Evidence map›Paper›PMID 18502812›Full record

ArticleBiophysical journal2008

A simulation study on the activation of cardiac CaMKII delta-isoform and its regulation by phosphatases.

Hiroaki Chiba, Natalie S Schneider, Satoshi Matsuoka, Akinori Noma

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 34 citations in OpenAlex.

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  9. The delicate bistability of CaMKII.Biophysical journal · 2013
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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

4 authors at 1 institution in 1 country.

Hiroaki ChibaCell/Biodynamics Simulation Project, Kyoto University, Kyoto, Japan.
Natalie S Schneider
Satoshi Matsuoka
Akinori Noma
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although the highly conserved Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is known to play an essential role in cardiac myocytes, its involvement in the frequency-dependent acceleration of relaxation is still controversial. To investigate the functional significance of CaMKII autophosphorylation and its regulation by protein phosphatases (PPs) in heart, we developed a new mathematical model for the CaMKIIdelta isoform. Due to better availability of experimental data, the model was first adjusted to the kinetics of the neuronal CaMKIIalpha isoform and then converted to a CaMKIIdelta model by fitting to kinetic data of the delta isoform. Both models satisfactorily reproduced experimental data of the CaMKII-calmodulin interaction, the autophosphorylation rate, and the frequency dependence of activation. The level of autophosphorylated CaMKII cumulatively increased upon starting the Ca(2+) stimulation at 3 Hz in the delta model. Variations in PP concentration remarkably affected the frequency-dependent activation of CaMKIIdelta, suggesting that cellular PP activity plays a key role in adjusting CaMKII activation in heart. The inhibitory effect of PP was stronger for CaMKIIalpha compared to CaMKIIdelta. Simulation results revealed a potential involvement of CaMKIIdelta autophosphorylation in the frequency-dependent acceleration of relaxation at physiological heart rates and PP concentrations.

Indexed as

Computer SimulationModels, BiologicalAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Enzyme ActivationIsoenzymesKineticsMyocytes, CardiacPhosphoric Monoester HydrolasesPhosphorylationCalcium-Calmodulin-Dependent Protein Kinase Type 2IsoenzymesPhosphoric Monoester Hydrolases

Identifiers

PMID18502812
PMCPMC2517018
OpenAlexW2008198783

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.