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- Title
The JNK/AP1/ATF2 pathway is involved in H<sub>2</sub>O<sub>2</sub>-induced acetylcholinesterase expression during apoptosis.
- Authors
Zhang, J.-Y.; Jiang, H.; Gao, W.; Wu, J.; Peng, K.; Shi, Y.-F.; Zhang, X.-J.
- Abstract
We show that H2O2 increases acetylcholinesterase (AChE) expression via transcriptional activation through c-Jun N-terminal kinase (JNK), since the JNK inhibitor SP600125, but not the extracellular signal-regulated kinase (ERK) pathway inhibitor PD98059 or p38 kinase inhibitor SB203580, attenuated H2O2- induced AChE expression and its promoter activity. Over expression of hemagglutinin (HA)-JNK increases H2O2-induced AChE expression and its promoter activity, whereas the dominant negative mutant form of JNK suppressed H2O2-induced AChE expression and promoter activity. Mutation analysis indicates that the major response elements for JNK in the AChE promoter are the AP1–like element (TGAGTCT) site, located within the -1565/-1569 region of the AChE promoter, and the ATF2 element (CCACGTCA), within the -2185/-2177 region. The AP1-like element binds to the transcription factors, c-jun and ATF2, while the ATF2 element binds mainly ATF2. Taken together, our results strongly suggest that H2O2 induces AChE expression via the JNK/AP1/ATF2 signaling pathway.
- Subjects
ACETYLCHOLINESTERASE; APOPTOSIS; FREE radicals; HEMAGGLUTININ; TRANSCRIPTION factors; CHOLINESTERASES
- Publication
Cellular & Molecular Life Sciences, 2008, Vol 65, Issue 9, p1435
- ISSN
1420-682X
- Publication type
Article
- DOI
10.1007/s00018-008-8047-9