Evidence map›Paper›PMID 2170564›Full record

ArticleThe Journal of general physiology1990

GTP-dependent regulation of myometrial KCa channels incorporated into lipid bilayers.

L Toro, J Ramos-Franco, E Stefani

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of general physiology, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.2field-weighted citation impact, top 5% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. Article
  3. MaxiK channel and cell signalling.Pflugers Archiv : European journal of physiology · 2014
    Review
  4. Review
  5. Article
  6. Article
  7. MaxiK channel partners: physiological impact.The Journal of physiology · 2006
    Review
  8. Article
  9. Article
  10. Article
  11. dSLo interacting protein 1, a novel protein that interacts with large-conductance calcium-activated potassium channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998
    Article
  12. Article
  13. Article
  14. Stimulatory and inhibitory regulation of calcium-activated potassium channels by guanine nucleotide-binding proteins.Proceedings of the National Academy of Sciences of the United States of America · 1992
    Article
  15. Article
  16. Calcium-activated K+ channels: metabolic regulation.Journal of bioenergetics and biomembranes · 1991
    Review
  17. Calcium-activated potassium channels: regulation by calcium.Journal of bioenergetics and biomembranes · 1991
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

L ToroDepartment of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas 77030.
J Ramos-Franco
E Stefani
Baylor College of Medicine · US

Funding

NICHD NIH HHS HD-25616
6 · The paper itself

Abstract

The regulation of calcium-activated K (KCa) channels by a G protein-mediated mechanism was studied. KCa channels were reconstituted in planar lipid bilayers by fusion of membrane vesicles from rat or pig myometrium. The regulatory process was studied by exploring the actions of GTP and GTP gamma S on single channel activity. KCa channels had a conductance of 260 +/- 6 pS (n = 25, +/- SE, 250/50 mM KCl gradient) and were voltage dependent. The open probability (Po) vs. voltage relationships were well fit by a Boltzmann distribution. The slope factor (11 mV) was insensitive to internal Ca2+. The half activation potential (V1/2) was shifted -70 mV by raising internal Ca2+ from pCa 6.2 to pCa 4. Addition of GTP or GTP gamma S activated channel activity only in the presence of Mg2+, a characteristic typical of G protein-mediated mechanisms. The Po increased from 0.18 +/- 0.08 to 0.49 +/- 0.07 (n = 7, 0 mV, pCa 6 to 6.8). The channel was also activated (Po increased from 0.03 to 0.37) in the presence of AMP-PNP, a nonphosphorylating ATP analogue, suggesting a direct G protein gating of KCa channels. Upon nucleotide activation, mean open time increased by a factor of 2.7 +/- 0.7 and mean closed time decreased by 0.2 +/- 0.07 of their initial values (n = 6). Norepinephrine (NE) or isoproterenol potentiated the GTP-mediated activation of KCa channels (Po increased from 0.17 +/- 0.06 to 0.35 +/- 0.07, n = 10). These results suggest that myometrium possesses beta-adrenergic receptors coupled to a GTP-dependent protein that can directly gate KCa channels. Furthermore, KCa channels, beta-adrenergic receptors, and G proteins can be reconstituted in lipid bilayers as a stable, functionally coupled, molecular complex.

Indexed as

Adenosine TriphosphateAnimalsFemaleGTP-Binding ProteinsGuanosine 5'-O-(3-Thiotriphosphate)Guanosine DiphosphateGuanosine TriphosphateIsoproterenolLipid BilayersMagnesiumMyometriumNorepinephrinePotassium ChannelsRatsRats, Inbred StrainsReceptors, Adrenergic, betaAdenosine TriphosphateGTP-Binding Proteinsguanosine 5'-O-(2-thiodiphosphate)Guanosine 5'-O-(3-Thiotriphosphate)Guanosine DiphosphateGuanosine TriphosphateIsoproterenolLipid BilayersMagnesiumNorepinephrinePotassium ChannelsReceptors, Adrenergic, betaSympathomimeticsThionucleotides

Identifiers

PMID2170564
PMCPMC2228995
OpenAlexW2164627338

What OpenQuestion holds

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LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.