S-nitrosylation of Parkin regulates ubiquitination and compromises Parkin's protective function

被引：628

作者：

Chung, KKK

Thomas, B

Li, XJ

Pletnikova, O

Troncoso, JC

Marsh, L

Dawson, VL

Dawson, TM ^{[1
]}

机构：

[1] Johns Hopkins Univ, Sch Med, Inst Cell Engn, Baltimore, MD 21205 USA

[2] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA

[3] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA

[4] Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD 21205 USA

[5] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA

[6] Johns Hopkins Univ, Sch Med, Dept Physiol, Baltimore, MD 21205 USA

来源：

SCIENCE | 2004年 / 304卷 / 5675期

关键词：

D O I：

10.1126/science.1093891

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Parkin is an E3 ubiquitin ligase involved in the ubiquitination of proteins that are important in the survival of dopamine neurons in Parkinson's disease (PD). We show that parkin is S-nitrosylated in vitro, as well as in vivo in a mouse model of PD and in brains of patients with PD and diffuse Lewy body disease. Moreover, S-nitrosylation inhibits parkin's ubiquitin E3 ligase activity and its protective function. The inhibition of parkin's ubiquitin E3 ligase activity by S-nitrosylation could contribute to the degenerative process in these disorders by impairing the ubiquitination of parkin substrates.

引用

页码：1328 / 1331

页数：4

共 33 条

[1] Mutations in the DJ-1 gene associated with autosomal recessive early-onset parkinsonism
Bonifati, V
Rizzu, P
van Baren, MJ
Schaap, O
Breedveld, GJ
Krieger, E
Dekker, MCJ
Squitieri, F
Ibanez, P
Joosse, M
van Dongen, JW
Vanacore, N
van Swieten, JC
Brice, A
Meco, G
van Duijn, CM
Oostra, BA
Heutink, P
[J]. SCIENCE, 2003, 299 (5604) : 256 - 259
[2] New insights into Parkinson's disease
Chung, KKK
Dawson, VL
Dawson, TM
[J]. JOURNAL OF NEUROLOGY, 2003, 250 (Suppl 3) : 15 - 24
[3] The role of the ubiquitin-proteasomal pathway in Parkinson's disease and other neurodegenerative disorders
Chung, KKK
Dawson, VL
Dawson, TM
[J]. TRENDS IN NEUROSCIENCES, 2001, 24 (11) : S7 - S14
[4] Parkin ubiquitinates the α-synuclein-interacting protein, synphilin-1:: implications for Lewy-body formation in Parkinson disease
Chung, KKK
Zhang, Y
Lim, KL
Tanaka, Y
Huang, H
Gao, J
Ross, CA
Dawson, VL
Dawson, TM
[J]. NATURE MEDICINE, 2001, 7 (10) : 1144 - 1150
[5] Convenient colorimetric and fluorometric assays for S-nitrosothiols
Cook, JA
Kim, SY
Teague, D
Krishna, MC
Pacelli, R
Mitchell, JB
Vodovotz, Y
Nims, RW
Christodoulou, D
Miles, AM
Grisham, MB
Wink, DA
[J]. ANALYTICAL BIOCHEMISTRY, 1996, 238 (02) : 150 - 158
[6] The p38 subunit of the aminoacyl-tRNA synthetase complex is a Parkin substrate: linking protein biosynthesis and neurodegeneration
Corti, O
Hampe, C
Koutnikova, H
Darios, F
Jacquier, S
Prigent, A
Robinson, JC
Pradier, L
Ruberg, M
Mirande, M
Hirsch, E
Rooney, T
Fournier, A
Brice, A
[J]. HUMAN MOLECULAR GENETICS, 2003, 12 (12) : 1427 - 1437
[7] Parkin: A multipurpose neuroprotective agent?
Feany, MB
Pallanck, LJ
[J]. NEURON, 2003, 38 (01) : 13 - 16
[8] Oxidative damage linked to neurodegeneration by selective α-synuclein nitration in synucleinopathy lesions
Giasson, BI
Duda, JE
Murray, IVJ
Chen, QP
Souza, JM
Hurtig, HI
Ischiropoulos, H
Trojanowski, JQ
Lee, VMY
[J]. SCIENCE, 2000, 290 (5493) : 985 - 989
[9] Redox regulatory and anti-apoptotic functions of thioredoxin depend on S-nitrosylation at cysteine 69
Haendeler, J
Hoffmann, J
Tischler, V
Berk, BC
Zeiher, AM
Dimmeler, S
[J]. NATURE CELL BIOLOGY, 2002, 4 (10) : 743 - 749
[10] Familial Parkinson's disease: a hint to elucidate the mechanisms of nigral degeneration
Hattori, N
Kobayashi, H
Sasaki-Hatano, Y
Sato, K
Mizuno, Y
[J]. JOURNAL OF NEUROLOGY, 2003, 250 (Suppl 3) : 2 - 10

← 1 2 3 4 →