ArticleThe Journal of cell biology1998
Cystic fibrosis transmembrane conductance regulator-associated ATP release is controlled by a chloride sensor.
Article in The Journal of cell biology, 1998. 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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 106 citations in OpenAlex.
- Physiologic roles of P2 receptors in leukocytes.Journal of leukocyte biology · 2022Review
- Improved Chloride Ion Sensing Performance of Flexible Ag-NPs/AgCl Electrode Sensor Using Cu-BTC as an Effective Adsorption Layer.Frontiers in chemistry · 2019Article
- Human Keratinocytes Respond to Extracellular UTP by Induction of Hyaluronan Synthase 2 Expression and Increased Hyaluronan Synthesis.The Journal of biological chemistry · 2017Article
- Activation of the metabolic sensor AMP-activated protein kinase inhibits aquaporin-2 function in kidney principal cells.American journal of physiology. Renal physiology · 2016Article
- Cellular chloride and bicarbonate retention alters intracellular pH regulation in Cftr KO crypt epithelium.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Regulation of ACh release from guinea pig bladder urothelial cells: potential role in bladder filling sensations.British journal of pharmacology · 2014Article
- The cystic fibrosis transmembrane conductance regulator (CFTR): three-dimensional structure and localization of a channel gate.The Journal of biological chemistry · 2011Article
- Phosphopeptide screen uncovers novel phosphorylation sites of Nedd4-2 that potentiate its inhibition of the epithelial Na+ channel.The Journal of biological chemistry · 2010Article
- Role of purinergic signaling pathways in V-ATPase recruitment to apical membrane of acidifying epididymal clear cells.American journal of physiology. Cell physiology · 2010Article
- ATP release from non-excitable cells.Purinergic signalling · 2009Article
- Connexin 30 deficiency impairs renal tubular ATP release and pressure natriuresis.Journal of the American Society of Nephrology : JASN · 2009Article
- Amperometric Sensor for Detection of Chloride Ions.Sensors (Basel, Switzerland) · 2008Article
- Chloride homeostasis in Saccharomyces cerevisiae: high affinity influx, V-ATPase-dependent sequestration, and identification of a candidate Cl- sensor.The Journal of general physiology · 2008Article
- International Union of Pharmacology LVIII: update on the P2Y G protein-coupled nucleotide receptors: from molecular mechanisms and pathophysiology to therapy.Pharmacological reviews · 2006Review
- Mutual enhancement of virulence by enterotoxigenic and enteropathogenic Escherichia coli.Infection and immunity · 2006Article
- Characterization of ammonia transport by the kidney Rh glycoproteins RhBG and RhCG.American journal of physiology. Renal physiology · 2006Article
- ATP release via anion channels.Purinergic signalling · 2005Article
- Spontaneous channel activity of the inositol 1,4,5-trisphosphate (InsP3) receptor (InsP3R). Application of allosteric modeling to calcium and InsP3 regulation of InsP3R single-channel gating.The Journal of general physiology · 2003Article
- Novel regulation of calcium inhibition of the inositol 1,4,5-trisphosphate receptor calcium-release channel.The Journal of general physiology · 2003Article
- Release of ATP induced by hypertonic solutions in Xenopus oocytes.The Journal of physiology · 2003Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
The cystic fibrosis transmembrane conductance regulator (CFTR) is a chloride channel that is defective in cystic fibrosis, and has also been closely associated with ATP permeability in cells. Using a Xenopus oocyte cRNA expression system, we have evaluated the molecular mechanisms that control CFTR-modulated ATP release. CFTR-modulated ATP release was dependent on both cAMP activation and a gradient change in the extracellular chloride concentration. Activation of ATP release occurred within a narrow concentration range of external Cl- that was similar to that reported in airway surface fluid. Mutagenesis of CFTR demonstrated that Cl- conductance and ATP release regulatory properties could be dissociated to different regions of the CFTR protein. Despite the lack of a need for Cl- conductance through CFTR to modulate ATP release, alterations in channel pore residues R347 and R334 caused changes in the relative ability of different halides to activate ATP efflux (wtCFTR, Cl >> Br; R347P, Cl >> Br; R347E, Br >> Cl; R334W, Cl = Br). We hypothesize that residues R347 and R334 may contribute a Cl- binding site within the CFTR channel pore that is necessary for activation of ATP efflux in response to increases of extracellular Cl-. In summary, these findings suggest a novel chloride sensor mechanism by which CFTR is capable of responding to changes in the extracellular chloride concentration by modulating the activity of an unidentified ATP efflux pathway. This pathway may play an important role in maintaining fluid and electrolyte balance in the airway through purinergic regulation of epithelial cells. Insight into these molecular mechanisms enhances our understanding of pathogenesis in the cystic fibrosis lung.
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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.