Evidence map›Paper›PMID 21099262›Full record

ArticleIslets

Physiological significance of SK4 channels in pancreatic β-cell oscillations.

Gisela Drews

Abstract readComment
PubMed Publisher
In one paragraph

Article in Islets. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author.

Gisela DrewsInstitute of Pharmacy, Department of Pharmacology, University of Tübingen, Tübingen, Germany. gisela.drews@uni-tuebingen.de

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic beta-cells show oscillations in membrane potential (Vm), the cytosolic Ca (2+) concentration ([Ca (2+) ]c) and finally insulin secretion. It is well accepted that the initiation of a burst phase with action potentials is mediated by voltage-dependent Ca (2+) (and Na (+) ) channels. The mechanism triggering the onset of interburst phases is less clear. The exact nature of the K (+) channels that hyperpolarize Vm to maintain the rhythmic activity is unknown. In 1999 Göpel and co-workers (1) described a current termed Kslow and claimed that this current terminates the burst phases. KATP current is a part of the Kslow current. We could show that the Ca (2+) -dependent K (+) current through K (+) channels of intermediate conductance (SK4, KCa3.1 or IK1) also contributes to the Kslow current. We suggest that the Kslow current is composed of two currents through metabolism-regulated K (+) channels, KATP (regulated by ATP) and SK4 (regulated by Ca (2+) ). We further propose that the SK4 component of the Kslow current can trigger oscillations in mice without functioning KATP channels.

Indexed as

AnimalsBiological ClocksElectrophysiologyInsulin-Secreting CellsIntermediate-Conductance Calcium-Activated Potassium ChannelsMembrane PotentialsMiceModels, BiologicalIntermediate-Conductance Calcium-Activated Potassium ChannelsKcnn4 protein, mouse

Identifiers

PMID21099262

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.