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淘豆网网友近日为您收集整理了关于SIRT1-FoxO-自噬通路研究进展.pdf的文档，希望对您的工作和学习有所帮助。以下是文档介绍：中国药理学通报 Chinese Pharmacological Bulletin
·901· 网络出版时间: 16:35
网络出版地址:s/doi/10.3969/j.issn...html SIRT1-FoxO-自噬通路研究进展徐俊,黄秀兰(中央民族大学中国少数民族传统医学国家民委一教育部重点实验室,北京 100081) doi:10.3969/j.issn.. 文献标志码:A 文章编号:(01—04 中国图书分类号:R-05;R329.24;R339.38;R394.2;R587.1; R589.2;R73;R54 摘要:FoxO是一类重要自噬调控因子,其活性主要受 SIRT1 的去乙酰化调节。SIRT1一FoxO一自噬通路可能为糖尿病、衰老、肥胖、肿瘤、心血管疾病、肌肉萎缩等多种疾病提供新的防治策略。该文旨在分析 FoxO 的转录调节机制,综述 SIRTI—FoxO一自噬通路的研究进展。关键词:自噬;FoxO;SIRT1;去乙酰化;疾病;通路自噬是真核细胞内的蛋白质大分子、细胞器等在自噬溶酶体的作用下被降解的过程。生理情况下,自噬是细胞重塑、维持细胞内稳态的必要过程;而在炎症反应、氧化应激等病理情况下,细胞凋亡过程中伴有自噬过度激活,因此细胞内自噬活性的调控尤其重要 。FoxO (forkhead box-con— taining protein,O subfamily)转录因子是一类关键的自噬调收稿日期:,修回日期: 基金项目:国家自然科学基金资助项目(No );国家民族事务委员会资助项目(No 10ZY08) 作者简介:徐俊(1989一),男,硕士生,研究方向:中药/民族药心血管药理学,E-mail:jerry890529@sina. 黄秀兰(1964一),女,博士,教授,博士生导师,研究方向: 中药/民族药心血管药理学,通讯作者,Tel:010￣8933254, E.mail.hxlcun@ 126.con 控因子,以 FoxO1、FoxO3的作用最为广泛。FoxO可通过激活细胞自噬活性,在心脏、血管、骨骼肌、肝脏、脑组织等多种器官或组织中,参与调节细胞增殖、代谢、存活等过程。FoxO 的转录激活能力受其乙酰it/去乙酰化、磷酸化/去磷酸化过程的特异性调节 j。沉默信息凋节因子 Sir2(silent informa— tion regulator 2)基因家族是一类 NAD 依赖型去乙酰化酶, 作为其重要成员的 SIRT1对 FoxO的去乙酰化调节,在细胞自噬调控中具有重要作用,大量研究表明,SIRT1一FoxO一自噬通路对糖尿病、衰老、肥胖、肿瘤、心血管疾病等具有重要影响。本文将阐释 FoxO的转录调控机制,进而综述 SIRT1一 FoxO通路调控自噬,对多种组织、器官中病理生理过程的调节。 1
FoxO 的转录调节机制 FoxO1和 FoxO3是叉头蛋白转录因子大家族(Foxes)0 亚家族的重要成员,广泛表达于心脏、血管内皮、脂肪、肝脏、脑、骨骼肌等多种器官与组织。FoxO蛋白质结构可分为“叉头区”(FH)、核定位信号(NkS)、核输出信号(NES)、转录激活区(TA或 TAD)。FoxO中的乙酰化位点、磷酸化位点等转录后修饰位点,对其 DNA结合活性和亚细胞定位等具有重要影响。 1.1
FoxO 的乙酰化/去乙酰化调节其转录活-陛 CBP、 p3o0等细胞核蛋白具有组蛋白乙酰转移酶(HAT)活性,可对 FoxO蛋白结构中 DNA结合区域的赖氨酸残基乙酰化,导致 FoxO的转录激活能力降低。氧化应激时,FoxO被 CBP、 p300等乙酰化增多,乙酰化的 FoxO(Ac—FoxO)在细胞核内积累,并与核小体结合,以屏蔽其转录调节活性 ,而细胞核 CaM K lI:A m olecular switch of synaptic plasticity HE Wen.bin
,ZHANG Jun—long ,YU Long.chuan’,CHEN Nai—hong (1.Higher Education Key Laboratory of Brain Science in Shanxi Province School of Basic Medicine,Shanxi University of Traditional Chinese Medicine ,Taiyuan .State Key Laboratory of Bioactive Substance and Function of Natural Medicine,Institute of Materia Medica,Chinese Academy of Medical Sciences Peking Union Medical College, Beijing
.School ofLife Sciences,Peking University,Beijing 100871,China) Abstract:Calcium/calmodulin.dependent protein kinase
1/ (CaMK 11),which is an important protein kinase involved in learning and memo￣,is found in most tissues,but it is present in especially high concentrations in neurons.The relatively high expression of CaMK lI in nervous system suggests it plays an im- portant role in the function of nervous system. This paper re— views the research development of the molecular structure of CaMK II and its autophosphorylation,subcellular localization and its role in synaptic plasticity. Key words:calcium/calmodulin—dependent protein kinase I1;subc synaptic plastici—long—learning and memory ·902 ·
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中国药理学通报 Chinese Pharmacological Bulletin
·901· 网络出版时间: 16:35
网络出版地址:s/doi/10.3969/j.issn...html SIRT1-FoxO-自噬通路研究进展徐俊,黄秀兰(中央民族大学中国少数民族传统医学国家民委一教育部重点实验室,北京 100081) doi:10.3969/j.issn.. 文献标志码:A 文章编号:(01—04 中国图书分类号:R-05;R329.24;R339.38;R394.2;R587.1; R589.2;R73;R54 摘要:FoxO是一类重要自噬调控因子,其活性主要受 SIRT1 的去乙酰化调节。SIRT1一FoxO一自噬通路可能为糖尿病、衰老、肥胖、肿瘤、心血管疾病、肌肉萎缩等多种疾病提供新的防治策略。该文旨在分析 FoxO 的转录调节机制,综述 SIRTI—FoxO一自噬通路的研究进展。关键词:自噬;FoxO;SIRT1;去乙酰化;疾病;通路自噬是真核细胞内的蛋白质大分子、细胞器等在自噬溶酶体的作用下被降解的过程。生理情况下,自噬是细胞重塑、维持细胞内稳态的必要过程;而在炎症反应、氧化应激等病理情况下,细胞凋亡过程中伴有自噬过度激活,因此细胞内自噬活性的调控尤其重要 。FoxO (forkhead box-con— taining protein,O subfami...
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2016 Apr 27;309:1-8. doi: 10.1016/j.bbr.. [Epub ahead of print]Nrf2/antioxidant defense pathway is involved in the neuroprotective effects of Sirt1 against focal cerebral ischemia in rats after hyperbaric oxygen preconditioning.1, 2, 2, 2, 2, 2, 3, 4, 5.1Department of Psychiatry, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.2Department of Anesthesiology, Gansu Provincial Hospital, Lanzhou, China.3College of Life Science, Shaanxi Normal University, China.4Department of Psychiatry, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. Electronic address: .5Department of Anesthesiology, Gansu Provincial Hospital, Lanzhou, China. Electronic address: .AbstractSirtuin 1 (Sirt1) is a class III histone deacetylase involved in neuroprotection induced by hyperbaric oxygen preconditioning (HBO-PC) in animal models of ischemia. However, the underlying mechanisms remain to be illustrated. In the present study, rats exposed to middle cerebral artery occlusion (MCAO) were used to establish an ischemic stroke model. The infarct volume ratio, neurobehavioral score, and expressions of Sirt1, nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase 1 (HO-1), and superoxide dismutase 1 (SOD1) were evaluated at 7 days after reperfusion, and the level of malondialdehyde (MDA) was used to assess oxidative stress. HBO-PC increased the expression of Sirt1 and reduced infarct volume ratio and neurobehavioral deficit in MCAO rats. Meanwhile, HBO-PC also increased expression of Nrf2, HO-1, and SOD1 and decreased MDA content. Furthermore, either Sirt1 or Nrf2 knockdown by short interfering RNA (siRNA) inhibited the expression of Nrf2, HO-1, and SOD1 and eliminated the neuroprotective effects of HBO-PC. Taken together, the results suggest that the Nrf2/antioxidant defense pathway is involved in the long lasting neuroprotective effects of Sirt1 induced by HBO-PC against transient focal cerebral ischemia.Copyright (C) 2016 Elsevier B.V. All rights reserved.KEYWORDS: HBO-PC; MCAO; Nrf2; O Sirt1PMID:
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