ArticleThe Journal of general physiology1997
Redox regulation of large conductance Ca(2+)-activated K+ channels in smooth muscle cells.
Article in The Journal of general physiology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 102 citations in OpenAlex.
- Redox Regulation of KAntioxidants & redox signaling · 2024Review
- Redox Regulation of Mitochondrial Potassium Channels Activity.Antioxidants (Basel, Switzerland) · 2024Review
- The Potential of a Protein Model Synthesized Absent of Methionine.Molecules (Basel, Switzerland) · 2022Review
- Role of Airway Smooth Muscle in Inflammation Related to Asthma and COPD.Advances in experimental medicine and biology · 2021Article
- Endogenous and Agonist-induced Opening of Mitochondrial Big Versus Small Ca2+-sensitive K+ Channels on Cardiac Cell and Mitochondrial Protection.Journal of cardiovascular pharmacology · 2017Article
- Oxidative Stress and Maxi Calcium-Activated Potassium (BK) Channels.Biomolecules · 2015Review
- Role of in vivo vascular redox in resistance arteries.Hypertension (Dallas, Tex. : 1979) · 2015Article
- Distinct activity of BK channel β1-subunit in cerebral and pulmonary artery smooth muscle cells.American journal of physiology. Cell physiology · 2013Article
- Protection against cardiac injury by small Ca(2+)-sensitive K(+) channels identified in guinea pig cardiac inner mitochondrial membrane.Biochimica et biophysica acta · 2013Article
- Putative Structural and Functional Coupling of the Mitochondrial BKCa Channel to the Respiratory Chain.PloS one · 2013Article
- Hydrogen sulfide preconditioning or neutrophil depletion attenuates ischemia-reperfusion-induced mitochondrial dysfunction in rat small intestine.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Low resistance, large dimension entrance to the inner cavity of BK channels determined by changing side-chain volume.The Journal of general physiology · 2011Article
- The role of the large-conductance voltage-dependent and calcium-activated potassium (BK(Ca)) channels in the regulation of rat ductus arteriosus tone.Heart and vessels · 2010Article
- Hydrogen sulfide increases calcium-activated potassium (BK) channel activity of rat pituitary tumor cells.Pflugers Archiv : European journal of physiology · 2010Article
- Mitochondria, oxidative stress, and temporal lobe epilepsy.Epilepsy research · 2010Review
- Modulation of BKCa channel gating by endogenous signaling molecules.Physiology (Bethesda, Md.) · 2009Review
- Anoxia-induced changes in reactive oxygen species and cyclic nucleotides in the painted turtle.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2007Article
- Mitochondria-derived reactive oxygen species dilate cerebral arteries by activating Ca2+ sparks.Circulation research · 2005Article
- Homocysteine inhibits store-mediated calcium entry in human endothelial cells: evidence for involvement of membrane potential and actin cytoskeleton.Molecular and cellular biochemistry · 2005Article
- The beta1 subunit enhances oxidative regulation of large-conductance calcium-activated K+ channels.The Journal of general physiology · 2004Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The effects of sulfhydryl reduction/oxidation on the gating of large-conductance, Ca(2+)-activated K+ (maxi-K) channels were examined in excised patches from tracheal myocytes. Channel activity was modified by sulfhydryl redox agents applied to the cytosolic surface, but not the extracellular surface, of membrane patches. Sulfhydryl reducing agents dithiothreitol, beta-mercaptoethanol, and GSH augmented, whereas sulfhydryl oxidizing agents diamide, thimerosal, and 2,2'-dithiodipyridine inhibited, channel activity in a concentration-dependent manner. Channel stimulation by reduction and inhibition by oxidation persisted following washout of the compounds, but the effects of reduction were reversed by subsequent oxidation, and vice versa. The thiol-specific reagents N-ethylmaleimide and (2-aminoethyl)methanethiosulfonate inhibited channel activity and prevented the effect of subsequent sulfhydryl oxidation. Measurements of macroscopic currents in inside-out patches indicate that reduction only shifted the voltage/nP0 relationship without an effect on the maximum conductance of the patch, suggesting that the increase in nP0 following reduction did not result from recruitment of more functional channels but rather from changes of channel gating. We conclude that redox modulation of cysteine thiol groups, which probably involves thiol/disulfide exchange, alters maxi-K channel gating, and that this modulation likely affects channel activity under physiological conditions.
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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.