Pael-R is accumulated in Lewy bodies of Parkinson's disease

被引:123
作者
Murakami, T
Shoji, M
Imai, Y
Inoue, H
Kawarabayashi, T
Matsubara, E
Harigaya, Y
Sasaki, A
Takahashi, R
Abe, K
机构
[1] Okayama Univ, Grad Sch Med & Dent, Dept Neurol, Okayama 7008558, Japan
[2] Maebashi Red Cross Hosp, Dept Neurol, Maebashi, Gumma, Japan
[3] Gunma Univ, Sch Med, Dept Pathol 1, Gunma, Japan
关键词
D O I
10.1002/ana.20064
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
We examined the distribution of Pael-R, a newly identified substrate for Parkin, in Parkinson's disease (PD) and multiple system atrophy (MSA). Pael-R, Parkin, a-synuclein, and ubiquitin accumulated in Lewy bodies (LBs) and neurites. Pael-R was localized in the core of LBs. Parkin and a-synuclein accumulated in the halo, neuronal cell bodies, and processes. These findings potentially suggest the involvement of Pael-R in LB formation, and protection role of Parkin in Pael-R-mediated neurotoxicity in PD. The absence of Pael-R and Parkin in glial cytoplasmic inclusions (GCIs) in MSA implies a distinct pathway involved in the formation of LBs and GCIs.
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页码:439 / 442
页数:4
相关论文
共 21 条
[1]  
Baba M, 1998, AM J PATHOL, V152, P879
[2]   Parkin ubiquitinates the α-synuclein-interacting protein, synphilin-1:: implications for Lewy-body formation in Parkinson disease [J].
Chung, KKK ;
Zhang, Y ;
Lim, KL ;
Tanaka, Y ;
Huang, H ;
Gao, J ;
Ross, CA ;
Dawson, VL ;
Dawson, TM .
NATURE MEDICINE, 2001, 7 (10) :1144-1150
[3]   The p38 subunit of the aminoacyl-tRNA synthetase complex is a Parkin substrate: linking protein biosynthesis and neurodegeneration [J].
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 .
HUMAN MOLECULAR GENETICS, 2003, 12 (12) :1427-1437
[4]   Neuropathology of Parkinson's disease [J].
Forno, LS .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1996, 55 (03) :259-272
[5]   α-Synuclein is phosphorylated in synucleinopathy lesions [J].
Fujiwara, H ;
Hasegawa, M ;
Dohmae, N ;
Kawashima, A ;
Masliah, E ;
Goldberg, MS ;
Shen, J ;
Takio, K ;
Iwatsubo, T .
NATURE CELL BIOLOGY, 2002, 4 (02) :160-164
[6]   The autosomal recessive juvenile Parkinson disease gene product, parkin, interacts with and ubiquitinates synaptotagmin XI [J].
Huynh, DP ;
Scoles, DR ;
Nguyen, D ;
Pulst, SM .
HUMAN MOLECULAR GENETICS, 2003, 12 (20) :2587-2597
[7]   Parkin suppresses unfolded protein stress-induced cell death through its E3 ubiquitin-protein ligase activity [J].
Imai, Y ;
Soda, M ;
Takahashi, R .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (46) :35661-35664
[8]   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
[9]   Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism [J].
Kitada, T ;
Asakawa, S ;
Hattori, N ;
Matsumine, H ;
Yamamura, Y ;
Minoshima, S ;
Yokochi, M ;
Mizuno, Y ;
Shimizu, N .
NATURE, 1998, 392 (6676) :605-608
[10]   Ala30Pro mutation in the gene encoding α-synuclein in Parkinson's disease [J].
Krüger, R ;
Kuhn, W ;
Müller, T ;
Woitalla, D ;
Graeber, M ;
Kösel, S ;
Przuntek, H ;
Epplen, JT ;
Schöls, L ;
Riess, O .
NATURE GENETICS, 1998, 18 (02) :106-108