Evidence map›Paper›PMID 20566856›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Localization-dependent activity of the Kv2.1 delayed-rectifier K+ channel.

Kristen M S O'Connell, Robert Loftus, Michael M Tamkun

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing 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

95 citing papers in PubMed.

  1. Article
  2. Article
  3. Ion channels and actin: A tale of two friends.Histology and histopathology · 2025
    Review
  4. Article
  5. Article
  6. Glucocorticoids Rapidly Modulate CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. The formation of KCommunications biology · 2023
    Article
  11. The formation of KResearch square · 2023
    Article
  12. Article
  13. Review
  14. Article
  15. Increased KCells · 2022
    Article
  16. Activity-dependent endoplasmic reticulum CaProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  17. Review
  18. Mechanism of use-dependent Kv2 channel inhibition by RY785.The Journal of general physiology · 2022
    Article
  19. Article
  20. Article

35 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

3 authors.

Kristen M S O'ConnellDepartment of Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA.
Robert Loftus
Michael M Tamkun

Funding

Kv2.1 membrane corrals:Regulators of K+ channel function and traffickingR01GM084136 · NIGMS · COLORADO STATE UNIVERSITY · PI TAMKUN, MICHAEL M. · 2009 to 2012
$1.6M
Cell Biology of Cardiac Kv ChannelsR00HL087591 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI O'CONNELL, KRISTEN M · 2009 to 2011
$740k
NHLBI NIH HHS R00 HL087591NIGMS NIH HHS R01 GM084136NIGMS NIH HHS R01GM084136
6 · The paper itself

Abstract

The Kv2.1 K(+) channel is highly expressed throughout the brain, where it regulates excitability during periods of high-frequency stimulation. Kv2.1 is unique among Kv channels in that it targets to large surface clusters on the neuronal soma and proximal dendrites. These clusters also form in transfected HEK cells. Following excessive excitatory stimulation, Kv2.1 declusters with an accompanying 20- to 30-mV hyperpolarizing shift in the activation threshold. Although most Kv2.1 channels are clustered, there is a pool of Kv2.1 resident outside of these domains. Using the cell-attached patch clamp technique, we investigated the hypothesis that Kv2.1 activity varies as a function of cell surface location. We found that clustered Kv2.1 channels do not efficiently conduct K(+), whereas the nonclustered channels are responsible for the high threshold delayed rectifier K(+) current typical of Kv2.1. Comparison of gating and ionic currents indicates only 2% of the surface channels conduct, suggesting that the clustered channels still respond to membrane potential changes. Declustering induced via either actin depolymerization or alkaline phosphatase treatment did not increase whole-cell currents. Dephosphorylation resulted in a 25-mV hyperpolarizing shift, whereas actin depolymerization did not alter the activation midpoint. Taken together, these data demonstrate that clusters do not contain high threshold Kv2.1 channels whose voltage sensitivity shifts upon declustering; nor are they a reservoir of nonconducting channels that are activated upon release. On the basis of these findings, we propose unique roles for the clustered Kv2.1 that are independent of K(+) conductance.

Indexed as

AlgorithmsCell LineCell MembraneGreen Fluorescent ProteinsHumansIon Channel GatingMembrane PotentialsPatch-Clamp TechniquesPotassiumQuantum DotsRecombinant Fusion ProteinsShab Potassium ChannelsTransfectionGreen Fluorescent ProteinsPotassiumRecombinant Fusion ProteinsShab Potassium Channels

Identifiers

PMID20566856
PMCPMC2901471

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.