c-Jun Amino-Terminal Kinase-1 Mediates Glucose-Responsive Upregulation of the RNA Editing Enzyme ADAR2 in Pancreatic Beta-Cells
文献类型：期刊论文
| 作者 | Yang, Liu（杨柳）; Huang, Ping; Li, Feng; Zhao, Liyun; Zhang, Yongliang; Li, Shoufeng; Gan, Zhenji; Lin, Anning; Li, Wenjun; Liu, Yong（刘勇）
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| 刊名 | PLOS ONE
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| 出版日期 | 2012 |
| 卷号 | 7期号:11页码:e48611 |
| 通讯作者 | Liu, Y (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Key Lab Nutr & Metab, Shanghai, Peoples R China. |
| 英文摘要 | A-to-I RNA editing catalyzed by the two main members of the adenosine deaminase acting on RNA (ADAR) family, ADAR1 and ADAR2, represents a RNA-based recoding mechanism implicated in a variety of cellular processes. Previously we have demonstrated that the expression of ADAR2 in pancreatic islet beta-cells is responsive to the metabolic cues and ADAR2 deficiency affects regulated cellular exocytosis. To investigate the molecular mechanism by which ADAR2 is metabolically regulated, we found that in cultured beta-cells and primary islets, the stress-activated protein kinase JNK1 mediates the upregulation of ADAR2 in response to changes of the nutritional state. In parallel with glucose induction of ADAR2 expression, JNK phosphorylation was concurrently increased in insulin-secreting INS-1 beta-cells. Pharmacological inhibition of JNKs or siRNA knockdown of the expression of JNK1 prominently suppressed glucose-augmented ADAR2 expression, resulting in decreased efficiency of ADAR2 auto-editing. Consistently, the mRNA expression of Adar2 was selectively reduced in the islets from JNK1 null mice in comparison with that of wild-type littermates or JNK2 null mice, and ablation of JNK1 diminished high-fat diet-induced Adar2 expression in the islets from JNK1 null mice. Furthermore, promoter analysis of the mouse Adar2 gene identified a glucose-responsive region and revealed the transcription factor c-Jun as a driver of Adar2 transcription. Taken together, these results demonstrate that JNK1 serves as a crucial component in mediating glucose-responsive upregulation of ADAR2 expression in pancreatic beta-cells. Thus, the JNK1 pathway may be functionally linked to the nutrient-sensing actions of ADAR2-mediated RNA editing in professional secretory cells. |
| 类目[WOS] | Multidisciplinary Sciences |
| 研究领域[WOS] | Science & Technology - Other Topics |
| 关键词[WOS] | ADENOSINE-DEAMINASE ADAR1 ; SPLICE-SITE VARIANTS ; STIMULATED INSULIN-SECRETION ; PRE-MESSENGER-RNA ; ENERGY HOMEOSTASIS ; SIGNAL-TRANSDUCTION ; AGRP NEURONS ; MAP KINASES ; INTERFERON ; JNK |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000311315300045 |
| 公开日期 | 2015-12-24 |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.144/handle/331004/280]  |
| 专题 | 中国科学院上海生命科学研究院营养科学研究所_糖脂代谢与调控研究组 |
| 推荐引用方式 GB/T 7714 | Yang, Liu,Huang, Ping,Li, Feng,et al. c-Jun Amino-Terminal Kinase-1 Mediates Glucose-Responsive Upregulation of the RNA Editing Enzyme ADAR2 in Pancreatic Beta-Cells[J]. PLOS ONE,2012,7(11):e48611. |
| APA | Yang, Liu.,Huang, Ping.,Li, Feng.,Zhao, Liyun.,Zhang, Yongliang.,...&Liu, Yong.(2012).c-Jun Amino-Terminal Kinase-1 Mediates Glucose-Responsive Upregulation of the RNA Editing Enzyme ADAR2 in Pancreatic Beta-Cells.PLOS ONE,7(11),e48611. |
| MLA | Yang, Liu,et al."c-Jun Amino-Terminal Kinase-1 Mediates Glucose-Responsive Upregulation of the RNA Editing Enzyme ADAR2 in Pancreatic Beta-Cells".PLOS ONE 7.11(2012):e48611. |
入库方式： OAI收割
来源：上海营养与健康研究所
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