Evidence map›Paper›PMID 36077279›Full record

ArticleInternational journal of molecular sciences2022

Direct Analysis of Mitochondrial Damage Caused by Misfolded/Destabilized Proteins.

Jannatul Aklima, Sawaros Onchaiya, Tomonori Saotome, Punitha Velmurugan, Taihei Motoichi, Jannatul Naima, Yutaka Kuroda, Yoshihiro Ohta

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 54% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
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

8 authors at 3 institutions in 2 countries.

Jannatul AklimaDivision of Biotechnology and Life Sciences, Tokyo University of Agriculture and Technology, 2-24-16 Nakacho, Koganei, Tokyo 184-8588, Japan.
Sawaros OnchaiyaDivision of Biotechnology and Life Sciences, Tokyo University of Agriculture and Technology, 2-24-16 Nakacho, Koganei, Tokyo 184-8588, Japan.
Tomonori SaotomeDivision of Biotechnology and Life Sciences, Tokyo University of Agriculture and Technology, 2-24-16 Nakacho, Koganei, Tokyo 184-8588, Japan.
Punitha VelmuruganDivision of Biotechnology and Life Sciences, Tokyo University of Agriculture and Technology, 2-24-16 Nakacho, Koganei, Tokyo 184-8588, Japan.
Taihei MotoichiDivision of Biotechnology and Life Sciences, Tokyo University of Agriculture and Technology, 2-24-16 Nakacho, Koganei, Tokyo 184-8588, Japan.
Jannatul NaimaDivision of Biotechnology and Life Sciences, Tokyo University of Agriculture and Technology, 2-24-16 Nakacho, Koganei, Tokyo 184-8588, Japan.
Yutaka KurodaDivision of Biotechnology and Life Sciences, Tokyo University of Agriculture and Technology, 2-24-16 Nakacho, Koganei, Tokyo 184-8588, Japan.ORCID 0000-0002-3221-4295
Yoshihiro OhtaDivision of Biotechnology and Life Sciences, Tokyo University of Agriculture and Technology, 2-24-16 Nakacho, Koganei, Tokyo 184-8588, Japan.ORCID 0000-0001-7416-0507
Tokyo University of Agriculture and Technology · JPNagaoka University of Technology · JPUniversity of Chittagong · BD

Funding

Japan Science and Technology Agency OPERA(JPMJOP1833)
6 · The paper itself

Abstract

Protein quality control is essential for cellular homeostasis. In this study, we examined the effect of improperly folded proteins that do not form amyloid fibrils on mitochondria, which play important roles in ATP production and cell death. First, we prepared domain 3 of the dengue envelope protein in wild type and four mutants with widely different biophysical properties in misfolded/aggregated or destabilized states. The effects of the different proteins were detected using fluorescence microscopy and Western blotting, which revealed that three of the five proteins disrupted both inner and outer membrane integrity, while the other two proteins, including the wild type, did not. Next, we examined the common characteristics of the proteins that displayed toxicity against mitochondria by measuring oligomer size, molten globule-like properties, and thermal stability. The common feature of all three toxic proteins was thermal instability. Therefore, our data strongly suggest that thermally unstable proteins generated in the cytosol can cause cellular damage by coming into direct contact with mitochondria. More importantly, we revealed that this damage is not amyloid-specific.

Indexed as

AmyloidAmyloidosisCytosolHomeostasisHumansMitochondriaMitochondrial ProteinsAmyloidMitochondrial Proteinsdengue envelope protein domain 3membranemisfolded proteinmitochondriathermal instability

Identifiers

PMID36077279
PMCPMC9456338
OpenAlexW4293771169

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.