ArticleMolecular pharmacology2009
Activation of (Na+ + K+)-ATPase modulates cardiac L-type Ca2+ channel function.
Article in Molecular pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- TiDrug delivery and translational research · 2024Review
- Sensational site: the sodium pump ouabain-binding site and its ligands.American journal of physiology. Cell physiology · 2024Review
- Rutin Improves Cardiac and Erythrocyte Membrane-Bound ATPase Activities in Male Rats Exposed to Cadmium Chloride and Lead Acetate.Biological trace element research · 2022Article
- Ultrathin 2D Titanium Carbide MXene (TiAdvanced healthcare materials · 2021Article
- DR region of NaScientific reports · 2018Article
- Na+/K+‑ATPase DR region‑specific antibody protects U251 cells against hypoxia reperfusion‑induced injury via the PI3K/AKT and ERK pathways.Molecular medicine reports · 2017Article
- Article
- CaMKII in the cardiovascular system: sensing redox states.Physiological reviews · 2011Review
- Acute lead exposure increases arterial pressure: role of the renin-angiotensin system.PloS one · 2011Article
- Mechanistic distinction between activation and inhibition of (Na(+)+K(+))-ATPase-mediated Ca2+ influx in cardiomyocytes.Biochemical and biophysical research communications · 2011Article
- Serine496 of β2 subunit of L-type Ca2+ channel participates in molecular crosstalk between activation of (Na++K+)-ATPase and the channel.Biochemical and biophysical research communications · 2010Article
- Soybean oil increases SERCA2a expression and left ventricular contractility in rats without change in arterial blood pressure.Lipids in health and disease · 2010Article
- Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Cellular Ca(2+) signaling underlies diverse vital biological processes, including muscle contractility, memory encoding, fertilization, cell survival, and cell death. Despite extensive studies, the fundamental control mechanisms that regulate intracellular Ca(2+) movement remain enigmatic. We have found recently that activation of the (Na(+)+K(+))-ATPase markedly potentiates intracellular Ca(2+) transients and contractility of rat heart cells. Little is known about the pathway responsible for the activation of the (Na(+)+K(+))-ATPase-initiated Ca(2+) signaling. Here, we demonstrate a novel mechanism in which activation of the (Na(+)+K(+))-ATPase is coupled to increased L-type Ca(2+) channel function through a signaling cascade involving Src and ERK1/2 but not well established regulators of the channel, such as adrenergic receptor system or activation of PKA or CaMKII. We have also identified Ser(1928), a phosphorylation site for the alpha1 subunit of the L-type Ca(2+) channel that may participate in the activation of the (Na(+)+K(+))-ATPase-mediated Ca(2+) signaling. The findings reported here uncover a novel molecular cross-talk between activation of the (Na(+)+K(+))-ATPase and L-type Ca(2+) channel and provide new insights into Ca(2+) signaling mechanisms for deeper understanding of the nature of cellular Ca(2+) handling in heart.
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