Evidence map›Paper›PMID 16006035›Full record

ArticleNeuroscience letters2005

Obligatory role of ASK1 in the apoptotic surge of K+ currents.

Mandar A Aras, Elias Aizenman

Open access · greenAbstract read
In one paragraph

Article in Neuroscience letters, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

17 citing papers in PubMed, 33 citations in OpenAlex.

  1. Redox Regulation of KAntioxidants & redox signaling · 2024
    Review
  2. Review
  3. Tyrosine Phosphorylation of the KInternational journal of molecular sciences · 2020
    Article
  4. ZnExperimental neurology · 2018
    Article
  5. Targeting a Potassium Channel/Syntaxin Interaction Ameliorates Cell Death in Ischemic Stroke.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Convergent Ca2+ and Zn2+ signaling regulates apoptotic Kv2.1 K+ currents.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  11. Review
  12. Article
  13. The neurophysiology and pathology of brain zinc.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Review
  14. Suppression of a pro-apoptotic K+ channel as a mechanism for hepatitis C virus persistence.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  15. Article
  16. Article
  17. Apoptotic surface delivery of K+ channels.Cell death and differentiation · 2006
    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

2 authors at 1 institution in 1 country.

Mandar A ArasDepartment of Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.
Elias Aizenman
University of Pittsburgh · US

Funding

Liberation of Intracellular Zinc and Neuronal Cell DeathR01NS043277 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AIZENMAN, ELIAS · 2002 to 2022
$8.2M
Liberation of Intracellular Zinc and Neuronal Cell DeathR56NS043277 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AIZENMAN, ELIAS · 2007 to 2007
$371k
NINDS NIH HHS NS43277NINDS NIH HHS R01 NS043277NINDS NIH HHS R56 NS043277
6 · The paper itself

Abstract

Apoptosis signal-regulating kinase 1 (ASK1) is a critical component of mitogen-activated protein kinase signaling pathways leading to cell death in response to cytokines and cellular stress. We use a dominant-negative (DN) form of ASK1 to show that this enzyme is necessary for the delayed surge in neuronal K+ channel activity, a required step in apoptosis. Furthermore, expression of ASK1 DN also suppresses the apoptotic increase in Kv2.1 currents transiently expressed in Chinese hamster ovary cells. Finally, over-expression of thioredoxin, an inhibitory binding partner of ASK1, is sufficient to halt the apoptotic current surge in neurons. Thus, ASK1 is an obligatory component of the pro-apoptotic modulation of K+ channels.

Indexed as

AnimalsApoptosisCells, CulturedCerebral CortexCHO CellsCricetinaeMAP Kinase Kinase Kinase 5MAP Kinase Signaling SystemNerve DegenerationOxidative StressPotassium ChannelsRatsThioredoxinsUp-RegulationMAP Kinase Kinase Kinase 5Potassium ChannelsThioredoxins

Identifiers

PMID16006035
PMCPMC2947746
OpenAlexW2038787225

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.