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Differential Regulation of the Antiapoptotic Action of B-Cell Lymphoma 2 (Bcl-2) and B-Cell Lymphoma Extra Long (Bcl-xL) by c-Jun N-Terminal Protein Kinase (JNK) 1-Involved Pathway in Neuroglioma Cells

Here, we confirmed that stable expression of B-cell lymphoma-xL (Bcl-xL) in N18TG neuroglioma cells could suppress c-Jun N-terminal protein kinase (JNK) activation, nuclear fragmentation, and cell death caused by etoposide treatment. Moreover, additional overexpression of JNK1 led to partially antag...

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Bibliographic Details
Published in:Biological & Pharmaceutical Bulletin 2008/09/01, Vol.31(9), pp.1686-1690
Main Authors: Jeong, Hyo-Soon, Choi, Hye-Yeon, Choi, Tae-Won, Kim, Bong-Woo, Kim, Jung-Hyun, Lee, Eung-Ryoung, Cho, Ssang-Goo
Format: Article
Language:English
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Summary:Here, we confirmed that stable expression of B-cell lymphoma-xL (Bcl-xL) in N18TG neuroglioma cells could suppress c-Jun N-terminal protein kinase (JNK) activation, nuclear fragmentation, and cell death caused by etoposide treatment. Moreover, additional overexpression of JNK1 led to partially antagonize the antiapoptotic environment attained by Bcl-xL, implying that JNK1-involved pathway may play a role in down-regulation of the antiapoptotic effect of Bcl-xL. However, the antagonistic effect of JNK1 on the antiapoptotic action of Bcl-xL was significantly weaker than that on the action of Bcl-2. Interestingly, we found that overexpression of JNK1 led to increase of Bcl-xL expression. Thus, these results suggest that Bcl-xL and Bcl-2 may induce its antiapoptotic effect in a different mechanism, provoking the possibility of involvement of JNK1-involved pathway in Bcl-xL expression.
ISSN:0918-6158
1347-5215
DOI:10.1248/bpb.31.1686