ArticleThe Journal of general physiology1996
A recombinant inwardly rectifying potassium channel coupled to GTP-binding proteins.
Article in The Journal of general physiology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 71 citations in OpenAlex.
- Tcf4 Deficiency causes recurrent seizures in mice.Progress in neurobiology · 2025Article
- Mechanism of PKCε regulation of cardiac GIRK channel gating.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Kir Channel Molecular Physiology, Pharmacology, and Therapeutic Implications.Handbook of experimental pharmacology · 2021Review
- The small molecule GAT1508 activates brain-specific GIRK1/2 channel heteromers and facilitates conditioned fear extinction in rodents.The Journal of biological chemistry · 2020Article
- G protein-coupled receptor signaling to Kir channels in Xenopus oocytes.Current pharmaceutical biotechnology · 2014Review
- Gating of a G protein-sensitive mammalian Kir3.1 prokaryotic Kir channel chimera in planar lipid bilayers.The Journal of biological chemistry · 2010Article
- A sodium-mediated structural switch that controls the sensitivity of Kir channels to PtdIns(4,5)P(2).Nature chemical biology · 2008Article
- Phosphoinositide-mediated gating of inwardly rectifying K(+) channels.Pflugers Archiv : European journal of physiology · 2007Review
- Diverse Kir modulators act in close proximity to residues implicated in phosphoinositide binding.The Journal of physiology · 2007Review
- Specificity of activation by phosphoinositides determines lipid regulation of Kir channels.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Cloning and characterization of G protein-gated inward rectifier K+ channel (GIRK1) isoforms from heart and brain.Journal of molecular neuroscience : MN · 2001Article
- Slow modal gating of single G protein-activated K+ channels expressed in Xenopus oocytes.The Journal of physiology · 2000Article
- Evidence of elevated intracellular calcium levels in weaver homozygote mice.The Journal of physiology · 2000Article
- Synergistic activation of G protein-gated inwardly rectifying potassium channels by the betagamma subunits of G proteins and Na(+) and Mg(2+) ions.The Journal of general physiology · 1999Article
- Selective activation of heterologously expressed G protein-gated K+ channels by M2 muscarinic receptors in rat sympathetic neurones.The Journal of physiology · 1999Article
- Characterization of inositol-1,4,5-trisphosphate-gated channels in the plasma membrane of rat olfactory neurons.Biophysical journal · 1999Article
- Activation of the atrial KACh channel by the betagamma subunits of G proteins or intracellular Na+ ions depends on the presence of phosphatidylinositol phosphates.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Identification of regions that regulate the expression and activity of G protein-gated inward rectifier K+ channels in Xenopus oocytes.The Journal of physiology · 1997Article
- Control of channel activity through a unique amino acid residue of a G protein-gated inwardly rectifying K+ channel subunit.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- Na+ activation of the muscarinic K+ channel by a G-protein-independent mechanism.The Journal of general physiology · 1996Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
GTP-binding (G) proteins have been shown to mediate activation of inwardly rectifying potassium (K+) channels in cardiac, neuronal and neuroendocrine cells. Here, we report functional expression of a recombinant inwardly rectifying channel which we call KGP (or hpKir3.4), to signify that it is K+ selective, G-protein-gated and isolated from human pancreas. KGP expression in Xenopus oocytes resulted in sizeable basal (or agonist-independent) currents while coexpression with a G-protein-linked receptor, yielded additional agonist-induced currents. Coexpression of KGP and hGIRK1 (a human brain homolog of GIRK1/Kir3.1) produced much larger basal currents than those observed with KGP or hGIRK1 alone, and upon coexpression with receptor, similarly large agonist-induced currents could be obtained. Pertussis toxin treatment significantly diminished agonist-dependent currents due to either KGP or KGP/hGIRK1 expression. Interestingly, PTX also significantly reduced basal KGP or KGP/hGIRK1 currents, suggesting that basal activity is largely the result of G-protein gating as well. When the two channels were coexpressed with receptor, the relative increase in current elicited by agonist was similar whether KGP and hGIRK1 were expressed alone or together. When in vitro translated or when expressed in Xenopus oocytes or CHO mammalian cells, KGP gave rise to a nonglycosylated 45-kD protein. Antibodies directed against either KGP or hGIRK1 coprecipitated both proteins coexpressed in oocytes, providing evidence for the heteromeric assembly of the two channels and suggesting that the current potentiation seen with coexpression of the two channel subunits is due to specific interactions between them. An endogenous oocyte protein similar in size to KGP was also coprecipitated with hGIRK1.
Indexed as
Identifiers
What OpenQuestion holds
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.