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Emerging Role of GCN1 in Disease and Homeostasis

発表形態:
資料・解説・論説・研究報告・総合雑誌の論文
主要業績:
主要業績
単著・共著:
共著
発表年月:
2024年03月
DOI:
10.3390/ijms25052998
会議属性:
指定なし
査読:
有り
リンク情報:

日本語フィールド

著者:
Tatara, Yota; Kasai, Shuya; Kokubu, Daichi; Tsujita, Tadayuki; Mimura, Junsei; Itoh, Ken
題名:
Emerging Role of GCN1 in Disease and Homeostasis
発表情報:
International Journal of Molecular Sciences 巻: 25 号: 5 ページ: -
キーワード:
概要:
GCN1 is recognized as a factor that is essential for the activation of GCN2, which is a sensor of amino acid starvation. This function is evolutionarily conserved from yeast to higher eukaryotes. However, recent studies have revealed non-canonical functions of GCN1 that are independent of GCN2, such as its participation in cell proliferation, apoptosis, and the immune response, beyond the borders of species. Although it is known that GCN1 and GCN2 interact with ribosomes to accomplish amino acid starvation sensing, recent studies have reported that GCN1 binds to disomes (i.e., ribosomes that collide each other), thereby regulating both the co-translational quality control and stress response. We propose that GCN1 regulates ribosome-mediated signaling by dynamically changing its partners among RWD domain-possessing proteins via unknown mechanisms. We recently demonstrated that GCN1 is essential for cell proliferation and whole-body energy regulation in mice. However, the manner in which ribosome-initiated signaling via GCN1 is related to various physiological functions warrants clarification. GCN1-mediated mechanisms and its interaction with other quality control and stress response signals should be important for proteostasis during aging and neurodegenerative diseases, and may be targeted for drug development.
抄録:

英語フィールド

Author:
Tatara, Yota; Kasai, Shuya; Kokubu, Daichi; Tsujita, Tadayuki; Mimura, Junsei; Itoh, Ken
Title:
Emerging Role of GCN1 in Disease and Homeostasis
Announcement information:
International Journal of Molecular Sciences Vol: 25 Issue: 5 Page: -
An abstract:
GCN1 is recognized as a factor that is essential for the activation of GCN2, which is a sensor of amino acid starvation. This function is evolutionarily conserved from yeast to higher eukaryotes. However, recent studies have revealed non-canonical functions of GCN1 that are independent of GCN2, such as its participation in cell proliferation, apoptosis, and the immune response, beyond the borders of species. Although it is known that GCN1 and GCN2 interact with ribosomes to accomplish amino acid starvation sensing, recent studies have reported that GCN1 binds to disomes (i.e., ribosomes that collide each other), thereby regulating both the co-translational quality control and stress response. We propose that GCN1 regulates ribosome-mediated signaling by dynamically changing its partners among RWD domain-possessing proteins via unknown mechanisms. We recently demonstrated that GCN1 is essential for cell proliferation and whole-body energy regulation in mice. However, the manner in which ribosome-initiated signaling via GCN1 is related to various physiological functions warrants clarification. GCN1-mediated mechanisms and its interaction with other quality control and stress response signals should be important for proteostasis during aging and neurodegenerative diseases, and may be targeted for drug development.


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