Evidence map›Paper›PMID 17573431›Full record

ArticleBiophysical journal2007

The electrophysiology of the beta-cell based on single transmembrane protein characteristics.

Michael E Meyer-Hermann

Abstract read
In one paragraph

Article in Biophysical journal, 2007. 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
–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

16 citing papers in PubMed.

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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

1 author.

Michael E Meyer-HermannFrankfurt Institute for Advanced Studies, Frankfurt, Germany. m.meyer-hermann@fias.uni-frankfurt.de

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The electrophysiology of beta-cells is at the origin of insulin secretion. beta-Cells exhibit a complex behavior upon stimulation with glucose including repeated bursts and continuous spiking. Mathematical modeling is most suitable to improve knowledge about the function of various transmembrane currents provided the model is based on reliable data. This is the first attempt to build a mathematical model for the beta-cell electrophysiology in a bottom-up approach that relies on single protein conductance data. The results of previous whole-cell-based models are reconsidered. The full simulation including all prominent transmembrane proteins in beta-cells is used to provide a functional interpretation of their role in beta-cell bursting and an updated vantage point of beta-cell electrophysiology. As a result of a number of in silico knock-out and block experiments the novel model makes some unexpected predictions: single-channel conductance data imply that large-conductance calcium-gated potassium currents acquire the potential of driving oscillations at supralarge glucose levels. A more complex burst interruption model is presented. It also turns out that, depending on the species, sodium currents may be more relevant than considered so far. Experiments are proposed to verify these predictions.

Indexed as

Models, BiologicalAction PotentialsAnimalsBiological ClocksCalcium SignalingCells, CulturedComputer SimulationHumansInsulin-Secreting CellsIon Channel GatingMembrane PotentialsMembrane ProteinsMembrane Proteins

Identifiers

PMID17573431
PMCPMC1989707

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.