Evidence map›Paper›PMID 32029570›Full record

ArticleLife science alliance2020

ER-resident sensor PERK is essential for mitochondrial thermogenesis in brown adipose tissue.

Hironori Kato, Kohki Okabe, Masato Miyake, Kazuki Hattori, Tomohiro Fukaya, Kousuke Tanimoto, Shi Beini, Mariko Mizuguchi, Satoru Torii, Satoko Arakawa and 10 more

Abstract read
In one paragraph

Article in Life science alliance, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
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

27 citing papers in PubMed.

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  10. CLCF1 inhibits energy expenditure via suppressing brown fat thermogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

20 authors.

Hironori KatoLaboratory of Biochemistry and Molecular Biology, Department of Medical Sciences, University of Miyazaki, Miyazaki, Japan.
Kohki OkabeLaboratory of Bioanalytical Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Masato MiyakeDivision of Molecular Biology, Institute for Genome Research, Institute of Advanced Medical Sciences, Tokushima University, Tokushima, Japan.
Kazuki HattoriLaboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-5592-4257
Tomohiro FukayaDivision of Immunology, Department of Infectious Diseases, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Kousuke TanimotoGenome Laboratory, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Shi BeiniLaboratory of Bioanalytical Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Mariko MizuguchiDepartment of Immunology, Graduate School of Medicine, University of the Ryukyus, Okinawa, Japan.
Satoru ToriiDepartment of Pathological Cell Biology, Medical Research Institute, TMDU, Tokyo, Japan.
Satoko ArakawaDepartment of Pathological Cell Biology, Medical Research Institute, TMDU, Tokyo, Japan.
Masaya OnoDepartment of Clinical Proteomics, National Cancer Center Research Institute, Tokyo, Japan.
Yusuke SaitoDivision of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Takashi SugiyamaLaboratory of Biochemistry and Molecular Biology, Department of Medical Sciences, University of Miyazaki, Miyazaki, Japan.
Takashi FunatsuLaboratory of Bioanalytical Chemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-9656-8308
Katsuaki SatoDivision of Immunology, Department of Infectious Diseases, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
Shigeomi ShimizuDepartment of Pathological Cell Biology, Medical Research Institute, TMDU, Tokyo, Japan.
Seiichi OyadomariDivision of Molecular Biology, Institute for Genome Research, Institute of Advanced Medical Sciences, Tokushima University, Tokushima, Japan.
Hidenori IchijoLaboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Hisae KadowakiLaboratory of Biochemistry and Molecular Biology, Department of Medical Sciences, University of Miyazaki, Miyazaki, Japan.
Hideki NishitohLaboratory of Biochemistry and Molecular Biology, Department of Medical Sciences, University of Miyazaki, Miyazaki, Japan nishitoh@med.miyazaki-u.ac.jp.ORCID 0000-0002-8652-4109

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria play a central role in the function of brown adipocytes (BAs). Although mitochondrial biogenesis, which is indispensable for thermogenesis, is regulated by coordination between nuclear DNA transcription and mitochondrial DNA transcription, the molecular mechanisms of mitochondrial development during BA differentiation are largely unknown. Here, we show the importance of the ER-resident sensor PKR-like ER kinase (PERK) in the mitochondrial thermogenesis of brown adipose tissue. During BA differentiation, PERK is physiologically phosphorylated independently of the ER stress. This PERK phosphorylation induces transcriptional activation by GA-binding protein transcription factor α subunit (GABPα), which is required for mitochondrial inner membrane protein biogenesis, and this novel role of PERK is involved in maintaining the body temperatures of mice during cold exposure. Our findings demonstrate that mitochondrial development regulated by the PERK-GABPα axis is indispensable for thermogenesis in brown adipose tissue.

Indexed as

Adipocytes, BrownAdipose Tissue, BrownAnimalsCell DifferentiationDNA, MitochondrialeIF-2 KinaseEndoplasmic ReticulumFemaleMaleMiceMice, Inbred ICRMitochondriaOrganelle BiogenesisPhosphorylationSignal TransductionThermogenesisDNA, MitochondrialeIF-2 Kinase

Identifiers

PMID32029570
PMCPMC7010021

What OpenQuestion holds

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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.