Evidence map›Paper›PMID 9185532›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997

Redox modulation of hslo Ca2+-activated K+ channels.

T J DiChiara, P H Reinhart

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
4.0field-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

61 citing papers in PubMed, 145 citations in OpenAlex.

  1. Article
  2. Article
  3. Redox Regulation of KAntioxidants & redox signaling · 2024
    Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Effects of Single Nucleotide Polymorphisms in HumanFrontiers in molecular neuroscience · 2019
    Article
  9. Sleep and circadian defects in aNeurobiology of sleep and circadian rhythms · 2019
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Role of in vivo vascular redox in resistance arteries.Hypertension (Dallas, Tex. : 1979) · 2015
    Article
  18. Article
  19. Oxidative modulation of voltage-gated potassium channels.Antioxidants & redox signaling · 2014
    Review
  20. Adenosine APhysiological reports · 2013
    Article

1 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

T J DiChiaraDepartment of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA.
P H Reinhart
Duke University · USDuke University Hospital · US

Funding

NEUROMODULATION OF ION CHANNELSR01NS031253 · NINDS · DUKE UNIVERSITY · PI REINHART, PETER H · 1997 to 2000
$232k
INFORMATION PROCESSING BY CALCIUM-ACTIVATED K+ CHANNELSF31MH010930 · NIMH · DUKE UNIVERSITY · PI DI CHIARA, TIMOTHY J · 1995 to 1997
–
NEUROMODULATION OF ION CHANNELSR29NS031253 · NINDS · DUKE UNIVERSITY · PI REINHART, PETER H · 1993 to 1997
–
NIMH NIH HHS F31 MH010930NIMH NIH HHS MH10930-F31NINDS NIH HHS NS31253
6 · The paper itself

Abstract

The modulation of ion channel proteins by cellular redox potential has emerged recently as a significant determinant of channel function. We have investigated the influence of sulfhydryl redox reagents on human brain Ca2+-activated K+ channels (hslo) expressed in both human embryonic kidney 293 cells and Xenopus oocytes using macropatch and single-channel analysis. Intracellular application of the reducing agent dithiothreitol (DTT): (1) shifts the voltage of half-maximal channel activation (V0.5) approximately 18 mV to more negative potentials without affecting the maximal conductance or the slope of the voltage dependence; (2) slows by approximately 10-fold a time-dependent right-shift in V0.5 values ("run-down"); (3) speeds macroscopic current activation kinetics by approximately 33%; and (4) increases the single-channel open probability without affecting the unitary conductance. In contrast to DTT treatment, oxidation with hydrogen peroxide shifts macropatch V0.5 values to more positive potentials, increases the rate of channel run-down, and decreases the single-channel open probability. KCa channels cloned from Drosophila differ from hslo channels in that they show very little run-down and are not modulated by the addition of DTT. These data indicate that hslo Ca2+-activated K+ channels may be modulated by changes in the cellular redox potential as well as by the transmembrane voltage and the cytoplasmic Ca2+ concentration.

Indexed as

Potassium Channels, Calcium-ActivatedAnimalsCell LineDithiothreitolElectrophysiologyEmbryo, NonmammalianFemaleHydrogen PeroxideKidneyKineticsLarge-Conductance Calcium-Activated Potassium ChannelsOocytesOxidation-ReductionPotassium ChannelsProbabilityReducing AgentsDithiothreitolHydrogen PeroxideLarge-Conductance Calcium-Activated Potassium ChannelsPotassium ChannelsPotassium Channels, Calcium-ActivatedReducing AgentsSulfhydryl Reagents

Identifiers

PMID9185532
PMCPMC6573296
OpenAlexW1641032390

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.