Evidence map›Paper›PMID 16273079›Full record

ArticleCell death and differentiation2006

Apoptotic surface delivery of K+ channels.

S K Pal, K Takimoto, E Aizenman, E S Levitan

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Cell death and differentiation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

53 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
  2. Antagonistic roles of Ras-MAPK and Akt signaling in integrin-KFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Voltage-Gated Potassium Channels as Regulators of Cell Death.Frontiers in cell and developmental biology · 2020
    Review
  10. Ions, the Movement of Water and the Apoptotic Volume Decrease.Frontiers in cell and developmental biology · 2020
    Review
  11. Review
  12. Defining the Kv2.1-syntaxin molecular interaction identifies a first-in-class small molecule neuroprotectant.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  13. Article
  14. Disruption of KNeuroscience · 2017
    Article
  15. 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
  16. Review
  17. Article
  18. Article
  19. 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 at 1 institution in 1 country.

S K PalDepartment of Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15217, USA.
K Takimoto
E Aizenman
E S Levitan
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 R01 NS043277NINDS NIH HHS R56 NS043277
6 · The paper itself

Abstract

Apoptosis in cortical neurons requires efflux of cytoplasmic potassium mediated by a surge in Kv2.1 channel activity. Pharmacological blockade or molecular disruption of these channels in neurons prevents apoptotic cell death, while ectopic expression of Kv2.1 channels promotes apoptosis in non-neuronal cells. Here, we use a cysteine-containing mutant of Kv2.1 and a thiol-reactive covalent inhibitor to demonstrate that the increase in K+ current during apoptosis is due to de novo insertion of functional channels into the plasma membrane. Biotinylation experiments confirmed the delivery of additional Kv2.1 protein to the cell surface following an apoptotic stimulus. Finally, expression of botulinum neurotoxins that cleave syntaxin and synaptosome-associated protein of 25 kDa (SNAP-25) blocked upregulation of surface Kv2.1 channels in cortical neurons, suggesting that target soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins support proapoptotic delivery of K+ channels. These data indicate that trafficking of Kv2.1 channels to the plasma membrane causes the apoptotic surge in K+ current.

Indexed as

ApoptosisAnimalsBiotinylationCell MembraneCells, CulturedCerebral CortexCHO CellsCricetinaeCricetulusMembrane PotentialsNeuronsPotassiumPyridinesRatsRats, Sprague-DawleyShab Potassium ChannelsPotassiumPyridinesShab Potassium ChannelsSNARE Proteins

Identifiers

PMID16273079
PMCPMC1403161
OpenAlexW2021797855

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.