Evidence map›Paper›PMID 17624316›Full record

ArticleBiochemical pharmacology2007

Functional consequences of methionine oxidation of hERG potassium channels.

Zhi Su, James Limberis, Ruth L Martin, Rong Xu, Katrin Kolbe, Stefan H Heinemann, Toshinori Hoshi, Bryan F Cox, Gary A Gintant

Open access · greenAbstract read
In one paragraph

Article in Biochemical pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Oxidative modulation of voltage-gated potassium channels.Antioxidants & redox signaling · 2014
    Review
  10. Article
  11. Article
  12. Article
  13. Metabolic stress, reactive oxygen species, and arrhythmia.Journal of molecular and cellular cardiology · 2012
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Repolarization abnormalities and afterdepolarizations in a canine model of sudden cardiac death.American journal of physiology. Regulatory, integrative and comparative physiology · 2008
    Article
  20. Oxidation of multiple methionine residues impairs rapid sodium channel inactivation.Pflugers Archiv : European journal of physiology · 2008
    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

9 authors at 3 institutions in 3 countries.

Zhi SuDepartment of Integrative Pharmacology, Abbott Laboratories, 100 Abbott Park Road, Abbott Park, IL 60064, USA. zhi.su@abbott.com
James Limberis
Ruth L Martin
Rong Xu
Katrin Kolbe
Stefan H Heinemann
Toshinori Hoshi
Bryan F Cox
Gary A Gintant
Abbott Fund · USFriedrich Schiller University Jena · DEUniversity of Pennsylvania · US

Funding

REGULATION OF ION CHANNELS BY METHIONINE OXIDATIONR01GM057654 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI HOSHI, TOSHINORI, OLCESE, RICCARDO · 1998 to 2014
$5.0M
NIGMS NIH HHS R01 GM057654
6 · The paper itself

Abstract

Reactive species oxidatively modify numerous proteins including ion channels. Oxidative sensitivity of ion channels is often conferred by amino acids containing sulfur atoms, such as cysteine and methionine. Functional consequences of oxidative modification of methionine in human ether à go-go related gene 1 (hERG1), which encodes cardiac I(Kr) channels, are unknown. Here we used chloramine-T (ChT), which preferentially oxidizes methionine, to examine the functional consequences of methionine oxidation of hERG channels stably expressed in a human embryonic kidney cell line (HEK 293) and native hERG channels in a human neuroblastoma cell line (SH-SY5Y). ChT (300 microM) significantly decreased whole-cell hERG current in both HEK 293 and SH-SY5Y cells. In HEK 293 cells, the effects of ChT on hERG current were time- and concentration-dependent, and were markedly attenuated in the presence of enzyme methionine sulfoxide reductase A that specifically repairs oxidized methionine. After treatment with ChT, the channel deactivation upon repolarization to -60 or -100 mV was significantly accelerated. The effect of ChT on channel activation kinetics was voltage-dependent; activation slowed during depolarization to +30 mV but accelerated during depolarization to 0 or -10mV. In contrast, the reversal potential, inactivation kinetics, and voltage-dependence of steady-state inactivation remained unaltered. Our results demonstrate that the redox status of methionine is an important modulator of hERG channel.

Indexed as

Action PotentialsCell LineChloraminesERG1 Potassium ChannelEther-A-Go-Go Potassium ChannelsHumansMethionineOxidation-ReductionPotassiumTosyl CompoundsChloramineschloramine-TERG1 Potassium ChannelEther-A-Go-Go Potassium ChannelsKCNH2 protein, humanMethioninePotassiumTosyl Compounds

Identifiers

PMID17624316
PMCPMC3905454
OpenAlexW2079309179

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.