Oxidative stress-enhanced SUMOylation and aggregation of ataxin-1: Implication of JNK pathway

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Title
Oxidative stress-enhanced SUMOylation and aggregation of ataxin-1: Implication of JNK pathway
Author(s)
J Ryu; S Cho; Byoung Chul Park; D H Lee
Bibliographic Citation
Biochemical and Biophysical Research Communications, vol. 393, no. 2, pp. 280-285
Publication Year
2010
Abstract
Although the polyglutamine protein ataxin-1 is modified by SUMO at multiple sites, the functions of such modification or how it is regulated are still unknown. Here we report that SUMO-1 or Ubc9 over-expression stimulated the aggregation of ataxin-1 and that oxidative stress, such as hydrogen peroxide treatment, further enhanced SUMO conjugation and aggregation of ataxin-1. Accordingly, co-treatment with antioxidant N-acetyl-cysteine attenuated the effect of oxidative stress. Ataxin-1, which can activate c-Jun N-terminal kinase (JNK) pathway by itself, strongly associated with apoptosis signal-regulating kinase 1 (ASK1) while not interacting with JNK. Finally, treatment of JNK-specific inhibitor caused a reduction in the oxidant-enhanced SUMOylation and aggregation of ataxin-1. Together these results indicate that SUMO modification of ataxin-1 promotes the aggregation of ataxin-1 and that oxidative stress and JNK pathway play roles in this process.
Keyword
ASK1Ataxin-1JNKOxidative stressPolyglutamine diseasesSUMO-1
ISSN
0006-291X
Publisher
Elsevier
DOI
http://dx.doi.org/10.1016/j.bbrc.2010.01.122
Type
Article
Appears in Collections:
Division of Biomedical Research > Disease Target Structure Research Center > 1. Journal Articles
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