ArticleThe Journal of biological chemistry2001
Eicosanoids inhibit the G-protein-gated inwardly rectifying potassium channel (Kir3) at the Na+/PIP2 gating site.
Article in The Journal of biological chemistry, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Membrane-associated estrogen receptor α prevents the amyloid β-induced suppression of GIRK channel activity in hippocampal neurons from female mice.Biology of sex differences · 2025Article
- Amyloid-β oligomers trigger sex-dependent inhibition of GIRK channel activity in hippocampal neurons in mice.Science signaling · 2024Article
- Capsaicin inhibits intestinal ClThe Journal of biological chemistry · 2022Article
- Mutual action by Gγ and Gβ for optimal activation of GIRK channels in a channel subunit-specific manner.Scientific reports · 2019Article
- Eag1 KOxidative medicine and cellular longevity · 2017Review
- Genetic defects in the hotspot of inwardly rectifying K(+) (Kir) channels and their metabolic consequences: a review.Molecular genetics and metabolism · 2012Review
- Regulation of voltage-gated Ca2+ channels by lipids.Cell calcium · 2009Review
- Arachidonic acid and ion channels: an update.British journal of pharmacology · 2008Review
- Arachidonic acid-induced activation of large-conductance potassium channels and membrane hyperpolarization in mouse B cells.Pflugers Archiv : European journal of physiology · 2008Article
- Decrease in PIP(2) channel interactions is the final common mechanism involved in PKC- and arachidonic acid-mediated inhibitions of GABA(B)-activated K+ current.The Journal of physiology · 2007Article
- Diverse Kir modulators act in close proximity to residues implicated in phosphoinositide binding.The Journal of physiology · 2007Review
- Receptor-specific inhibition of GABAB-activated K+ currents by muscarinic and metabotropic glutamate receptors in immature rat hippocampus.The Journal of physiology · 2007Article
- Activation of hEAG1 potassium channels by arachidonic acid.Pflugers Archiv : European journal of physiology · 2007Article
- M1 muscarinic receptors inhibit L-type Ca2+ current and M-current by divergent signal transduction cascades.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Mechanism of arachidonic acid modulation of the T-type Ca2+ channel alpha1G.The Journal of general physiology · 2004Article
- G protein-independent inhibition of GIRK current by adenosine in rat atrial myocytes overexpressing A1 receptors after adenovirus-mediated gene transfer.The Journal of physiology · 2003Article
- Reciprocal regulation of capacitative and non-capacitative Ca2+ entry in A7r5 vascular smooth muscle cells: only the latter operates during receptor activation.The Biochemical journal · 2002Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
We previously showed that activation of the human endothelin A receptor (HETAR) by endothelin-1 (Et-1) selectively inhibits the response to mu opioid receptor (MOR) activation of the G-protein-gated inwardly rectifying potassium channel (Kir3). The Et-1 effect resulted from PLA2 production of an eicosanoid that inhibited Kir3. In this study, we show that Kir3 inhibition by eicosanoids is channel subunit-specific, and we identify the site within the channel required for arachidonic acid sensitivity. Activation of the G-protein-coupled MOR by the selective opioid agonist D-Ala(2)Glyol, enkephalin, released Gbetagamma that activated Kir3. The response to MOR activation was significantly inhibited by Et-1 activation of HETAR in homomeric channels composed of either Kir3.2 or Kir3.4. In contrast, homomeric channels of Kir3.1 were substantially less sensitive. Domain deletion and channel chimera studies suggested that the sites within the channel required for Et-1-induced inhibition were within the region responsible for channel gating. Mutation of a single amino acid in the homomeric Kir3.1 to produce Kir3.1(F137S)(N217D) dramatically increased the channel sensitivity to arachidonic acid and Et-1 treatment. Complementary mutation of the equivalent amino acid in Kir3.4 to produce Kir3.4(S143T)(D223N) significantly reduced the sensitivity of the channel to arachidonic acid- and Et-1-induced inhibition. The critical aspartate residue required for eicosanoid sensitivity is the same residue required for Na(+) regulation of PIP(2) gating. The results suggest a model of Kir3 gating that incorporates a series of regulatory steps, including Gbetagamma, PIP(2), Na(+), and arachidonic acid binding to the channel gating domain.
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