Delayed activation and regulation of MKK7 in hippocampal CA1 region following global cerebral ischemia in rats
Life Sciences, ISSN: 0024-3205, Vol: 74, Issue: 1, Page: 37-45
2003
- 9Citations
- 3Captures
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Metrics Details
- Citations9
- Citation Indexes9
- CrossRef6
- Captures3
- Readers3
Article Description
c-Jun N-terminal protein kinase (JNK) activation and subsequent c-Jun phosphorylation which stimulates its transcriptional activity have been well studied in cerebral ischemia. To determine whether mitogen-activated protein kinase kinase 7 (MKK7) play a role in JNK activation in response to the stress of global cerebral ischemia, we tested the activation of such a kinase by using phospho-Ser and phospho-Thr antibodies. Immunoprecipitation and Western blot analysis revealed that MKK7 was expressed at similar levels in all conditions, whereas phospho-MKK7 was highly augmented from 1 to 5 days and reached its peak at 3 days after 15 min of ischemia. Consistent with the active phase, the interaction of MLK3, ASK1 and phospho-JNK with MKK7 was increased compared with sham control, as shown by coimmunoprecipitation experiments. Moreover, MKK7 activation was markedly reduced by pretreatment of the free radical scavenging thiol antioxidant N -acetylcysteine (NAC). Together with previous studies, the late activation of MKK7 in hippocampal CA1 region may contribute to delayed cell death, and the protective effects of antioxidant against ischemia-induced injury may be partially mediated by the down-regulation of JNK signal pathway.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0024320503008828; http://dx.doi.org/10.1016/j.lfs.2003.06.025; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0142186311&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/14575811; https://linkinghub.elsevier.com/retrieve/pii/S0024320503008828; https://dx.doi.org/10.1016/j.lfs.2003.06.025
Elsevier BV
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