ArticleProceedings of the National Academy of Sciences of the United States of America1997
Inactivation of calcium-activated chloride channels in smooth muscle by calcium/calmodulin-dependent protein kinase.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 109 citations in OpenAlex.
- TMEM16A Antagonism: Therapeutic Potential with Desensitization of β-Agonist Responsiveness in Asthma.American journal of respiratory cell and molecular biology · 2025Article
- 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
- Molecular mechanisms of activation and regulation of ANO1-Encoded CaChannels (Austin, Tex.) · 2021Review
- Calmodulin-Dependent Regulation of Overexpressed but Not Endogenous TMEM16A Expressed in Airway Epithelial Cells.Membranes · 2021Article
- Anoctamin 1 antagonism potentiates conventional tocolytic-mediated relaxation of pregnant human uterine smooth muscle.The journal of physiological sciences : JPS · 2021Article
- Gating and Regulatory Mechanisms of TMEM16 Ion Channels and Scramblases.Frontiers in physiology · 2021Review
- Reciprocal Correlations of Inflammatory and Calcium Signaling in Asthma Pathogenesis.Advances in experimental medicine and biology · 2021Article
- Molecular mechanism of TMEM16A regulation: role of CaMKII and PP1/PP2A.American journal of physiology. Cell physiology · 2019Article
- Molecular basis of PIPNature communications · 2019Article
- CaNature communications · 2019Article
- Drug Repurposing: The Anthelmintics Niclosamide and Nitazoxanide Are Potent TMEM16A Antagonists That Fully Bronchodilate Airways.Frontiers in pharmacology · 2019Article
- Intraluminal pressure triggers myogenic response via activation of calcium spark and calcium-activated chloride channel in rat renal afferent arteriole.American journal of physiology. Renal physiology · 2018Article
- Calcium-activated chloride current determines action potential morphology during calcium alternans in atrial myocytes.The Journal of physiology · 2016Article
- Molecular and functional significance of Ca(2+)-activated Cl(-) channels in pulmonary arterial smooth muscle.Pulmonary circulation · 2015Review
- TP53 oncomorphic mutations predict resistance to platinum‑ and taxane‑based standard chemotherapy in patients diagnosed with advanced serous ovarian carcinoma.International journal of oncology · 2015Article
- Calcineurin upregulates local Ca(2+) signaling through ryanodine receptor-1 in airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- New pulmonary therapies directed at targets other than CFTR.Cold Spring Harbor perspectives in medicine · 2013Review
- Functional regulation of ClC-3 in the migration of vascular smooth muscle cells.Hypertension (Dallas, Tex. : 1979) · 2013Article
- Role of ROS signaling in differential hypoxic Ca2+ and contractile responses in pulmonary and systemic vascular smooth muscle cells.Respiratory physiology & neurobiology · 2010Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
To determine the mechanisms responsible for the termination of Ca2+-activated Cl- currents (ICl(Ca)), simultaneous measurements of whole cell currents and intracellular Ca2+ concentration ([Ca2+]i) were made in equine tracheal myocytes. In nondialyzed cells, or cells dialyzed with 1 mM ATP, ICl(Ca) decayed before the [Ca2+]i decline, whereas the calcium-activated potassium current decayed at the same rate as [Ca2+]i. Substitution of AMP-PNP or ADP for ATP markedly prolonged the decay of ICl(Ca), resulting in a rate of current decay similar to that of the fall in [Ca2+]i. In the presence of ATP, dialysis of the calmodulin antagonist W7, the Ca2+/calmodulin-dependent kinase II (CaMKII) inhibitor KN93, or a CaMKII-specific peptide inhibitor the rate of ICl(Ca) decay was slowed and matched the [Ca2+]i decline, whereas H7, a nonspecific kinase inhibitor with low affinity for CaMKII, was without effect. When a sustained increase in [Ca2+]i was produced in ATP dialyzed cells, the current decayed completely, whereas in cells loaded with 5'-adenylylimidodiphosphate (AMP-PNP), KN93, or the CaMKII inhibitory peptide, ICl(Ca) did not decay. Slowly decaying currents were repeatedly evoked in ADP- or AMP-PNP-loaded cells, but dialysis of adenosine 5'-O-(3-thiotriphosphate) or okadaic acid resulted in a smaller initial ICl(Ca), and little or no current (despite a normal [Ca2+]i transient) with a second stimulation. These data indicate that CaMKII phosphorylation results in the inactivation of calcium-activated chloride channels, and that transition from the inactivated state to the closed state requires protein dephosphorylation.
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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.