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.

引用

收藏

页码：73 / 87

页数：17

相关论文

共 106 条

[11]

Bursztajn S, 1998, J NEUROSCI, V18, P9790

[12] Apaf1 (CED-4 homolog) regulates programmed cell death in mammalian development [J].

Cecconi, F ;

Alvarez-Bolado, G ;

Meyer, BI ;

Roth, KA ;

Gruss, P .

CELL, 1998, 94 (06) :727-737

[13] FADD, A NOVEL DEATH DOMAIN-CONTAINING PROTEIN, INTERACTS WITH THE DEATH DOMAIN OF FAS AND INITIATES APOPTOSIS [J].

CHINNAIYAN, AM ;

OROURKE, K ;

TEWARI, M ;

DIXIT, VM .

CELL, 1995, 81 (04) :505-512

[14] REGRESSIVE EVENTS IN NEUROGENESIS [J].

COWAN, WM ;

FAWCETT, JW ;

OLEARY, DDM ;

STANFIELD, BB .

SCIENCE, 1984, 225 (4668) :1258-1265

[15] NEUROPATHOLOGICAL CHANGES IN 2 LINES OF MICE CARRYING A TRANSGENE FOR MUTANT HUMAN CU,ZN SOD, AND IN MICE OVEREXPRESSING WILD-TYPE HUMAN SOD - A MODEL OF FAMILIAL AMYOTROPHIC-LATERAL-SCLEROSIS (FALS) [J].

DALCANTO, MC ;

GURNEY, ME .

BRAIN RESEARCH, 1995, 676 (01) :25-40

[16] Formation of neuronal intranuclear inclusions underlies the neurological dysfunction in mice transgenic for the HD mutation [J].

Davies, SW ;

Turmaine, M ;

Cozens, BA ;

DiFiglia, M ;

Sharp, AH ;

Ross, CA ;

Scherzinger, E ;

Wanker, EE ;

Mangiarini, L ;

Bates, GP .

CELL, 1997, 90 (03) :537-548

[17] BAX is required for neuronal death after trophic factor deprivation and during development [J].

Deckwerth, TL ;

Elliott, JL ;

Knudson, CM ;

Johnson, EM ;

Snider, WD ;

Korsmeyer, SJ .

NEURON, 1996, 17 (03) :401-411

[18] Alzheimer-associated presenilin-2 confers increased sensitivity to apoptosis in PC12 cells [J].

Deng, GM ;

Pike, CJ ;

Cotman, CW .

FEBS LETTERS, 1996, 397 (01) :50-54

[19] AMYOTROPHIC-LATERAL-SCLEROSIS AND STRUCTURAL DEFECTS IN CU,ZN SUPEROXIDE-DISMUTASE [J].

DENG, HX ;

HENTATI, A ;

TAINER, JA ;

IQBAL, Z ;

CAYABYAB, A ;

HUNG, WY ;

GETZOFF, ED ;

HU, P ;

HERZFELDT, B ;

ROOS, RP ;

WARNER, C ;

DENG, G ;

SORIANO, E ;

SMYTH, C ;

PARGE, HE ;

AHMED, A ;

ROSES, AD ;

HALLEWELL, RA ;

PERICAKVANCE, MA ;

SIDDIQUE, T .

SCIENCE, 1993, 261 (5124) :1047-1051

[20] Evidence of a novel event during neuronal death: Development of competence-to-die in response to cytoplasmic cytochrome c [J].

Deshmukh, M ;

Johnson, EM .

NEURON, 1998, 21 (04) :695-705

← 1 2 3 4 5 6 7 8 9 10 →