ArticleThe Journal of physiology2002
Regulation of an ATP-conductive large-conductance anion channel and swelling-induced ATP release by arachidonic acid.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 71 citations in OpenAlex.
- The ATP-Releasing Maxi-Cl Channel: Its Identity, Molecular Partners and Physiological/Pathophysiological Implications.Life (Basel, Switzerland) · 2021Review
- Extracellular ATP released by copper stress could act as diffusible signal in alleviating the copper stress-induced cell death.Protoplasma · 2019Article
- Protective mechanism of shenmai on myocardial ischemia-reperfusion through the energy metabolism pathway.American journal of translational research · 2019Article
- X-ray crystallographic studies of the extracellular domain of the first plant ATP receptor, DORN1, and the orthologous protein from Camelina sativa.Acta crystallographica. Section F, Structural biology communications · 2016Article
- The properties, functions, and pathophysiology of maxi-anion channels.Pflugers Archiv : European journal of physiology · 2016Review
- Extracellular ATP: a potential regulator of plant cell death.Molecular plant pathology · 2015Review
- Synthesis and antiplatelet activity of antithrombotic thiourea compounds: biological and structure-activity relationship studies.Molecules (Basel, Switzerland) · 2015Article
- Abnormal unsaturated fatty acid metabolism in cystic fibrosis: biochemical mechanisms and clinical implications.International journal of molecular sciences · 2014Review
- Bacterial RTX toxins allow acute ATP release from human erythrocytes directly through the toxin pore.The Journal of biological chemistry · 2014Article
- Suppression of cell membrane permeability by suramin: involvement of its inhibitory actions on connexin 43 hemichannels.British journal of pharmacology · 2014Article
- The Concise Guide to PHARMACOLOGY 2013/14: ion channels.British journal of pharmacology · 2013Article
- Imaging exocytosis of ATP-containing vesicles with TIRF microscopy in lung epithelial A549 cells.Purinergic signalling · 2012Article
- Identification of an Arabidopsis plasma membrane-located ATP transporter important for anther development.The Plant cell · 2011Article
- Swelling-activated anion channels are essential for volume regulation of mouse thymocytes.International journal of molecular sciences · 2011Article
- Extracellular ATP signaling in plants.Trends in cell biology · 2010Review
- ATP release from non-excitable cells.Purinergic signalling · 2009Article
- The maxi-anion channel: a classical channel playing novel roles through an unidentified molecular entity.The journal of physiological sciences : JPS · 2009Review
- Arachidonic acid-induced activation of large-conductance potassium channels and membrane hyperpolarization in mouse B cells.Pflugers Archiv : European journal of physiology · 2008Article
- Spatial distribution of maxi-anion channel on cardiomyocytes detected by smart-patch technique.Biophysical journal · 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
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mouse mammary C127 cells responded to hypotonic stimulation with activation of the volume-dependent ATP-conductive large conductance (VDACL) anion channel and massive release of ATP. Arachidonic acid downregulated both VDACL currents and swelling-induced ATP release in the physiological concentration range with K(d) of 4- 6 microM. The former effect observed in the whole-cell or excised patch mode was more prominent than the latter effect observed in intact cells. The arachidonate effects were direct and not mediated by downstream metabolic products, as evidenced by their insensitivity to inhibitors of arachidonate-metabolizing oxygenases, and by the observation that they were mimicked by cis-unsaturated fatty acids, which are not substrates for oxygenases. A membrane-impermeable analogue, arachidonyl coenzyme A was effective only from the cytosolic side of membrane patches suggesting that the binding site is localized intracellularly. Non-charged arachidonate analogues as well as trans-unsaturated and saturated fatty acids had no effect on VDACL currents and ATP release, indicating the importance of arachidonate's negative charge and specific hydrocarbon chain conformation in the inhibitory effect. VDACL anion channels were inhibited by arachidonic acid in two different ways: channel shutdown (K(d) of 4- 5 microM) and reduced unitary conductance (K(d) of 13-14 microM) without affecting voltage dependence of open probability. ATP(4-)-conducting inward currents measured in the presence of 100 mM ATP in the bath were reversibly inhibited by arachidonic acid. Thus, we conclude that swelling-induced ATP release and its putative pathway, the VDACL anion channel, are under a negative control by intracellular arachidonic acid signalling in mammary C127 cells.
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