c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) are involved in Mycobacterium tuberculosis-induced expression of Leukotactin-1
In: BMB Reports, Jg. 45 (2012), Heft 10, S. 583-588
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Zugriff:
Leukotactin(Lkn)-1 is a CC chemokine and is upregulated inmacrophages in response to Mycobacterium tuberculosis (MTB)infection. We investigated whether mitogen-activated proteinkinases (MAPKs) are involved in MTB-induced expression ofLkn-1. The up-regulation of Lkn-1 by infection with MTB wasinhibited in cells treated with inhibitors specific for JNK(SP600125) or p38 MAPK (SB202190). Since the up-regulation ofLkn-1 by MTB has been reported to be mediated by thePI3-K/PDK1/Akt signaling, we examined whether JNK and/orp38 MAPK are also involved in this signal pathway.MTB-induced Akt phosphorylation was blocked by treatmentwith JNK- or p38 MAPK-specific inhibitors implying that p38 andJNK are upstream of Akt. In addition, treatment with thePI3-K-specific inhibitor inhibited MTB-stimulated activation ofJNK or p38 MAPK implying that PI3-K is upstream of JNK andp38 MAPK. These results collectively suggest that JNK and p38MAPK are involved in the signal pathway responsible forMTB-induced up-regulation of Lkn-1.
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c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) are involved in Mycobacterium tuberculosis-induced expression of Leukotactin-1
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Autor/in / Beteiligte Person: | Jang-Eun Cho1, Sangjung Park2, Sang-Nae Cho3, Hyeyoung Lee2 & Yoon Suk Kim2, |
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Zeitschrift: | BMB Reports, Jg. 45 (2012), Heft 10, S. 583-588 |
Veröffentlichung: | Korean Society for Biochemistry and Molecular Biology, 2012 |
Medientyp: | academicJournal |
ISSN: | 1976-6696 (print) ; 1976-670X (print) |
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