Evidence map›Paper›PMID 8887775›Full record

ArticleThe Journal of physiology1996

Protein kinase C inhibition of cloned inward rectifier (HRK1/KIR2.3) K+ channels expressed in Xenopus oocytes.

P Henry, W L Pearson, C G Nichols

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
  2. PKC regulation of ion channels: The involvement of PIPThe Journal of biological chemistry · 2022
    Review
  3. Role of plasma membrane-associated AKAPs for the regulation of cardiac INaunyn-Schmiedeberg's archives of pharmacology · 2017
    Article
  4. Boosting the signal: Endothelial inward rectifier KMicrocirculation (New York, N.Y. : 1994) · 2017
    Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Molecular basis for genistein-induced inhibition of Kir2.3 currents.Pflugers Archiv : European journal of physiology · 2008
    Article
  15. Article
  16. Article
  17. Article
  18. The orexin OX1 receptor regulates Ca2+ entry via diacylglycerol-activated channels in differentiated neuroblastoma cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006
    Article
  19. Article
  20. Article
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.

P HenryDepartment of Cell Biology and Physiology, Washington University School of Medicine, St Louis, MO 63110, USA.
W L Pearson
C G Nichols
Washington University in St. Louis · US

Funding

Rectification &Block of Ion Channel CurrentsR01HL054171 · NHLBI · WASHINGTON UNIVERSITY · PI NICHOLS, COLIN G · 1995 to 2017
$4.5M
NHLBI NIH HHS HL451231NHLBI NIH HHS HL54171
6 · The paper itself

Abstract

1. The effect of protein kinase activators on cloned inward rectifier channels expressed in Xenopus oocytes was examined using a two-electrode voltage clamp. PKA activators caused no change in KIR1.1, KIR2.1, or KIR2.3 current. The PKC activators phorbol 12-myristate 14-acetate (PMA) and phorbol 12, 13-dibutyrate (PDBu) inhibited KIR2.3 currents, but not KIR2.1 or KIR1.1 current. This inhibition was blocked by staurosporine. An inactive phorbol ester, 4 alpha-phorbol 12, 13-didecanoate (4 alpha-PDD), had no effect on KIR2.3. 2. Upon changing solution from 2 to 98 microM K+, KIR2.3 but not KIR1.1 or KIR2.1 currents typically 'ran down' over 5 min to 60-80% of maximum amplitude. Rundown occurred even if PMA was applied before changing to high [K+] solution, indicating that rundown was independent of PKC activity. Rundown was evoked by substituting NMG+ for Na+, showing that it results from low [Na+] and not from high [K+]. 3. These results suggest that KIR2.3, but not KIR1.1 or KIR2.1, is subject to regulation, both by PKC activation and as a consequence of low [Na+]o. The difference in secondary regulation may account for specific responses to PKC stimulation of tissues expressing otherwise nearly identical KIR channels.

Indexed as

Potassium Channel BlockersPotassium Channels, Inwardly RectifyingAnimalsCloning, MolecularEnzyme ActivationEnzyme InhibitorsFemaleIn Vitro TechniquesMembrane PotentialsMutagenesis, Site-DirectedOocytesPhorbol EstersPotassiumPotassium ChannelsProtein Kinase CSodiumEnzyme InhibitorsKCNJ4 protein, humanPhorbol EstersPotassiumPotassium Channel BlockersPotassium ChannelsPotassium Channels, Inwardly RectifyingProtein Kinase CSodiumStaurosporine

Identifiers

PMID8887775
PMCPMC1160774
OpenAlexW2135035055

What OpenQuestion holds

Textmetadata
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.