Neuronal expression of constitutive heat shock proteins: implications for neurodegenerative diseases

被引：83

作者：

Chen, Sheng ^{[1
]}

Brown, Ian R. ^{[1
]}

机构：

[1] Univ Toronto Scarborough, Ctr Neurobiol Stress, Toronto, ON M1C 1A4, Canada

来源：

CELL STRESS & CHAPERONES | 2007年 / 12卷 / 01期

关键词：

D O I：

10.1379/CSC-236R.1

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 [细胞生物学]; 090102 [作物遗传育种];

摘要：

Neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis have been termed "protein misfolding disorders." These diseases differ widely in frequency and impact different classes of neurons. Heat shock proteins provide a line of defense against misfolded, aggregation-prone proteins and are among the most potent suppressors of neurodegeneration in animal models. Analysis of constitutively expressed heat shock proteins revealed variable levels of Hsc70 and Hsp27 in different classes of neurons in the adult rat brain. The differing levels of these constitutively expressed heat shock proteins in neuronal cell populations correlated with the relative frequencies of the previously mentioned neurodegenerative diseases.

引用

页码：51 / 58

页数：8

共 28 条

[1]

Chaperone suppression of α-synuclein toxicity in a Drosophila model for Parkinson's disease [J].

Auluck, PK ;

Chan, HYE ;

Trojanowski, JQ ;

Lee, VMY ;

Bonini, NM .

SCIENCE, 2002, 295 (5556) :865-868

[2]

HEAT-SHOCK PROTEINS AS MOLECULAR CHAPERONES [J].

BECKER, J ;

CRAIG, EA .

EUROPEAN JOURNAL OF BIOCHEMISTRY, 1994, 219 (1-2) :11-23

[3]

Molecular pathways to neurodegeneration [J].

Bossy-Wetzel, E ;

Schwarzenbacher, R ;

Lipton, SA .

NATURE MEDICINE, 2004, 10 (07) :S2-S9

[4]

Brown IR, 1999, HANDB EXP PHARM, V136, P243

[5]

Up-regulation of protein chaperones preserves viability of cells expressing toxic Cu/Zn-superoxide dismutase mutants associated with amyotrophic lateral sclerosis [J].

Bruening, W ;

Roy, J ;

Giasson, B ;

Figlewicz, DA ;

Mushynski, WE ;

Durham, HD .

JOURNAL OF NEUROCHEMISTRY, 1999, 72 (02) :693-699

[6]

Unraveling the mechanisms involved in motor neuron degeneration in ALS [J].

Bruijn, LI ;

Miller, TM ;

Cleveland, DW .

ANNUAL REVIEW OF NEUROSCIENCE, 2004, 27 :723-749

[7]

β-amyloid immunotherapy prevents synaptic degeneration in a mouse model of Alzheimer's disease [J].

Buttini, M ;

Masliah, E ;

Barbour, R ;

Grajeda, H ;

Motter, R ;

Johnson-Wood, K ;

Khan, K ;

Seubert, P ;

Freedman, S ;

Schenk, D ;

Games, D .

JOURNAL OF NEUROSCIENCE, 2005, 25 (40) :9096-9101

[8]

Protein folding and misfolding [J].

Dobson, CM .

NATURE, 2003, 426 (6968) :884-890

[9]

Chaperones increase association of tau protein with microtubules [J].

Dou, F ;

Netzer, WJ ;

Tanemura, K ;

Li, F ;

Hartl, FU ;

Takashima, A ;

Gouras, GK ;

Greengard, P ;

Xu, HX .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (02) :721-726

[10]

Common structure of soluble amyloid oligomers implies common mechanism of pathogenesis [J].

Kayed, R ;

Head, E ;

Thompson, JL ;

McIntire, TM ;

Milton, SC ;

Cotman, CW ;

Glabe, CG .

SCIENCE, 2003, 300 (5618) :486-489

← 1 2 3 →