期刊
CELL DEATH AND DIFFERENTIATION
卷 11, 期 1, 页码 38-48出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.cdd.4401352
关键词
Bcl-2; caspase; kinase; mitochondria; neurotrophin; transcription factor
资金
- NIA NIH HHS [R37AG12947] Funding Source: Medline
- NINDS NIH HHS [R01NS38651] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS038651] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R37AG012947] Funding Source: NIH RePORTER
Awarding the 2002 Nobel Prize in Physiology or Medicine to Sydney Brenner, H Robert Horvitz, and John E Sulston for 'their discoveries concerning the genetic regulation of organ development and programmed cell death (PCD)' highlights the significant contribution that the study of experimental organisms, such as the nematode Caenorhabditis elegans, has made to our understanding of human physiology and pathophysiology. Their studies of lineage determination in worms established the 'central dogma' of apoptosis: The BH3-only protein EGL-1 is induced in cells destined to die, interacts with the BCL-2-like inhibitor CED-9, displacing the adaptor CED-4, which then promotes activation of the caspase CED-3. The vast majority of cells undergoing PCD during development in C. elegans, as in vertebrates, are neurons. Accordingly, the genetic regulation of apoptosis is strikingly similar in nematode and vertebrate neurons. This review summarizes these similarities - and the important differences - in the molecular mechanisms responsible for neuronal PCD in C. elegans and vertebrates, and examines the implications that our understanding of physiological neuronal apoptosis may have for the diagnosis and treatment of acute and chronic human neurodegenerative disorders.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据