ArticleThe Journal of general physiology2006
Mechanism of the inhibition of Ca2+-activated Cl- currents by phosphorylation in pulmonary arterial smooth muscle cells.
Article in The Journal of general physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 64 citations in OpenAlex.
- Function and Regulation of the Calcium-Activated Chloride Channel Anoctamin 1 (TMEM16A).Handbook of experimental pharmacology · 2024Article
- Polymodal Control of TMEM16x Channels and Scramblases.International journal of molecular sciences · 2022Review
- Positive modulation of the TMEM16B mediated currents by TRPV4 antagonist.Biochemistry and biophysics reports · 2021Article
- Molecular mechanisms of activation and regulation of ANO1-Encoded CaChannels (Austin, Tex.) · 2021Review
- Allosteric modulation of alternatively spliced CaProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Molecular mechanism of TMEM16A regulation: role of CaMKII and PP1/PP2A.American journal of physiology. Cell physiology · 2019Article
- Importance of Altered Levels of SERCA, IPBiophysical journal · 2017Article
- DNA methylation patterns and gene expression associated with litter size in Berkshire pig placenta.PloS one · 2017Article
- Influence of intracellular Ca2+ and alternative splicing on the pharmacological profile of ANO1 channels.American journal of physiology. Cell physiology · 2016Article
- The molecular basis of the genesis of basal tone in internal anal sphincter.Nature communications · 2016Article
- Role of Quercetin in Modulating Chloride Transport in the Intestine.Frontiers in physiology · 2016Article
- Molecular and functional significance of Ca(2+)-activated Cl(-) channels in pulmonary arterial smooth muscle.Pulmonary circulation · 2015Review
- Calcium-activated chloride channels anoctamin 1 and 2 promote murine uterine smooth muscle contractility.American journal of obstetrics and gynecology · 2014Article
- Inhibitory role of phosphatidylinositol 4,5-bisphosphate on TMEM16A-encoded calcium-activated chloride channels in rat pulmonary artery.British journal of pharmacology · 2014Article
- Calmodulin-dependent activation and inactivation of anoctamin calcium-gated chloride channels.The Journal of general physiology · 2013Article
- TMEM16F (Anoctamin 6), an anion channel of delayed Ca(2+) activation.The Journal of general physiology · 2013Article
- Distinct activity of BK channel β1-subunit in cerebral and pulmonary artery smooth muscle cells.American journal of physiology. Cell physiology · 2013Article
- Potent vasorelaxant activity of the TMEM16A inhibitor T16A(inh) -A01.British journal of pharmacology · 2013Article
- Increased TMEM16A-encoded calcium-activated chloride channel activity is associated with pulmonary hypertension.American journal of physiology. Cell physiology · 2012Article
- New mechanisms of pulmonary arterial hypertension: role of Ca²⁺ signaling.American journal of physiology. Heart and circulatory physiology · 2012Review
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
The aim of the present study was to provide a mechanistic insight into how phosphatase activity influences calcium-activated chloride channels in rabbit pulmonary artery myocytes. Calcium-dependent Cl- currents (I(ClCa)) were evoked by pipette solutions containing concentrations between 20 and 1000 nM Ca2+ and the calcium and voltage dependence was determined. Under control conditions with pipette solutions containing ATP and 500 nM Ca2+, I(ClCa) was evoked immediately upon membrane rupture but then exhibited marked rundown to approximately 20% of initial values. In contrast, when phosphorylation was prohibited by using pipette solutions containing adenosine 5'-(beta,gamma-imido)-triphosphate (AMP-PNP) or with ATP omitted, the rundown was severely impaired, and after 20 min dialysis, I(ClCa) was approximately 100% of initial levels. I(ClCa) recorded with AMP-PNP-containing pipette solutions were significantly larger than control currents and had faster kinetics at positive potentials and slower deactivation kinetics at negative potentials. The marked increase in I(ClCa) was due to a negative shift in the voltage dependence of activation and not due to an increase in the apparent binding affinity for Ca2+. Mathematical simulations were carried out based on gating schemes involving voltage-independent binding of three Ca2+, each binding step resulting in channel opening at fixed calcium but progressively greater "on" rates, and voltage-dependent closing steps ("off" rates). Our model reproduced well the Ca2+ and voltage dependence of I(ClCa) as well as its kinetic properties. The impact of global phosphorylation could be well mimicked by alterations in the magnitude, voltage dependence, and state of the gating variable of the channel closure rates. These data reveal that the phosphorylation status of the Ca2+-activated Cl- channel complex influences current generation dramatically through one or more critical voltage-dependent steps.
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