The REGγ-proteasome forms a regulatory circuit with IκBɛ and NFκB in experimental colitis
REGγ is a component of ubiquitin-independent 20S proteasome that targets many regulatory proteins for degradation. Here the authors show that REGγ is induced in DSS colitis and promotes degradation of IκBɛ, and that REGγ-deficient mice have less NFκB activation and are more resistant to the disease....
| Main Authors: | , , , , , , , , , , , , , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Nature Publishing Group
2016-02-01
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| Series: | Nature Communications |
| Online Access: | https://doi.org/10.1038/ncomms10761 |
| id |
doaj-815ed3c7811843c397e9095adc1ff9cf |
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| record_format |
Article |
| collection |
DOAJ |
| language |
English |
| format |
Article |
| sources |
DOAJ |
| author |
Jinjin Xu Lei Zhou Lei Ji Fengyuan Chen Karen Fortmann Kun Zhang Qingwu Liu Ke Li Weicang Wang Hao Wang Wei Xie Qingwei Wang Jiang Liu Biao Zheng Pei Zhang Shixia Huang Tieliu Shi Biaohong Zhang Yongyan Dang Jiwu Chen Bert W. O’Malley Robb E. Moses Ping Wang Lei Li Jianru Xiao Alexander Hoffmann Xiaotao Li |
| spellingShingle |
Jinjin Xu Lei Zhou Lei Ji Fengyuan Chen Karen Fortmann Kun Zhang Qingwu Liu Ke Li Weicang Wang Hao Wang Wei Xie Qingwei Wang Jiang Liu Biao Zheng Pei Zhang Shixia Huang Tieliu Shi Biaohong Zhang Yongyan Dang Jiwu Chen Bert W. O’Malley Robb E. Moses Ping Wang Lei Li Jianru Xiao Alexander Hoffmann Xiaotao Li The REGγ-proteasome forms a regulatory circuit with IκBɛ and NFκB in experimental colitis Nature Communications |
| author_facet |
Jinjin Xu Lei Zhou Lei Ji Fengyuan Chen Karen Fortmann Kun Zhang Qingwu Liu Ke Li Weicang Wang Hao Wang Wei Xie Qingwei Wang Jiang Liu Biao Zheng Pei Zhang Shixia Huang Tieliu Shi Biaohong Zhang Yongyan Dang Jiwu Chen Bert W. O’Malley Robb E. Moses Ping Wang Lei Li Jianru Xiao Alexander Hoffmann Xiaotao Li |
| author_sort |
Jinjin Xu |
| title |
The REGγ-proteasome forms a regulatory circuit with IκBɛ and NFκB in experimental colitis |
| title_short |
The REGγ-proteasome forms a regulatory circuit with IκBɛ and NFκB in experimental colitis |
| title_full |
The REGγ-proteasome forms a regulatory circuit with IκBɛ and NFκB in experimental colitis |
| title_fullStr |
The REGγ-proteasome forms a regulatory circuit with IκBɛ and NFκB in experimental colitis |
| title_full_unstemmed |
The REGγ-proteasome forms a regulatory circuit with IκBɛ and NFκB in experimental colitis |
| title_sort |
regγ-proteasome forms a regulatory circuit with iκbɛ and nfκb in experimental colitis |
| publisher |
Nature Publishing Group |
| series |
Nature Communications |
| issn |
2041-1723 |
| publishDate |
2016-02-01 |
| description |
REGγ is a component of ubiquitin-independent 20S proteasome that targets many regulatory proteins for degradation. Here the authors show that REGγ is induced in DSS colitis and promotes degradation of IκBɛ, and that REGγ-deficient mice have less NFκB activation and are more resistant to the disease. |
| url |
https://doi.org/10.1038/ncomms10761 |
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| _version_ |
1721446651837546496 |
| spelling |
doaj-815ed3c7811843c397e9095adc1ff9cf2021-05-11T11:22:59ZengNature Publishing GroupNature Communications2041-17232016-02-017111410.1038/ncomms10761The REGγ-proteasome forms a regulatory circuit with IκBɛ and NFκB in experimental colitisJinjin Xu0Lei Zhou1Lei Ji2Fengyuan Chen3Karen Fortmann4Kun Zhang5Qingwu Liu6Ke Li7Weicang Wang8Hao Wang9Wei Xie10Qingwei Wang11Jiang Liu12Biao Zheng13Pei Zhang14Shixia Huang15Tieliu Shi16Biaohong Zhang17Yongyan Dang18Jiwu Chen19Bert W. O’Malley20Robb E. Moses21Ping Wang22Lei Li23Jianru Xiao24Alexander Hoffmann25Xiaotao Li26Shanghai Key Laboratory of Regulatory Biology, Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Biomedical Sciences, East China Normal UniversityShanghai Key Laboratory of Regulatory Biology, Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Biomedical Sciences, East China Normal UniversityShanghai Key Laboratory of Regulatory Biology, Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Biomedical Sciences, East China Normal UniversityThe Fifth Hospital of Shanghai, Fudan UniversitySignaling Systems Laboratory and San Diego Center for Systems Biology, University of CaliforniaShanghai Key Laboratory of Regulatory Biology, Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Biomedical Sciences, East China Normal UniversityShanghai Key Laboratory of Regulatory Biology, Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Biomedical Sciences, East China Normal UniversityShanghai Key Laboratory of Regulatory Biology, Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Biomedical Sciences, East China Normal UniversityShanghai Key Laboratory of Regulatory Biology, Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Biomedical Sciences, East China Normal UniversityShanghai Key Laboratory of Regulatory Biology, Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Biomedical Sciences, East China Normal UniversityShanghai Key Laboratory of Regulatory Biology, Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Biomedical Sciences, East China Normal UniversityShanghai Key Laboratory of Regulatory Biology, Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Biomedical Sciences, East China Normal UniversityThe Institute of Aging Research, School of Medicine, Hangzhou Normal UniversityShanghai Key Laboratory of Regulatory Biology, Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Biomedical Sciences, East China Normal UniversityDepartment of Pathology, the Second Chengdu Municipal HospitalDepartment of Molecular and Cellular Biology, The Dan L. Duncan Cancer Center, Baylor College of Medicine. One Baylor PlazaShanghai Key Laboratory of Regulatory Biology, Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Biomedical Sciences, East China Normal UniversityShanghai Key Laboratory of Regulatory Biology, Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Biomedical Sciences, East China Normal UniversityShanghai Key Laboratory of Regulatory Biology, Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Biomedical Sciences, East China Normal UniversityShanghai Key Laboratory of Regulatory Biology, Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Biomedical Sciences, East China Normal UniversityDepartment of Molecular and Cellular Biology, The Dan L. Duncan Cancer Center, Baylor College of Medicine. One Baylor PlazaDepartment of Molecular and Cellular Biology, The Dan L. Duncan Cancer Center, Baylor College of Medicine. One Baylor PlazaShanghai Key Laboratory of Regulatory Biology, Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Biomedical Sciences, East China Normal UniversityShanghai Key Laboratory of Regulatory Biology, Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Biomedical Sciences, East China Normal UniversityDepartment of Orthopedic Oncology, Changzheng Hospital, The Second Military Medical UniversitySignaling Systems Laboratory and San Diego Center for Systems Biology, University of CaliforniaShanghai Key Laboratory of Regulatory Biology, Shanghai Key Laboratory of Brain Functional Genomics (Ministry of Education), Institute of Biomedical Sciences, East China Normal UniversityREGγ is a component of ubiquitin-independent 20S proteasome that targets many regulatory proteins for degradation. Here the authors show that REGγ is induced in DSS colitis and promotes degradation of IκBɛ, and that REGγ-deficient mice have less NFκB activation and are more resistant to the disease.https://doi.org/10.1038/ncomms10761 |