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Oxidative stress-enhanced SUMOylation and aggregation of ataxin-1: Implication of JNK pathway.
Biochem Biophys Res Commun. 2010 Mar 05; 393(2):280-5.BB

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.

Authors+Show Affiliations

Department of Biology, Kongju National University, Republic of Korea.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20132795

Citation

Ryu, Joohyun, et al. "Oxidative Stress-enhanced SUMOylation and Aggregation of Ataxin-1: Implication of JNK Pathway." Biochemical and Biophysical Research Communications, vol. 393, no. 2, 2010, pp. 280-5.
Ryu J, Cho S, Park BC, et al. Oxidative stress-enhanced SUMOylation and aggregation of ataxin-1: Implication of JNK pathway. Biochem Biophys Res Commun. 2010;393(2):280-5.
Ryu, J., Cho, S., Park, B. C., & Lee, D. H. (2010). Oxidative stress-enhanced SUMOylation and aggregation of ataxin-1: Implication of JNK pathway. Biochemical and Biophysical Research Communications, 393(2), 280-5. https://doi.org/10.1016/j.bbrc.2010.01.122
Ryu J, et al. Oxidative Stress-enhanced SUMOylation and Aggregation of Ataxin-1: Implication of JNK Pathway. Biochem Biophys Res Commun. 2010 Mar 5;393(2):280-5. PubMed PMID: 20132795.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oxidative stress-enhanced SUMOylation and aggregation of ataxin-1: Implication of JNK pathway. AU - Ryu,Joohyun, AU - Cho,Sayeon, AU - Park,Byoung Chul, AU - Lee,Do Hee, Y1 - 2010/02/02/ PY - 2010/01/22/received PY - 2010/01/29/accepted PY - 2010/2/6/entrez PY - 2010/2/6/pubmed PY - 2010/3/20/medline SP - 280 EP - 5 JF - Biochemical and biophysical research communications JO - Biochem. Biophys. Res. Commun. VL - 393 IS - 2 N2 - 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. SN - 1090-2104 UR - https://www.unboundmedicine.com/medline/citation/20132795/Oxidative_stress_enhanced_SUMOylation_and_aggregation_of_ataxin_1:_Implication_of_JNK_pathway_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-291X(10)00187-7 DB - PRIME DP - Unbound Medicine ER -