Evidence map›Paper›PMID 11222629›Full record

ArticleThe Journal of general physiology2001

Oxidative regulation of large conductance calcium-activated potassium channels.

X D Tang, H Daggett, M Hanner, M L Garcia, O B McManus, N Brot, H Weissbach, S H Heinemann, T Hoshi

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of general physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing 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

65 citing papers in PubMed, 126 citations in OpenAlex.

  1. Article
  2. Redox Regulation of KAntioxidants & redox signaling · 2024
    Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Coronary Large Conductance CaFrontiers in physiology · 2021
    Review
  10. Article
  11. Article
  12. Oxidation of methionine residues activates the high-threshold heat-sensitive ion channel TRPV2.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  13. Review
  14. Review
  15. Effect of Oxidative Stress on the Estrogen-NOS-NO-KOxidative medicine and cellular longevity · 2019
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

5 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

9 authors at 3 institutions in 1 country.

X D TangDepartment of Physiology and Biophysics, The University of Iowa, Iowa City, Iowa 52242, USA.
H Daggett
M Hanner
M L Garcia
O B McManus
N Brot
H Weissbach
S H Heinemann
T Hoshi
University of Iowa · USFlorida Atlantic University · USHospital for Special Surgery · US

Funding

VASOPRESSIN IN CARDIOVASCULAR REGULATIONP01HL014388 · NHLBI · UNIVERSITY OF IOWA · PI ABBOUD, FRANCOIS M · 1985 to 2018
$40.3M
REGULATION OF ION CHANNELS BY METHIONINE OXIDATIONR01GM057654 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI HOSHI, TOSHINORI, OLCESE, RICCARDO · 1998 to 2014
$5.0M
NHLBI NIH HHS HL14388NHLBI NIH HHS P01 HL014388NIGMS NIH HHS GM57654NIGMS NIH HHS R01 GM057654
6 · The paper itself

Abstract

Reactive oxygen/nitrogen species are readily generated in vivo, playing roles in many physiological and pathological conditions, such as Alzheimer's disease and Parkinson's disease, by oxidatively modifying various proteins. Previous studies indicate that large conductance Ca(2+)-activated K(+) channels (BK(Ca) or Slo) are subject to redox regulation. However, conflicting results exist whether oxidation increases or decreases the channel activity. We used chloramine-T, which preferentially oxidizes methionine, to examine the functional consequences of methionine oxidation in the cloned human Slo (hSlo) channel expressed in mammalian cells. In the virtual absence of Ca(2+), the oxidant shifted the steady-state macroscopic conductance to a more negative direction and slowed deactivation. The results obtained suggest that oxidation enhances specific voltage-dependent opening transitions and slows the rate-limiting closing transition. Enhancement of the hSlo activity was partially reversed by the enzyme peptide methionine sulfoxide reductase, suggesting that the upregulation is mediated by methionine oxidation. In contrast, hydrogen peroxide and cysteine-specific reagents, DTNB, MTSEA, and PCMB, decreased the channel activity. Chloramine-T was much less effective when concurrently applied with the K(+) channel blocker TEA, which is consistent with the possibility that the target methionine lies within the channel pore. Regulation of the Slo channel by methionine oxidation may represent an important link between cellular electrical excitability and metabolism.

Indexed as

Ion Channel GatingPotassium Channels, Calcium-ActivatedAnimalsCalciumCell Culture TechniquesChloraminesElectrophysiologyHumansLarge-Conductance Calcium-Activated Potassium ChannelsMethionineOxidation-ReductionPolymerase Chain ReactionPotassium ChannelsReactive Oxygen SpeciesTosyl CompoundsUp-RegulationCalciumChloramineschloramine-TLarge-Conductance Calcium-Activated Potassium ChannelsMethioninePotassium ChannelsPotassium Channels, Calcium-ActivatedReactive Oxygen SpeciesTosyl Compounds

Identifiers

PMID11222629
PMCPMC2225619
OpenAlexW2100326827

What OpenQuestion holds

Textmetadata
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.