A proteomic analysis of the effect of MAPK pathway activation on L-glutamate-induced neuronal cell death = HT22 세포주에서의 glutamate 유도 세포사멸 과정중의 MAPK pathway 효과

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Title
A proteomic analysis of the effect of MAPK pathway activation on L-glutamate-induced neuronal cell death = HT22 세포주에서의 glutamate 유도 세포사멸 과정중의 MAPK pathway 효과
Author(s)
Sunghyun Kang; E Y Kim; Young Jae Bahn; Jin Woong Chung; Do Hee Lee; Sung Goo ParkTae-Sung YoonByoung Chul ParkKwang-Hee Bae
Bibliographic Citation
Cellular & Molecular Biology Letters, vol. 12, no. 1, pp. 139-147
Publication Year
2007
Abstract
Oxidative stress has been implicated in the pathogenesis of neuronal degenerative diseases. It is also widely known that oxidative stress induces mitogen-activated protein kinase (MAPK) signaling cascades. In this study, we used proteomic analysis to investigate the role of the MAPK pathway in oxidative stress-induced neuronal cell death. The results demonstrated that several proteins, including eukaryotic translation elongation factor 2 (eEF2) and enolase I, showed a differential expression pattern during the neuronal cell death process, and this was MAPK pathway dependent. Several chaperone and cytoskeletal proteins including heat shock protein 70, calreticulin, vimentin, prolyl 4-hydroxylase β polypeptide, and transgelin 2 were up- or down-regulated, despite their expressions not depending on the MAPK pathway. These findings strongly suggest that the expressions of proteins which play protective roles are independent of the MAPK pathway. On the other hand, eEF2 and enolase I may be the downstream targets of the MAPK pathway.
Keyword
ApoptosisHT22MAPKOxidative stressReactive oxygen speciesU0126
ISSN
1425-8153
Publisher
Springer-BMC
DOI
http://dx.doi.org/10.2478/s11658-006-0057-8
Type
Article
Appears in Collections:
Critical Diseases Diagnostics Convergence Research Center > 1. Journal Articles
Division of Biomedical Research > Disease Target Structure Research Center > 1. Journal Articles
Division of Biomedical Research > Metabolic Regulation Research Center > 1. Journal Articles
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