Evidence map›Paper›PMID 25799407›Full record

ArticlePloS one2015

Development of a molecularly evolved, highly sensitive CaMKII FRET sensor with improved expression pattern.

Akihiro C E Shibata, Hiroshi K Maebashi, Yoshihisa Nakahata, Junichi Nabekura, Hideji Murakoshi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

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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

5 authors at 3 institutions in 1 country.

Akihiro C E ShibataSupportive Center for Brain Research, National Institute for Physiological Science, Okazaki, Aichi, Japan; Okazaki Institute for Integrative Bioscience, Okazaki, Aichi, Japan.
Hiroshi K MaebashiSupportive Center for Brain Research, National Institute for Physiological Science, Okazaki, Aichi, Japan.
Yoshihisa NakahataDivision of Homeostatic Development, National Institute for Physiological Science, Okazaki, Aichi, Japan.
Junichi NabekuraDivision of Homeostatic Development, National Institute for Physiological Science, Okazaki, Aichi, Japan; Department of Physiological Sciences, The Graduate University for Advanced Studies, Okazaki, Aichi, Japan; Core Research for Evolutional Science and Technology, Japan Science and Technology Agency (JST), Kawaguchi, Saitama, Japan.
Hideji MurakoshiSupportive Center for Brain Research, National Institute for Physiological Science, Okazaki, Aichi, Japan; Department of Physiological Sciences, The Graduate University for Advanced Studies, Okazaki, Aichi, Japan; Precursory Research for Embryonic Science and Technology, Japan Science and Technology Agency (JST), Kawaguchi, Saitama, Japan.
National Institute for Physiological Sciences · JPJapan Science and Technology Agency · JPThe Graduate University for Advanced Studies, SOKENDAI · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetically encoded fluorescence resonance energy transfer (FRET) biosensors have been successfully used to visualize protein activity in living cells. The sensitivity and accuracy of FRET measurements directly depend on biosensor folding efficiency, expression pattern, sensitivity, and dynamic range. Here, to improve the folding efficiency of the Ca2+/calmodulin-dependent protein kinase II alpha (CaMKIIα) FRET biosensor, we amplified the association domain of the CaMKIIα gene using error-prone polymerase chain reaction (PCR) and fused it to the N-terminus of mCherry in a bacterial expression vector. We also created an Escherichia coli expression library based on a previously reported fluorescent protein folding reporter method, and found a bright red fluorescent colony that contained the association domain with four mutations (F394L, I419V, A430T, and I434T). In vitro assays using the purified mutant protein confirmed improved folding kinetics of the downstream fluorescent protein, but not of the association domain itself. Furthermore, we introduced these mutations into the previously reported CaMKIIα FRET sensor and monitored its Ca2+/calmodulin-dependent activation in HeLa cells using 2-photon fluorescence lifetime imaging microscopy (2pFLIM), and found that the expression pattern and signal reproducibility of the mutant sensor were greatly improved without affecting the autophosphorylation function and incorporation into oligomeric CaMKIIα. We believe that our improved CaMKIIα FRET sensor would be useful in various types of cells and tissues, providing data with high accuracy and reproducibility. In addition, the method described here may also be applicable for improving the performance of all currently available FRET sensors.

Indexed as

MutationAnimalsBiosensing TechniquesCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Escherichia coliFluorescence Resonance Energy TransferHeLa CellsHumansLuminescent ProteinsModels, MolecularProtein FoldingProtein Structure, TertiaryRatsRecombinant ProteinsRed Fluorescent ProteinCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Luminescent ProteinsRecombinant ProteinsRed Fluorescent Protein

Identifiers

PMID25799407
PMCPMC4370617
OpenAlexW2013860167

What OpenQuestion holds

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LicenceCC BY
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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.