Lithium Down-regulates Histone Deacetylase 1 (HDAC1) and Induces Degradation of Mutant Huntingtin
文献类型：期刊论文
| 作者 | Wu, S; Zheng, SD; Huang, HL; Yan, LC; Yin, XF; Xu, HN; Zhang, KJ; Gui, JH; Chu, L; Liu, XY |
| 刊名 | JOURNAL OF BIOLOGICAL CHEMISTRY
 |
| 出版日期 | 2013 |
| 卷号 | 288期号:49页码:35500-35510 |
| 关键词 | Cell Biology Cell Signaling Histone Deacetylase Histone Deacetylase Inhibitors Huntington Disease Neurodegeneration MicroRNA Autophagy |
| 通讯作者 | Chu, L (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Shanghai Inst Biochem & Cell Biol, State Key Lab Cell Biol, Yueyang Rd, Shanghai 200031, Peoples R China.,lchu@sibcb.ac.cn ; xyliu@sibcb.ac.cn |
| 英文摘要 | Background: Lithium and valproic acid (VPA) exhibit a robust neuroprotective and anti-tumor effects in neural cells and tumor cells. Results: Lithium significantly down-regulates HDAC1 at the translational level by targeting HDAC1 mRNA. Conclusion: The decrease in HDAC1 is essential for the lithium-mediated, autophagic degradation of mutant huntingtin. Significance: This report is the first demonstration that HDAC1 decreases in response to lithium treatment. Lithium is an effective mood stabilizer that has been clinically used to treat bipolar disorder for several decades. Recent studies have suggested that lithium possesses robust neuroprotective and anti-tumor properties. Thus far, a large number of lithium targets have been discovered. Here, we report for the first time that HDAC1 is a target of lithium. Lithium significantly down-regulated HDAC1 at the translational level by targeting HDAC1 mRNA. We also showed that depletion of HDAC1 is essential for the neuroprotective effects of lithium and for the lithium-mediated degradation of mutant huntingtin through the autophagic pathway. Our studies explain the multiple functions of lithium and reveal a novel mechanism for the function of lithium in neurodegeneration. |
| 学科主题 | Biochemistry & Molecular Biology |
| 类目[WOS] | Biochemistry & Molecular Biology |
| 关键词[WOS] | CELL-CYCLE ARREST ; ALZHEIMERS-DISEASE ; INDUCED NEURODEGENERATION ; INHIBITS PROLIFERATION ; LIVER PROLIFERATION ; GENE-TRANSCRIPTION ; BIPOLAR DISORDER ; BINDING PROTEIN ; CANCER-CELLS ; C/EBP-BETA |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000329867600045 |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.143/handle/331003/480]  |
| 专题 | 上海生化细胞研究所_上海生科院生化细胞研究所 |
| 推荐引用方式 GB/T 7714 | Wu, S,Zheng, SD,Huang, HL,et al. Lithium Down-regulates Histone Deacetylase 1 (HDAC1) and Induces Degradation of Mutant Huntingtin[J]. JOURNAL OF BIOLOGICAL CHEMISTRY,2013,288(49):35500-35510. |
| APA | Wu, S.,Zheng, SD.,Huang, HL.,Yan, LC.,Yin, XF.,...&Liu, XY.(2013).Lithium Down-regulates Histone Deacetylase 1 (HDAC1) and Induces Degradation of Mutant Huntingtin.JOURNAL OF BIOLOGICAL CHEMISTRY,288(49),35500-35510. |
| MLA | Wu, S,et al."Lithium Down-regulates Histone Deacetylase 1 (HDAC1) and Induces Degradation of Mutant Huntingtin".JOURNAL OF BIOLOGICAL CHEMISTRY 288.49(2013):35500-35510. |
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