Evidence map›Paper›PMID 10024359›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

Identification of the Kv2.1 K+ channel as a major component of the delayed rectifier K+ current in rat hippocampal neurons.

H Murakoshi, J S Trimmer

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 169 papers.

0numbers the graph read from it
0cells of the map it votes in
169citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

169 citing papers in PubMed, 307 citations in OpenAlex.

  1. Article
  2. Review
  3. Glucocorticoids Rapidly Modulate CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  4. The involvement of KTranslational psychiatry · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Flavonoids as Modulators of Potassium Channels.International journal of molecular sciences · 2023
    Review
  14. Increased KCells · 2022
    Article
  15. Activity-dependent endoplasmic reticulum CaProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  16. Review
  17. Mechanism of use-dependent Kv2 channel inhibition by RY785.The Journal of general physiology · 2022
    Article
  18. Article
  19. Review
  20. Article

109 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

2 authors at 1 institution in 1 country.

H MurakoshiDepartment of Biochemistry and Cell Biology and Institute for Cell and Developmental Biology, State University of New York, Stony Brook, New York 11794-5215, USA.
J S Trimmer
State University of New York · US

Funding

REGULATION OF THE PERIPHERAL NERVE SPECIFIC SODIUM CHANNEL, PN1P01NS034375 · NINDS · STATE UNIVERSITY NEW YORK STONY BROOK · PI HALEGOUA, SIMON · 1996 to 2000
$1.0M
NINDS NIH HHS NS34375
6 · The paper itself

Abstract

Molecular cloning studies have revealed the existence of a large family of voltage-gated K+ channel genes expressed in mammalian brain. This molecular diversity underlies the vast repertoire of neuronal K+ channels that regulate action potential conduction and neurotransmitter release and that are essential to the control of neuronal excitability. However, the specific contribution of individual K+ channel gene products to these neuronal K+ currents is poorly understood. We have shown previously, using an antibody, "KC, " specific for the Kv2.1 K+ channel alpha-subunit, the high-level expression of Kv2.1 protein in hippocampal neurons in situ and in culture. Here we show that KC is a potent blocker of K+ currents expressed in cells transfected with the Kv2.1 cDNA, but not of currents expressed in cells transfected with other highly related K+ channel alpha-subunit cDNAs. KC also blocks the majority of the slowly inactivating outward current in cultured hippocampal neurons, although antibodies to two other K+ channel alpha-subunits known to be expressed in these cells did not exhibit blocking effects. In all cases the blocking effects of KC were eliminated by previous incubation with a recombinant fusion protein containing the KC antigenic sequence. Together these studies show that Kv2.1, which is expressed at high levels in most mammalian central neurons, is a major contributor to the delayed rectifier K+ current in hippocampal neurons and that the KC antibody is a powerful tool for the elucidation of the role of the Kv2.1 K+ channel in regulating neuronal excitability.

Indexed as

Potassium Channels, Voltage-GatedAnimalsAntibodiesAntibody SpecificityCells, CulturedDelayed Rectifier Potassium ChannelsDendritesEmbryo, MammalianFibroblastsHippocampusIn Vitro TechniquesMiceMicroscopy, FluorescenceNeuronsPatch-Clamp TechniquesPotassiumAntibodiesDelayed Rectifier Potassium ChannelsKcnb1 protein, mouseKcnb1 protein, ratPotassiumPotassium ChannelsPotassium Channels, Voltage-GatedShab Potassium Channels

Identifiers

PMID10024359
PMCPMC6782166
OpenAlexW2099949778

What OpenQuestion holds

Texttitle and abstract
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.