Axon degeneration: mechanisms and implications of a distinct program from cell death
文献类型：期刊论文
| 作者 | Yan, Tingting2; Feng, Yan2; Zhai, Qiwei1,2 |
| 刊名 | Neurochemistry international
 |
| 出版日期 | 2010-03-01 |
| 卷号 | 56期号:4页码:529-534 |
| 关键词 | Wallerian degeneration Wlds Nmnat Nad Neurodegenerative disease |
| ISSN号 | 0197-0186 |
| DOI | 10.1016/j.neuint.2010.01.013 |
| 通讯作者 | Zhai, qiwei(qwzhai@sibs.ac.cn) |
| 英文摘要 | Axon degeneration has been proposed to be a new therapeutic target for neurodegenerative diseases, because it usually occurs earlier than neuronal cell body death with a distinct active program from apoptosis and necrosis. overexpression of wld(s) or nmnats (nicotinamide mononucleotide adenylytransferase, ec2.7.7.1) has been demonstrated to delay axon degeneration initiated by various insults. nad synthesis activity of wld(s) and nmnats was shown to be responsible for their axon-protective function. the mitochondrial nmnat3 and cytoplasm-localized mutants of wld(s) and nmnat1 have similar or even stronger effect than wld(s) to delay axon degeneration, which suggest that increased mitochondrial or local nad synthesis might contribute to the protective function of wld(s) and nmnats. further studies show nad synthesis pathway and ubiquitin proteasome system play important roles in delaying axon degeneration. wld(s) mice are resistant to a variety of neurodegenerative diseases, but the role of nmnats in neurodegenerative diseases are largely unknown. nad plays key roles in energy metabolism, mitochondrial functions and aging, and is suggested to be involved in neuron degenerative diseases. future studies to identify the upstream factors inducing nad depletion and the downstream nad effectors responsible for the axon-protective function will provide more meaningful insights into the molecular mechanisms of axon degeneration in neurodegenerative diseases. (c) 2010 elsevier ltd. all rights reserved. |
| WOS关键词 | NICOTINAMIDE MONONUCLEOTIDE ADENYLYLTRANSFERASE ; UBIQUITIN-PROTEASOME SYSTEM ; WALLERIAN DEGENERATION ; ADENINE-DINUCLEOTIDE ; NEURONAL DEATH ; WLD(S) MICE ; IN-VIVO ; POLY(ADP-RIBOSE) POLYMERASE ; NEURODEGENERATIVE DISEASES ; ENZYMATIC-ACTIVITY |
| WOS研究方向 | Biochemistry & Molecular Biology ; Neurosciences & Neurology |
| WOS类目 | Biochemistry & Molecular Biology ; Neurosciences |
| 语种 | 英语 |
| WOS记录号 | WOS:000276597600001 |
| 出版者 | PERGAMON-ELSEVIER SCIENCE LTD |
| URI标识 | http://www.irgrid.ac.cn/handle/1471x/2413615 |
| 专题 | 中国科学院大学 |
| 通讯作者 | Zhai, Qiwei |
| 作者单位 | 1.Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Key Lab Nutr & Metab, Shanghai 200031, Peoples R China 2.Chinese Acad Sci, Grad Sch, Shanghai 200031, Peoples R China |
| 推荐引用方式 GB/T 7714 | Yan, Tingting,Feng, Yan,Zhai, Qiwei. Axon degeneration: mechanisms and implications of a distinct program from cell death[J]. Neurochemistry international,2010,56(4):529-534. |
| APA | Yan, Tingting,Feng, Yan,&Zhai, Qiwei.(2010).Axon degeneration: mechanisms and implications of a distinct program from cell death.Neurochemistry international,56(4),529-534. |
| MLA | Yan, Tingting,et al."Axon degeneration: mechanisms and implications of a distinct program from cell death".Neurochemistry international 56.4(2010):529-534. |
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来源：中国科学院大学
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