A proteomic analysis of the effect of MAPK pathway activation on L-glutamate-induced neuronal cell death

• Autorzy: Kang S , Kim E.Y. , Bahn Y.J. , Chung J.W. , Lee D.H. , Park S.G. , Yoon T.S. , Park B.C. , Bae K.H.
• Języki publikacji: EN

Abstrakty

EN

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.

Słowa kluczowe

EN

neuronal degenerative disease; pathogenesis; cell; neuronal cell; oxidative stress; reactive oxygen species; mitogen-activated protein kinase; apoptosis

• Wydawca: -
• Czasopismo: Cellular and Molecular Biology Letters
• Rocznik: 2007
• Tom: 12
• Numer: 1
• Opis fizyczny: p.139-147,fig.,ref.

Twórcy

autor

Kang S

• Korean Research Institute of Bioscience and Biotechnology, 52 Eoeun-Dong, Yusung-Gu, Daejeon, 305-333, Republic of Korea

autor

Kim E.Y.

autor

Bahn Y.J.

autor

Chung J.W.

autor

Lee D.H.

autor

Park S.G.

autor

Yoon T.S.

autor

Park B.C.

autor

Bae K.H.

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