ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Global loss of Na,K-ATPase and its nitric oxide-mediated regulation in a transgenic mouse model of amyotrophic lateral sclerosis.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
37 citing papers in PubMed.
- Oxidative Stress in the Regulation of Autosis-Related Proteins.Antioxidants (Basel, Switzerland) · 2025Review
- Dysregulation of Ion Channels and Transporters and Blood-Brain Barrier Dysfunction in Alzheimer's Disease and Vascular Dementia.Aging and disease · 2024Review
- Pathophysiology of ion channels in amyotrophic lateral sclerosis.Molecular brain · 2023Review
- G-Quadruplexes in Repeat Expansion Disorders.International journal of molecular sciences · 2023Review
- Recent Advances in the Study of NaCells · 2022Review
- Structure and Function of the Mammalian Neuromuscular Junction.Comprehensive Physiology · 2022Article
- The γ-Benzylidene Digoxin Derivative BD-15 Increases the α3-Na, K-ATPase Activity in Rat Hippocampus and Prefrontal Cortex and no Change on Heart.The Journal of membrane biology · 2021Article
- The Redox-Sensitive Na/K-ATPase Signaling in Uremic Cardiomyopathy.International journal of molecular sciences · 2020Review
- Fluoride Exposure Induces Inhibition of Sodium-and Potassium-Activated Adenosine Triphosphatase (NaInternational journal of environmental research and public health · 2019Review
- Cerebrospinal Fluid from Patients with Sporadic Amyotrophic Lateral Sclerosis Induces Degeneration of Motor Neurons Derived from Human Embryonic Stem Cells.Molecular neurobiology · 2019Article
- Can Proprioceptive Training Reduce Muscle Fatigue in Patients With Motor Neuron Diseases? A New Direction of Treatment.Frontiers in physiology · 2019Review
- S-Adenosylmethionine Promotes Oxidative Stress and Decreases NaMolecular neurobiology · 2018Article
- Sodium pump regulation of locomotor control circuits.Journal of neurophysiology · 2017Review
- Sodium potassium adenosine triphosphatase (Na/K-ATPase) as a therapeutic target for uremic cardiomyopathy.Expert opinion on therapeutic targets · 2017Review
- Sodium Pumps Mediate Activity-Dependent Changes in Mammalian Motor Networks.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Smn-Deficiency Increases the Intrinsic Excitability of Motoneurons.Frontiers in cellular neuroscience · 2017Article
- Axonal Excitability in Amyotrophic Lateral Sclerosis : Axonal Excitability in ALS.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017Review
- Glycoprotein nonmetastatic melanoma protein B extracellular fragment shows neuroprotective effects and activates the PI3K/Akt and MEK/ERK pathways via the Na+/K+-ATPase.Scientific reports · 2016Article
- Carbonylation Modification Regulates Na/K-ATPase Signaling and Salt Sensitivity: A Review and a Hypothesis.Frontiers in physiology · 2016Review
- Emerging Roles of Filopodia and Dendritic Spines in Motoneuron Plasticity during Development and Disease.Neural plasticity · 2016Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Na,K-ATPase plays a critical role in energy metabolism and ion fluxes. Its loss was investigated in the G93A mouse model of amyotrophic lateral sclerosis (ALS) in which the mutation of Cu/Zn superoxide dismutase (SOD1) is thought to lead to aberrant oxidative damage. Observed losses in spinal cord Na,K-ATPase activity exceeded all expectations. All three catalytic subunit isoforms (alpha1, alpha2, alpha3) were reduced, and the global alpha subunit loss affected not just neurons, glia, and myelinated axon tracts but even ependymal and pial membranes. Decreases in Na,K-ATPase activity were greater than losses of protein, and there were losses of Na,K-ATPase alpha, but not beta, subunits. Together, these observations are consistent with selective degradation of the alpha subunit after damage. Overexpression of normal SOD1 does not cause ALS-like symptoms, but it has other known pathological effects. In transgenic mice overexpressed normal human SOD1 had a smaller but still considerable effect on Na,K-ATPase. Furthermore, the nitric oxide-mediated regulatory pathway for Na,K-ATPase inhibition was undetectable in spinal cord tissue slices from mice overexpressing either mutant or normal human SOD1. Na,K-ATPase activity did not respond to nitric oxide donors, and the free radical-dependent step of the pathway could not be bypassed by the addition of the downstream protein kinase G activator, 8-Br-cGMP. The data demonstrate that Na,K-ATPase is vulnerable to aberrant SOD1 activity, making it a potential contributing factor in disease pathology. Moreover, the global cellular distribution of Na,K-ATPase loss indicates that SOD1 overexpression is far-reaching in its pathological effects.
Indexed as
Identifiers
12514200PMC6742130What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.