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

Joohyun Ryu, Sayeon Cho, Byoung Chul Park, Do Hee Lee

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42 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)280-285
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number2
StatePublished - Mar 5 2010
Externally publishedYes

Bibliographical note

Funding Information:
We are grateful to Prof. Chin Ha Chung for providing HA-tagged SUMO-1 construct and to Jung Young Choi and Jeong Hee Ryu for their assistance. This study was supported by a special research grant from Seoul Women’s University (2009) to Do Hee Lee and the grant of Korea Healthcare Technology R&D Project, Ministry for Health, Welfare and Family Affairs, Republic of Korea ( BGC0300912 ) to Byoung Chul Park.

Copyright 2010 Elsevier B.V., All rights reserved.


  • ASK1
  • Ataxin-1
  • JNK
  • Oxidative stress
  • Polyglutamine diseases
  • SUMO-1


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