Oxidative stress-enhanced SUMOylation and aggregation of ataxin-1: Implication of JNK pathway
- Authors
- Ryu, Joohyun; Cho, Sayeon; Park, Byoung Chul; Lee, Do Hee
- Issue Date
- Mar-2010
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Polyglutamine diseases; Ataxin-1; SUMO-1; Oxidative stress; JNK; ASK1
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.393, no.2, pp 280 - 285
- Pages
- 6
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 393
- Number
- 2
- Start Page
- 280
- End Page
- 285
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/22567
- DOI
- 10.1016/j.bbrc.2010.01.122
- ISSN
- 0006-291X
1090-2104
- 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. (C) 2010 Elsevier Inc. All rights reserved.
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