Evidence map›Paper›PMID 32637591›Full record

ArticleScience advances2020

Stress-responsive MTK1 SAPKKK serves as a redox sensor that mediates delayed and sustained activation of SAPKs by oxidative stress.

Moe Matsushita, Takanori Nakamura, Hisashi Moriizumi, Hiroaki Miki, Mutsuhiro Takekawa

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. The cellular model for Alzheimer's disease research: PC12 cells.Frontiers in molecular neuroscience · 2022
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  15. Neutrophil elastase: From mechanisms to therapeutic potential.Journal of pharmaceutical analysis · 2023
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  18. Reactive oxygen species signalling in plant stress responses.Nature reviews. Molecular cell biology · 2022
    Review
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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 2 institutions in 1 country.

Moe MatsushitaDivision of Cell Signaling and Molecular Medicine, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.ORCID 0000-0002-0835-9945
Takanori NakamuraDivision of Cell Signaling and Molecular Medicine, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.ORCID 0000-0002-2915-2257
Hisashi MoriizumiDivision of Cell Signaling and Molecular Medicine, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.ORCID 0000-0003-3257-5477
Hiroaki MikiDepartment of Cellular Regulation, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan.ORCID 0000-0003-0454-7006
Mutsuhiro TakekawaDivision of Cell Signaling and Molecular Medicine, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan.ORCID 0000-0002-8027-3847
The University of Tokyo · JPThe University of Osaka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cells respond to oxidative stress by inducing intracellular signaling, including stress-activated p38 and JNK MAPK (SAPK) pathways, but the underlying mechanisms remain unclear. Here, we report that the MAP three kinase 1 (MTK1) SAPK kinase kinase (SAPKKK) functions as an oxidative-stress sensor that perceives the cellular redox state and transduces it into SAPK signaling. Following oxidative stress, MTK1 is rapidly oxidized and gradually reduced at evolutionarily conserved cysteine residues. These coupled oxidation-reduction modifications of MTK1 elicit its catalytic activity. Gene knockout experiments showed that oxidative stress-induced SAPK signaling is mediated by coordinated activation of the two SAPKKKs, MTK1 and apoptosis signal-regulating kinase 1 (ASK1), which have different time and dose-response characteristics. The MTK1-mediated redox sensing system is crucial for delayed and sustained SAPK activity and dictates cell fate decisions including cell death and interleukin-6 production. Our results delineate a molecular mechanism by which cells generate optimal biological responses under fluctuating redox environments.

Identifiers

PMID32637591
PMCPMC7314524
OpenAlexW3037358576

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.