ArticleBritish journal of pharmacology2009
Phosphorylation alters the pharmacology of Ca(2+)-activated Cl channels in rabbit pulmonary arterial smooth muscle cells.
Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Pathophysiology and pathogenic mechanisms of pulmonary hypertension: role of membrane receptors, ion channels, and CaPhysiological reviews · 2023Review
- Polymodal Control of TMEM16x Channels and Scramblases.International journal of molecular sciences · 2022Review
- Molecular mechanisms of activation and regulation of ANO1-Encoded CaChannels (Austin, Tex.) · 2021Review
- Calcium-Activated Chloride Channels in Myometrial and Vascular Smooth Muscle.Frontiers in physiology · 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
- TMEM16A is implicated in the regulation of coronary flow and is altered in hypertension.British journal of pharmacology · 2019Article
- Molecular and functional significance of Ca(2+)-activated Cl(-) channels in pulmonary arterial smooth muscle.Pulmonary circulation · 2015Review
- Contribution of calcium-activated chloride channel to elevated pulmonary artery pressure in pulmonary arterial hypertension induced by high pulmonary blood flow.International journal of clinical and experimental pathology · 2015Article
- Pharmacological characterization of TMEM16A currents.Channels (Austin, Tex.) · 2014Article
- Increased TMEM16A-encoded calcium-activated chloride channel activity is associated with pulmonary hypertension.American journal of physiology. Cell physiology · 2012Article
- CaMKII inhibition hyperpolarizes membrane and blocks nitrergic IJP by closing a Cl(-) conductance in intestinal smooth muscle.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- New mechanisms of pulmonary arterial hypertension: role of Ca²⁺ signaling.American journal of physiology. Heart and circulatory physiology · 2012Review
- Expression profile and protein translation of TMEM16A in murine smooth muscle.American journal of physiology. Cell physiology · 2010Article
- Cholesterol depletion alters amplitude and pharmacology of vascular calcium-activated chloride channels.Cardiovascular research · 2010Article
- Complex phosphatase regulation of Ca2+-activated Cl- currents in pulmonary arterial smooth muscle cells.The Journal of biological chemistry · 2009Article
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4 authors.
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Abstract
background and purposeCa(2+)-activated Cl(-) currents (I(Cl(Ca))) in arterial smooth muscle cells are inhibited by phosphorylation. The Ca(2+)-activated Cl(-) channel (Cl(Ca)) blocker niflumic acid (NFA) produces a paradoxical dual effect on I(Cl(Ca)), causing stimulation or inhibition at potentials below or above 0 mV respectively. We tested whether the effects of NFA on I(Cl(Ca)) were modulated by phosphorylation. EXPERIMENTAL APPROACH: I(Cl(Ca)) was elicited with 500 nM free internal Ca(2+) in rabbit pulmonary artery myocytes. The state of global phosphorylation was altered by cell dialysis with either 5 mM ATP or 0 mM ATP with or without an inhibitor of calmodulin-dependent protein kinase type II, KN-93 (10 microM). KEY
resultsDephosphorylation enhanced the ability of 100 microM NFA to inhibit I(Cl(Ca)). This effect was attributed to a large negative shift in the voltage-dependence of block, which was converted to stimulation at potentials <-50 mV, approximately 70 mV more negative than cells dialysed with 5 mM ATP. NFA dose-dependently blocked I(Cl(Ca)) in the range of 0.1-250 microM in cells dialysed with 0 mM ATP and KN-93, which contrasted with the stimulation induced by 0.1 microM, which converted to block at concentrations >1 microM when cells were dialysed with 5 mM ATP. CONCLUSIONS AND IMPLICATIONS: Our data indicate that the presumed state of phosphorylation of the pore-forming or regulatory subunit of Cl(Ca) channels influenced the interaction of NFA in a manner that obstructs interaction of the drug with an inhibitory binding site.
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