c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) are involved in Mycobacterium tuberculosis-induced expression of Leukotactin-1.
作者： Jang-Eun Cho , Sang-Jung Park , Sang-Nae Cho , Hye-Young Lee , Yoon-Suk Kim
DOI: 10.5483/BMBREP.2012.45.10.120
关键词:
摘要: Leukotactin(Lkn)-1 is a CC chemokine and upregulated in macrophages response to Mycobacterium tuberculosis (MTB) infection. We investigated whether mitogen-activated protein kinases (MAPKs) are involved MTB-induced expression of Lkn-1. The up-regulation Lkn-1 by infection with MTB was inhibited cells treated inhibitors specific for JNK (SP600125) or p38 MAPK (SB202190). Since the has been reported be mediated PI3-K/PDK1/Akt signaling, we examined and/or also this signal pathway. Akt phosphorylation blocked treatment JNK- MAPK-specific implying that upstream Akt. In addition, PI3-K-specific inhibitor MTB-stimulated activation PI3-K MAPK. These results collectively suggest pathway responsible
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