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学科主题: 基础医学
题名:
Inactivation of bad by site-specific phosphorylation: The checkpoint for ischemic astrocytes to initiate or resist apoptosis
作者: Chen, XQ; Lau, LT; Fung, YWW; Yu, ACH
关键词: ischemia ; astrocyte ; bad ; apoptosis ; LY294002 ; U0126
刊名: JOURNAL OF NEUROSCIENCE RESEARCH
发表日期: 2005-03-15
DOI: 10.1002/jnr.20396
卷: 79, 期:6, 页:798-808
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Neurosciences
研究领域[WOS]: Neurosciences & Neurology
关键词[WOS]: CEREBRAL-ARTERY OCCLUSION ; IN-VITRO ISCHEMIA ; PRIMARY CULTURES ; CELL-DEATH ; DNA FRAGMENTATION ; ACTIVATION ; BCL-2 ; NEURONS ; PROTEIN ; INJURY
英文摘要:

Bcl-2-associated death protein (Bad), a member of the Bcl family, directs astrocytes in primary cultures to enter or resist apoptosis during ischemia in vitro. Under ischemia, Bad was the only Bcl family member whose expression was upregulated significantly during the early stages of an ischemic insult. Increased endogenous Bad was translocated from the cytoplasm to mitochondria to induce apoptosis in astrocytes. Concurrently, ischemia also induced Bad phosphorylation specifically on Ser112 to promote survival. This site-specific phosphorylation of Bad was mediated by an early activation of the mitogen-activated protein kinase/extracellular signal-regulated protein kinase (MAPK/ERK) intracellular signaling pathway. This study demonstrates that ischemia-induced Bad plays a dual role in determining whether astrocytes enter or resist apoptosis after an ischemic insult. (C) 2005 Wiley-Liss, Inc.

语种: 英语
WOS记录号: WOS:000227364700008
Citation statistics:
内容类型: 期刊论文
版本: 出版稿
URI标识: http://ir.bjmu.edu.cn/handle/400002259/68109
Appears in Collections:基础医学院_神经生物学系_期刊论文

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作者单位: 1.Peking Univ, Neurosci Res Inst, Beijing 100083, Peoples R China
2.Minist Educ, Key Lab Neurosci, PKU, Beijing, Peoples R China
3.Hong Kong DNA Chips Ltd, Hong Kong, Hong Kong, Peoples R China
4.Peking Univ, Hlth Sci Ctr, Dept Neurobiol, Beijing 100083, Peoples R China

Recommended Citation:
Chen, XQ,Lau, LT,Fung, YWW,et al. Inactivation of bad by site-specific phosphorylation: The checkpoint for ischemic astrocytes to initiate or resist apoptosis[J]. JOURNAL OF NEUROSCIENCE RESEARCH,2005,79(6):798-808.
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