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论文题目: BCCIP beta modulates the ribosomal and extraribosomal function of S7 through a direct interaction
英文论文题目: BCCIP beta modulates the ribosomal and extraribosomal function of S7 through a direct interaction
第一作者: Ba, Q; Li, XG; Huang, C; Li, JY; Fu, YJ; Chen, PZ; Duan, J; Hao, M; Zhang, YH; Li, JQ; Sun, CQ; Ying, H; Song, HY; Zhang, RW; Shen, ZY; Wang, H
英文第一作者: Ba, Q; Li, XG; Huang, C; Li, JY; Fu, YJ; Chen, PZ; Duan, J; Hao, M; Zhang, YH; Li, JQ; Sun, CQ; Ying, H; Song, HY; Zhang, RW; Shen, ZY; Wang, H
联系作者: Wang, H (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Key Lab Food Safety Res, Shanghai 200031, Peoples R China.
英文联系作者: Wang, H (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Key Lab Food Safety Res, Shanghai 200031, Peoples R China.
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发表年度: 2017
卷: 9
期: 3
页码: 209-219
摘要: Extraribosomal functions of ribosomal proteins (RPs) have gained much attention for their implications in tumorigenesis and progression. However, the regulations for transition between the ribosomal and extraribosomal functions of RPs are rarely reported. Herein, we identified a ribosomal protein S7-interacting partner, BCCIP beta, which modulates the functional conversion of S7. Through the N-terminal acidic domain, BCCIP beta interacts with the central basic region in S7 and regulates the extraribosomal distribution of S7. BCCIP beta deficiency abrogates the ribosomal accumulation but enhances the ribosome-free location of S7. This translocation further impairs protein synthesis and triggers ribosomal stress. Consequently, BCCIP beta deficiency suppresses the ribosomal function and initiates the extraribosomal function of S7, resulting in restriction of cell proliferation. Moreover, clinically relevant S7 mutations were found to dampen the interaction with BCCIP beta and facilitate the functional transition of S7. In conclusion, BCCIP beta, as a S7 modulator, contributes to the regulation of ribosomal and extraribosomal functions of S7 and has implications in cell growth and tumor development.
英文摘要: Extraribosomal functions of ribosomal proteins (RPs) have gained much attention for their implications in tumorigenesis and progression. However, the regulations for transition between the ribosomal and extraribosomal functions of RPs are rarely reported. Herein, we identified a ribosomal protein S7-interacting partner, BCCIP beta, which modulates the functional conversion of S7. Through the N-terminal acidic domain, BCCIP beta interacts with the central basic region in S7 and regulates the extraribosomal distribution of S7. BCCIP beta deficiency abrogates the ribosomal accumulation but enhances the ribosome-free location of S7. This translocation further impairs protein synthesis and triggers ribosomal stress. Consequently, BCCIP beta deficiency suppresses the ribosomal function and initiates the extraribosomal function of S7, resulting in restriction of cell proliferation. Moreover, clinically relevant S7 mutations were found to dampen the interaction with BCCIP beta and facilitate the functional transition of S7. In conclusion, BCCIP beta, as a S7 modulator, contributes to the regulation of ribosomal and extraribosomal functions of S7 and has implications in cell growth and tumor development.
刊物名称: JOURNAL OF MOLECULAR CELL BIOLOGY
英文刊物名称: JOURNAL OF MOLECULAR CELL BIOLOGY
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学科: Cell Biology
英文学科: Cell Biology
影响因子: 5.988
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论文类别: Article
英文论文类别: Article
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