Genome-wide identification and gene expression profiling of ubiquitin ligases for endoplasmic reticulum protein degradation
Scientific Reports 6 巻
30955- 頁
2016-08-03 発行
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| ファイル情報(添付) | |
| タイトル ( eng ) |
Genome-wide identification and gene expression profiling of ubiquitin ligases for endoplasmic reticulum protein degradation
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| 作成者 |
Iwase Ikuko
Yamasaki Yuki
Wu Yan
Matsuhisa Koji
Okuma Yasunobu
Watanabe Takeshi
Nomura Yausyuki
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| 収録物名 |
Scientific Reports
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| 巻 | 6 |
| 開始ページ | 30955 |
| 抄録 |
Endoplasmic reticulum (ER)-associated degradation (ERAD) is a mechanism by which unfolded proteins that accumulate in the ER are transported to the cytosol for ubiquitin–proteasome-mediated degradation. Ubiquitin ligases (E3s) are a group of enzymes responsible for substrate selectivity and ubiquitin chain formation. The purpose of this study was to identify novel E3s involved in ERAD. Thirty-seven candidate genes were selected by searches for proteins with RING-finger motifs and transmembrane regions, which are the major features of ERAD E3s. We performed gene expression profiling for the identified E3s in human and mouse tissues. Several genes were specifically or selectively expressed in both tissues; the expression of four genes (RNFT1, RNF185, CGRRF1 and RNF19B) was significantly upregulated by ER stress. To determine the involvement of the ER stress-responsive genes in ERAD, we investigated their ER localisation, in vitro autoubiquitination activity and ER stress resistance. All were partially localised to the ER, whereas CGRRF1 did not possess E3 activity. RNFT1 and RNF185, but not CGRRF1 and RNF19B, exhibited significant resistance to ER stressor in an E3 activity-dependent manner. Thus, these genes are possible candidates for ERAD E3s.
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| 内容記述 |
This study was supported by Grants-in-Aid for Scientific Research (KAKENHI) 15K21706, 26460099, 24300135, 22020032, 25251014, 15K15067, 15K20001, 15K18377 and 15K19516 from the Ministry of Education, Culture, Sports, Science and Technology, Japan and also supported by the Takeda Science Foundation. We thank H. Hishigaki and Otsuka GEN Research Institute for bioinformatic analysis. We also thank M. Minami and T. Uehara for the helpful discussions. We are grateful to T. Yoshikawa, T. Ike, Y. Maeoka, Y. Wada and Z. Cao for their technical assistance. The authors would like to thank Enago (www.enago.jp) for the English language review.
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| 言語 |
英語
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| 資源タイプ | 学術雑誌論文 |
| 出版者 |
Nature Research
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| 発行日 | 2016-08-03 |
| 権利情報 |
This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
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| 出版タイプ | Version of Record（出版社版。早期公開を含む） |
| アクセス権 | オープンアクセス |
| 収録物識別子 |
[ISSN] 2045-2322
[DOI] 10.1038/srep30955
[DOI] https://doi.org/10.1038/srep30955
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