p53-dependent cell death signaling in neurons

被引：167
作者：
Morrison, RS
Kinoshita, Y
Johnson, MD
Guo, WQ
Garden, GA
机构：
[1] Univ Washington, Sch Med, Dept Neurol Surg, Seattle, WA 98195 USA
[2] Univ Washington, Sch Med, Dept Neurol, Seattle, WA 98195 USA
来源：
NEUROCHEMICAL RESEARCH | 2003年 / 28卷 / 01期
关键词：
apoptosis; cell death; neurons/neurodegeneration; p53; caspase; Bcl-2; family;
D O I：
10.1023/A:1021687810103
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The p53 tumor suppressor gene is a sequence-specific transcription factor that activates the expression of genes engaged in promoting growth arrest or cell death in response to multiple forms of cellular stress. p53 expression is elevated in damaged neurons in acute models of injury such as ischemia and epilepsy and in brain tissue samples derived from animal models and patients with chronic neurodegenerative diseases. p53 deficiency or p53 inhibition protects neurons from a wide variety of acute toxic insults. Signal transduction pathways associated with p53-induced neuronal cell death are being characterized, suggesting that intervention may prove effective in maintaining neuronal viability and restoring function following neural injury and disease.
引用
收藏
页码：15 / 27
页数：13
相关论文
共 145 条
[41]   p53 facilitates pRb cleavage in IL-3-deprived cells: novel pro-apoptotic activity of p53 [J].
Gottlieb, E ;
Oren, M .
EMBO JOURNAL, 1998, 17 (13) :3587-3596
[42]   Hypoxia-inducible factor-1α mediates hypoxia-induced delayed neuronal death that involves p53 [J].
Halterman, MW ;
Miller, CC ;
Federoff, HJ .
JOURNAL OF NEUROSCIENCE, 1999, 19 (16) :6818-6824
[43]   Requirement for Atm in ionizing radiation-induced cell death in the developing central nervous system [J].
Herzog, KH ;
Chong, MJ ;
Kapsetaki, M ;
Morgan, JI ;
McKinnon, PJ .
SCIENCE, 1998, 280 (5366) :1089-1091
[44]  
Hirata H, 1997, J NEUROCHEM, V69, P780
[45]   Sensitivity and selectivity of the DNA damage sensor responsible for activating p53-dependent G(1) arrest [J].
Huang, LC ;
Clarkin, KC ;
Wahl, GM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (10) :4827-4832
[46]   Excitotoxic lesion of rat brain with quinolinic acid induces expression of p53 messenger RNA and protein and p53-inducible genes Bax and Gadd-45 in brain areas showing DNA fragmentation [J].
Hughes, PE ;
Alexi, T ;
Yoshida, T ;
Schreiber, SS ;
Knusel, B .
NEUROSCIENCE, 1996, 74 (04) :1143-1160
[47]   ACTIVATION OF P53 SEQUENCE-SPECIFIC DNA-BINDING BY SHORT SINGLE STRANDS OF DNA REQUIRES THE P53 C-TERMINUS [J].
JAYARAMAN, L ;
PRIVES, C .
CELL, 1995, 81 (07) :1021-1029
[48]   Mutation of the angelman ubiquitin ligase in mice causes increased cytoplasmic p53 and deficits of contextual learning and long-term potentiation [J].
Jiang, YH ;
Armstrong, D ;
Albrecht, U ;
Atkins, CM ;
Noebels, JL ;
Eichele, G ;
Sweatt, JD ;
Beaudet, AL .
NEURON, 1998, 21 (04) :799-811
[49]  
Johnson MD, 1998, J NEUROSCI RES, V54, P721, DOI 10.1002/(SICI)1097-4547(19981215)54:6<721::AID-JNR1>3.0.CO
[50]  
2-1
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