Apoptosis in neural development and disease

被引：237

作者：

Nijhawan, D

Honarpour, N

Wang, XD

机构：

[1] Univ Texas, SW Med Ctr, Howard Hughes Med Inst, Dallas, TX 75235 USA

[2] Univ Texas, SW Med Ctr, Dept Biochem, Dallas, TX 75235 USA

来源：

ANNUAL REVIEW OF NEUROSCIENCE | 2000年 / 23卷

关键词：

caspase; Bcl-2; cytochrome c; Apaf-1; neurodegenerative;

D O I：

10.1146/annurev.neuro.23.1.73

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Cell death via apoptosis is a prominent feature in mammalian neural development. Recent studies into the basic mechanism of apoptosis have revealed biochemical pathways that control and execute apoptosis in mammalian cells. Protein factors in these pathways play important roles during development in regulating the balance between neuronal life and death. Additionally, mounting evidence indicates such pathways may also be activated during several neurodegenerative diseases, resulting in improper loss of neurons.

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页码：73 / 87

页数：17

相关论文

共 106 条

[1] The Bcl-2 protein family: Arbiters of cell survival [J].

Adams, JM ;

Cory, S .

SCIENCE, 1998, 281 (5381) :1322-1326

[2] THE PROTOONCOGENE BCL-2 CAN SELECTIVELY RESCUE NEUROTROPHIC FACTOR-DEPENDENT NEURONS FROM APOPTOSIS [J].

ALLSOPP, TE ;

WYATT, S ;

PATERSON, HF ;

DAVIES, AM .

CELL, 1993, 73 (02) :295-307

[3] Death receptors: Signaling and modulation [J].

Ashkenazi, A ;

Dixit, VM .

SCIENCE, 1998, 281 (5381) :1305-1308

[4]

Bancher C, 1996, NEUROBIOL AGING, V17, P527

[5] A NOVEL PROTEIN THAT INTERACTS WITH THE DEATH DOMAIN OF FAS/APO1 CONTAINS A SEQUENCE MOTIF RELATED TO THE DEATH DOMAIN [J].

BOLDIN, MP ;

VARFOLOMEEV, EE ;

PANCER, Z ;

METT, IL ;

CAMONIS, JH ;

WALLACH, D .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (14) :7795-7798

[6] Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1- and TNF receptor-induced cell death [J].

Boldin, MP ;

Goncharov, TM ;

Goltsev, YV ;

Wallach, D .

CELL, 1996, 85 (06) :803-815

[7] AMYOTROPHIC-LATERAL-SCLEROSIS - RECENT INSIGHTS FROM GENETICS AND TRANSGENIC MICE [J].

BROWN, RH .

CELL, 1995, 80 (05) :687-692

[8] ALS-linked SOD1 mutant G85R mediates damage to astrocytes and promotes rapidly progressive disease with SOD1-containing inclusions [J].

Bruijn, LI ;

Becher, MW ;

Lee, MK ;

Anderson, KL ;

Jenkins, NA ;

Copeland, NG ;

Sisodia, SS ;

Rothstein, JD ;

Borchelt, DR ;

Price, DL ;

Cleveland, DW .

NEURON, 1997, 18 (02) :327-338

[9] Aggregation and motor neuron toxicity of an ALS-linked SOD1 mutant independent from wild-type SOD1 [J].

Bruijn, LI ;

Houseweart, MK ;

Kato, S ;

Anderson, KL ;

Anderson, SD ;

Ohama, E ;

Reaume, AG ;

Scott, RW ;

Cleveland, DW .

SCIENCE, 1998, 281 (5384) :1851-1854

[10]

Burek MJ, 1999, CELL DEATH AND DISEASES OF THE NERVOUS SYSTEM, P145

← 1 2 3 4 5 6 7 8 9 10 →