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SARS-CoV-2 ORF10 impairs cilia by enhancing CUL2ZYG11B activity.

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机构： [1]Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, China. [2]State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Stem Cell and Regenerative Medicine Innovation Institute, Chinese Academy of Sciences, Beijing, China. [3]Guangdong and Shenzhen Key Laboratory of Male Reproductive Medicine and Genetics, Institute of Urology, Peking University Shenzhen Hospital, Shenzhen PKU-HKUST Medical Center, Shenzhen, China. [4]State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, Jiangsu, China. [5]Department of Otolaryngology Head and Neck Surgery, Beijing TongRen Hospital, Capital Medical University, Beijing, China. [6]Beijing Key Laboratory of Nasal Diseases, Beijing Institute of Otolaryngology, Beijing, China. [7]Laboratory Animal Center, Institute of Zoology, Chinese Academy of Sciences, Beijing, China. [8]CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China. [9]School of Life Science and Technology, ShanghaiTech University, Shanghai, China. [10]Shanghai Institute for Advanced Immunochemical Studies and School of Life Science and Technology, ShanghaiTech University, Shanghai, China.

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causal pathogen of the ongoing global pandemic of coronavirus disease 2019 (COVID-19). Loss of smell and taste are symptoms of COVID-19, and may be related to cilia dysfunction. Here, we found that the SARS-CoV-2 ORF10 increases the overall E3 ligase activity of the CUL2ZYG11B complex by interacting with ZYG11B. Enhanced CUL2ZYG11B activity by ORF10 causes increased ubiquitination and subsequent proteasome-mediated degradation of an intraflagellar transport (IFT) complex B protein, IFT46, thereby impairing both cilia biogenesis and maintenance. Further, we show that exposure of the respiratory tract of hACE2 mice to SARS-CoV-2 or SARS-CoV-2 ORF10 alone results in cilia-dysfunction-related phenotypes, and the ORF10 expression in primary human nasal epithelial cells (HNECs) also caused a rapid loss of the ciliary layer. Our study demonstrates how SARS-CoV-2 ORF10 hijacks CUL2ZYG11B to eliminate IFT46 and leads to cilia dysfunction, thereby offering a powerful etiopathological explanation for how SARS-CoV-2 causes multiple cilia-dysfunction-related symptoms specific to COVID-19.© 2022 Wang et al.

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出版当年[2021]版：

大类 | 1 区

生物学

小类 | 2 区细胞生物学

最新[2023]版：

大类 | 1 区

生物学

小类 | 2 区细胞生物学

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出版当年[2020]版：

Q1 CELL BIOLOGY

最新[2023]版：

Q1 CELL BIOLOGY

影响因子： 7.3 最新[2023版] 8 最新五年平均 10.539 出版当年[2020版] 10.804 出版当年五年平均 8.811 出版前一年[2019版] 8.077 出版后一年[2021版]

第一作者：

第一作者机构： [1]Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, China. [2]State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Stem Cell and Regenerative Medicine Innovation Institute, Chinese Academy of Sciences, Beijing, China.

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通讯作者：

通讯机构： [1]Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, China. [2]State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Stem Cell and Regenerative Medicine Innovation Institute, Chinese Academy of Sciences, Beijing, China. [5]Department of Otolaryngology Head and Neck Surgery, Beijing TongRen Hospital, Capital Medical University, Beijing, China. [6]Beijing Key Laboratory of Nasal Diseases, Beijing Institute of Otolaryngology, Beijing, China.

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