Neurodegeneration: How does Parkin prevent Parkinson's disease?

被引：14

作者：

Cookson, MR ^{[1
]}

机构：

[1] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA

来源：

CURRENT BIOLOGY | 2003年 / 13卷 / 13期

关键词：

D O I：

10.1016/S0960-9822(03)00446-9

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：

Mutations in parkin cause Parkinson's disease due to the loss of the ubiquitin-protein ligase activity of Parkin protein. Recent data suggest we may be beginning to understand the nature of the proteins that are targeted by Parkin and how these cause neuronal damage.

引用

收藏

页码：R522 / R524

页数：3

相关论文

共 17 条

[1] Acceleration of oligomerization, not fibrillization, is a shared property of both α-synuclein mutations linked to early-onset Parkinson's disease:: Implications for pathogenesis and therapy [J].

Conway, KA ;

Lee, SJ ;

Rochet, JC ;

Ding, TT ;

Williamson, RE ;

Lansbury, PT .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (02) :571-576

[2] Parkin prevents mitochondrial swelling and cytochrome c release in mitochondria-dependent cell death [J].

Darios, F ;

Corti, O ;

Lücking, CB ;

Hampe, C ;

Muriel, MP ;

Abbas, N ;

Gu, WJ ;

Hirsch, EC ;

Rooney, T ;

Ruberg, M ;

Brice, A .

HUMAN MOLECULAR GENETICS, 2003, 12 (05) :517-526

[3] Parkin and CASK/LIN-2 associate via a PDZ-mediated interaction and are co-localized in lipid rafts and postsynaptic densities in brain [J].

Fallon, L ;

Moreau, F ;

Croft, BG ;

Labib, N ;

Gu, WJ ;

Fon, EA .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (01) :486-491

[4] Mitochondrial pathology and apoptotic muscle degeneration in Drosophila parkin mutants [J].

Greene, JC ;

Whitworth, AJ ;

Kuo, I ;

Andrews, LA ;

Feany, MB ;

Pallanck, LJ .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (07) :4078-4083

[5] Genes and parkinsonism [J].

Hardy, J ;

Cookson, MR ;

Singleton, A .

LANCET NEUROLOGY, 2003, 2 (04) :221-228

[6] An unfolded putative transmembrane polypeptide, which can lead to endoplasmic reticulum stress, is a substrate of parkin [J].

Imai, Y ;

Soda, M ;

Inoue, H ;

Hattori, N ;

Mizuno, Y ;

Takahashi, R .

CELL, 2001, 105 (07) :891-902

[7] The lore of the RINGs: substrate recognition and catalysis by ubiquitin ligases [J].

Jackson, PK ;

Eldridge, AG ;

Freed, E ;

Furstenthal, L ;

Hsu, JY ;

Kaiser, BK ;

Reimann, JDR .

TRENDS IN CELL BIOLOGY, 2000, 10 (10) :429-439

[8] Parkin protects against the toxicity associated with mutant α-synuclein:: Proteasome dysfunction selectively affects catecholaminergic neurons [J].

Petrucelli, L ;

O'Farrell, C ;

Lockhart, PJ ;

Baptista, M ;

Kehoe, K ;

Vink, L ;

Choi, P ;

Wolozin, B ;

Farrer, M ;

Hardy, J ;

Cookson, MR .

NEURON, 2002, 36 (06) :1007-1019

[9] Parkin binds the Rpn10 subunit of 26S proteasomes through its ubiquitin-like domain [J].

Sakata, E ;

Yamaguchi, Y ;

Kurimoto, E ;

Kikuchi, J ;

Yokoyama, S ;

Yamada, S ;

Kawahara, H ;

Yokosawa, H ;

Hattori, N ;

Mizuno, Y ;

Tanaka, K ;

Kato, K .

EMBO REPORTS, 2003, 4 (03) :301-306

[10] Ubiquitination of a new form of α-synuclein by parkin from human brain:: Implications for Parkinson's disease [J].

Shimura, H ;

Schlossmacher, MC ;

Hattori, N ;

Frosch, MP ;

Trockenbacher, A ;

Schneider, R ;

Mizuno, Y ;

Kosik, KS ;

Selkoe, DJ .

SCIENCE, 2001, 293 (5528) :263-269