| Literature DB >> 18758060 |
Hyo-Soon Jeong1, Hye-Yeon Choi, Tae-Won Choi, Bong-Woo Kim, Jung-Hyun Kim, Eung-Ryoung Lee, Ssang-Goo Cho.
Abstract
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.Entities:
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Year: 2008 PMID: 18758060 DOI: 10.1248/bpb.31.1686
Source DB: PubMed Journal: Biol Pharm Bull ISSN: 0918-6158 Impact factor: 2.233