.
Disruption of Ankyrin B and Caveolin-1 Interaction Sites Alters Na(+),K(+)-ATPase Membrane Diffusion
Mutations in ATP1A1 cause the excessive autonomous aldosterone secretion of Aldosterone-producing Adenomas.
Cardiotonic steroids activate NF-kappaB leading to proinflammatory cytokine production in primary macrophages through a signaling complex, including CD36, TLR4, 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 in renal proximal tubule cells through an angiotensin/AT1R-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).
Mutations in ATP1A1 gene is associated with aldosterone-producing adenomas.
Gal-3 interacts with ATP1A1 and induces the phosphorylation of MDR1, mediating multidrug resistance.
protein kinase A and C activation can increase Na,K-ATPase activity in human muscle but not via P2Y receptor stimulation.
Mutations of the ATP1A1 depolarize adrenocortical cells, disturb the K+ sensitivity, and lower intracellular pH but do not induce an overt increase of intracellular Ca2+.
Different mutations (KCNJ5, ATP1A1, ATP2B3, and CACNA1D) are found in different aldosterone-producing nodules from the same adrenal, suggesting that somatic mutations are independent events triggered by mechanisms that remain to be identified.
Data shows that a functional 12T-insertion polymorphism in the ATP1A1 promoter confers decreased susceptibility to hypertension in a male Sardinian population supporting ATP1A1 as a hypertension susceptibility gene in this population.
The extracellular entrance to the binding site on Sodium-Potassium-Exchanging ATPase has been characterized using spin-labeled derivatives of cardiotonic steroids.
This study determined the specificity of the interaction between the N-terminus of the alpha-subunit of the Na+,K+-ATPase and the surrounding membrane.
The findings are consistent with previous studies that indicate a link between Na,K-ATPase activity and SFK signaling.
Uroguanylin modulates (Na++K+)ATPase in a proximal tubule cells via cGMP/protein kinase G, cAMP/protein kinase A, and mTOR 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-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 interaction may represent an important sensing mechanism by which the cells regulate the sterol regulatory element-binding protein 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 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.
Na,K-ATPase is a new target of TGF-beta(1)-mediated Epithelial-to-mesenchymal transition in renal epithelial cells, a model system used in studies of both cancer progression and fibrosis.
Adenosine triphosphate binding to the E2P (intermediate) stage of the enzyme pump cycle causes a deceleration in its dephosphorylation when acting in the sodium ion (Na)+-ATPase mode, i.e., in the absence of monovalent potassium (K+) ions.
Results provide evidence for interaction of aspartic acid 443 in the N domain of Na(+),K(+)-ATPase with a magnesium ion.
addressed the question of how modification of the cholesterol content could affect the ATPase activity via changes in the membrane lipid phase and in the protein structure and dynamics
Neutralization of the charge on Asp 369 of Na+,K+-ATPase triggers conformational changes.
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
Inward current is a property inherent to Na/K pumps, not linked to the oocyte expression environment.
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.
examination of ion pathway through the pump
Na,K-ATPase interaction with magnesium ions
transient potassium(+)-induced peak Na(+)-K(+) pump current reflects the effect of conformation-dependent beta1 pump subunit glutathionylation, not restricted subsarcolemmal diffusion of sodium(+).
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.
The impact of alpha1 content on soleus muscle mass is consistent with a Na/K-ATPase alpha1-specific role in skeletal muscle growth that cannot be fulfilled by alpha2. The preserved running capacity in alpha1(+/-) is in sharp contrast with previously reported consequences of genetic manipulation of alpha2. These results lend further support to the concept of distinct isoform-specific functions of Na/K-ATPase alpha1 and ...
These results suggested the involvement of the actin binding site, but not tail regions, of class II non-muscle myosins in their interaction with Na(+)/K(+)-ATPase alpha1 subunits.
An antibody against the extracellular DR region (897-911) of Na(+)-K(+)-ATPase subunit alpha 1 disrupted the Na+-K+-ATPase/ROS amplifier and protected embryonic hearts in organ culture from ROS-induced injury and apoptosis.
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 recruits an Na/K-ATPase-Lyn complex in macrophages that promotes atherosclerosis.
TGFbeta1 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 transport through modulation of NKA-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.
Activation of Na,K-ATPase protects against oxidative damage in an animal model of pentylenetetrazol-induced seizures.
The results reveled that the NKAalpha1 subunit is found within alpha-motoneurons of spinal cord.
Reduction of Na+, K+-ATPase activity and expression in cerebral cortex of glutaryl-CoA dehydrogenase deficient mice is a possible mechanism for brain injury in glutaric aciduria type I.
Results indicate that Activation of Na+,K+-ATPase in skeletal muscle cells is AMPK-dependent.
the sodium pump alpha1 sub-unit has a role in progression of metastatic melanoma
ATP1A1 interaction with PKCeta and occludin was involved in the integrity of the blood-labyrinth-barrier
Both protein and mRNA expression of alpha1 and alpha2 isoforms of Na,K-ATPase and NKCC1 in the lateral wall were dramatically reduced following a long-term deafening
Data identify the K+-independent, ouabain-insensitive Na+-ATPase as a unique P-type ATPase.
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