Evidence map›Paper›PMID 17085590›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

SK channels mediate NADPH oxidase-independent reactive oxygen species production and apoptosis in granulocytes.

Alex J Fay, Xiang Qian, Yuh Nung Jan, Lily Yeh Jan

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
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

27 citing papers in PubMed.

  1. SK3 channel and mitochondrial ROS mediate NADPH oxidase-independent NETosis induced by calcium influx.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Trial
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Neutrophils' Extracellular Trap Mechanisms: From Physiology to Pathology.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Article
  10. Neutrophils: Many Ways to Die.Frontiers in immunology · 2021
    Review
  11. Review
  12. Physiological Roles and Therapeutic Potential of CaFrontiers in molecular neuroscience · 2018
    Review
  13. Identity and function of a cardiac mitochondrial small conductance CaBiochimica et biophysica acta. Bioenergetics · 2017
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. NLRP3 inflammasome activation induced by engineered nanomaterials.Small (Weinheim an der Bergstrasse, Germany) · 2013
    Review
  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

4 authors.

Alex J FayGraduate Group in Biophysics, University of California, San Francisco, CA 94143-0725, USA.
Xiang Qian
Yuh Nung Jan
Lily Yeh Jan

Funding

Genetic Studies of the SynapseR01MH065334 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JAN, LILY Y · 2001 to 2020
$3.8M
Genetic Studies of the SynapseR37MH065334 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JAN, LILY Y · 2006 to 2015
$3.8M
NIMH NIH HHS MH 065334NIMH NIH HHS R01 MH065334NIMH NIH HHS R37 MH065334
6 · The paper itself

Abstract

Neutrophils are immune cells that bind to, engulf, and destroy bacterial and fungal pathogens in infected tissue, and their clearance by apoptosis is essential for the resolution of inflammation. Killing involves both oxidative and nonoxidative processes, the oxidative pathway requiring electrogenic production of superoxide by the membrane-bound NADPH oxidase complex. A variety of stimuli, from bacterial chemotactic peptides to complement- or IgG-opsonized microbes, can induce the production of reactive oxygen species (ROS) by neutrophils, presumably by means of NADPH oxidase. We report here that 1-ethyl-2-benzimidazolinone (1-EBIO), an activator of Ca2+-activated potassium channels of small conductance (SK) and intermediate conductance (IK), causes production of superoxide and hydrogen peroxide by neutrophils and granulocyte-differentiated PLB-985 cells. This response can be partially inhibited by the SK blocker apamin, which inhibits a Ca2+-activated K+ current in these cells. Analysis of RNA transcripts indicates that channels encoded by the SK3 gene carry this current. The effects of 1-EBIO and apamin are independent of the NADPH oxidase pathway, as demonstrated by using a PLB-985 cell line lacking the gp91phox subunit. Rather, 1-EBIO and apamin modulate mitochondrial ROS production. Consistent with the enhanced ROS production and K+ efflux mediated by 1-EBIO, we found that this SK opener increased apoptosis of PLB-985 cells. Together, these findings suggest a previously uncharacterized mechanism for the regulation of neutrophil ROS production and programmed cell death.

Indexed as

ApoptosisApaminBenzimidazolesCalciumCell LineGranulocytesMitochondriaNADPH OxidasesOxidation-ReductionPotassiumPotassium Channel BlockersReactive Oxygen SpeciesSmall-Conductance Calcium-Activated Potassium ChannelsTranscription, Genetic1-ethyl-2-benzimidazolinoneApaminBenzimidazolesCalciumNADPH OxidasesPotassiumPotassium Channel BlockersReactive Oxygen SpeciesSmall-Conductance Calcium-Activated Potassium Channels

Identifiers

PMID17085590
PMCPMC1634413

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.