ArticleBiophysical journal1998
ATP inhibition and rectification of a Ca2+-activated anion channel in sarcoplasmic reticulum of skeletal muscle.
Article in Biophysical journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 32 citations in OpenAlex.
- Skeletal Muscle Fatigue in Rats Is More Consistently Related to Increased Inorganic Phosphate Concentration Than Acidosis.Acta physiologica (Oxford, England) · 2025Article
- Electrical signals in the ER are cell type and stimulus specific with extreme spatial compartmentalization in neurons.Cell reports · 2023Article
- ATP competes with PIP2 for binding to gelsolin.PloS one · 2018Article
- New and notable ion-channels in the sarcoplasmic/endoplasmic reticulum: do they support the process of intracellular Ca²⁺ release?The Journal of physiology · 2015Review
- Differential expression profile of membrane proteins in Aplysia pleural–pedal ganglia under the stress of methyl parathion.Environmental science and pollution research international · 2014Article
- Airway smooth muscle as a target of asthma therapy: history and new directions.Respiratory research · 2006Review
- Role of phosphate and calcium stores in muscle fatigue.The Journal of physiology · 2001Review
- Phosphate ion channels in sarcoplasmic reticulum of rabbit skeletal muscle.The Journal of physiology · 2001Article
- Inhibition of creatine kinase reduces the rate of fatigue-induced decrease in tetanic [Ca(2+)](i) in mouse skeletal muscle.The Journal of physiology · 2001Article
- Role of myoplasmic phosphate in contractile function of skeletal muscle: studies on creatine kinase-deficient mice.The Journal of physiology · 2001Article
- Modeling of the role of Cl- channels in Ca2+ translocation through endoplasmic reticulum membrane.Doklady. Biochemistry and biophysicsArticle
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We describe ATP-dependent inhibition of the 75-105-pS (in 250 mM Cl-) anion channel (SCl) from the sarcoplasmic reticulum (SR) of rabbit skeletal muscle. In addition to activation by Ca2+ and voltage, inhibition by ATP provides a further mechanism for regulating SCl channel activity in vivo. Inhibition by the nonhydrolyzable ATP analog 5'-adenylylimidodiphosphate (AMP-PNP) ruled out a phosphorylation mechanism. Cytoplasmic ATP (approximately 1 mM) inhibited only when Cl- flowed from cytoplasm to lumen, regardless of membrane voltage. Flux in the opposite direction was not inhibited by 9 mM ATP. Thus ATP causes true, current rectification in SCl channels. Inhibition by cytoplasmic ATP was also voltage dependent, having a K(I) of 0.4-1 mM at -40 mV (Hill coefficient approximately 2), which increased at more negative potentials. Luminal ATP inhibited with a K(I) of approximately 2 mM at +40 mV, and showed no block at negative voltages. Hidden Markov model analysis revealed that ATP inhibition 1) reduced mean open times without altering the maximum channel amplitude, 2) was mediated by a novel, single, voltage-independent closed state (approximately 1 ms), and 3) was much less potent on lower conductance substates than the higher conductance states. Therefore, the SCl channel is unlikely to pass Cl- from cytoplasm to SR lumen in vivo, and balance electrogenic Ca2+ uptake as previously suggested. Possible roles for the SCl channel in the transport of other anions are discussed.
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