Evidence map›Paper›PMID 27538565›Full record

ArticleScientific reports2016

Cellular growth defects triggered by an overload of protein localization processes.

Reiko Kintaka, Koji Makanae, Hisao Moriya

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

37 citing papers in PubMed, 69 citations in OpenAlex.

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  13. Intra-Frontiers in genetics · 2023
    Article
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  17. TheeLife · 2022
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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

3 authors at 1 institution in 1 country.

Reiko KintakaGraduate School of Natural Science and Technology, Okayama University, Okayama, Japan.
Koji MakanaeResearch Core for Interdisciplinary Sciences, Okayama University, Okayama, Japan.
Hisao MoriyaResearch Core for Interdisciplinary Sciences, Okayama University, Okayama, Japan.
Okayama University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High-level expression of a protein localized to an intracellular compartment is expected to cause cellular defects because it overloads localization processes. However, overloads of localization processes have never been studied systematically. Here, we show that the expression levels of green fluorescent proteins (GFPs) with localization signals were limited to the same degree as a toxic misfolded GFP in budding yeast cells, and that their high-level expression caused cellular defects associated with localization processes. We further show that limitation of the exportin Crm1 determined the expression limit of GFP with a nuclear export signal. Although misfolding of GFP with a vesicle-mediated transport signal triggered endoplasmic reticulum stress, it was not the primary determinant of its expression limit. The precursor of GFP with a mitochondrial targeting signal caused a cellular defect. Finally, we estimated the residual capacities of localization processes. High-level expression of a localized protein thus causes cellular defects by overloading the capacities of localization processes.

Indexed as

Exportin 1 ProteinGreen Fluorescent ProteinsKaryopherinsProtein TransportReceptors, Cytoplasmic and NuclearSaccharomyces cerevisiaeExportin 1 ProteinGreen Fluorescent ProteinsKaryopherinsReceptors, Cytoplasmic and Nuclear

Identifiers

PMID27538565
PMCPMC4990933
OpenAlexW2514377612

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.