Evidence map›Paper›PMID 14612577›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2003

Dissection of K+ currents in Caenorhabditis elegans muscle cells by genetics and RNA interference.

C M Santi, A Yuan, G Fawcett, Z-W Wang, A Butler, M L Nonet, A Wei, P Rojas, L Salkoff

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.5field-weighted citation impact, top 41% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

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  11. CLHM-1 is a functionally conserved and conditionally toxic Ca2+-permeable ion channel in Caenorhabditis elegans.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  12. Article
  13. Action potentials drive body wall muscle contractions in Caenorhabditis elegans.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  14. Article
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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

9 authors at 1 institution in 1 country.

C M SantiDepartment of Anatomy and Neurobiology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis MO 63110, USA.
A Yuan
G Fawcett
Z-W Wang
A Butler
M L Nonet
A Wei
P Rojas
L Salkoff
Centro de Estudios Científicos · CL

Funding

A COMPREHENSIVE RESOURCE BASE OF C. ELEGANS K+ CHANNELSR24RR017342 · NCRR · WASHINGTON UNIVERSITY · PI SALKOFF, LAWRENCE B · 2003 to 2007
$2.2M
Mutant Analysis of a Novel High Conductance K+ ChannelR01GM067154 · NIGMS · WASHINGTON UNIVERSITY · PI SALKOFF, LAWRENCE B · 2003 to 2006
$1.2M
NCRR NIH HHS R24 RR017342NCRR NIH HHS R24 RR017342-01NIGMS NIH HHS R01 GM067154NIGMS NIH HHS R01 GM067154-01A1
6 · The paper itself

Abstract

GFP-promoter experiments have previously shown that at least nine genes encoding potassium channel subunits are expressed in Caenorhabditis elegans muscle. By using genetic, RNA interference, and physiological techniques we revealed the molecular identity of the major components of the outward K+ currents in body wall muscle cells in culture. We found that under physiological conditions, outward current is dominated by the products of only two genes, Shaker (Kv1) and Shal (Kv4), both expressing voltage-dependent potassium channels. Other channels may be held in reserve to respond to particular circumstances. Because GFP-promoter experiments indicated that slo-2 expression is prominent, we created a deletion mutant to identify the SLO-2 current in vivo. In both whole-cell and single-channel modes, in vivo SLO-2 channels were active only when intracellular Ca2+ and Cl- were raised above normal physiological conditions, as occurs during hypoxia. Under such conditions, SLO-2 is the largest outward current, contributing up to 87% of the total current. Other channels are present in muscle, but our results suggest that they are unlikely to contribute a large outward component under physiological conditions. However, they, too, may contribute currents conditional on other factors. Hence, the picture that emerges is of a complex membrane with a small number of household conductances functioning under normal circumstances, but with additional conductances that are activated during unusual circumstances.

Indexed as

Potassium Channels, Voltage-GatedAnimalsAnimals, Genetically ModifiedCaenorhabditis elegansCaenorhabditis elegans ProteinsGenes, HelminthMembrane Transport ProteinsMusclesMutationPotassium ChannelsRNA InterferenceShaker Superfamily of Potassium ChannelsShal Potassium ChannelsCaenorhabditis elegans ProteinsMembrane Transport ProteinsPotassium ChannelsPotassium Channels, Voltage-GatedShaker Superfamily of Potassium ChannelsShal Potassium ChannelsSLO-2 protein, C elegans

Identifiers

PMID14612577
PMCPMC283602
OpenAlexW2109924563

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.