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ID 115577
Title Alternative
Role of PERK in mitochondrial function
Author
Kato, Hironori University of Miyazaki
Okabe, Kohki The University of Tokyo
Hattori, Kazuki The University of Tokyo
Fukaya, Tomohiro University of Miyazaki
Tanimoto, Kousuke Tokyo Medical and Dental University
Beini, Shi The University of Tokyo
Mizuguchi, Mariko University of the Ryukyus
Torii, Satoru TMDU
Arakawa, Satoko TMDU
Ono, Masaya National Cancer Center Research Institute
Saito, Yusuke University of Miyazaki
Sugiyama, Takashi University of Miyazaki
Funatsu, Takashi The University of Tokyo
Sato, Katsuaki University of Miyazaki
Shimizu, Shigeomi TMDU
Ichijo, Hidenori The University of Tokyo
Kadowaki, Hisae University of Miyazaki
Nishitoh, Hideki University of Miyazaki
Content Type
Journal Article
Description
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.
Journal Title
Life Science Alliance
ISSN
25751077
Publisher
Life Science Alliance
Volume
3
Issue
3
Start Page
e201900576
Published Date
2020-02-06
Rights
This article is available under a Creative Commons License (Attribution 4.0 International, as described at https://creativecommons.org/licenses/by/4.0/).
EDB ID
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Publisher
departments
Institute of Advanced Medical Sciences