%0 Journal Article
%T c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) are involved in Mycobacterium tuberculosis-induced expression of Leukotactin-1
%A Jang-Eun Cho1
%A Sangjung Park2
%A Sang-Nae Cho3
%A Hyeyoung Lee2 & Yoon Suk Kim2
%A *
%J BMB Reports
%D 2012
%I Korean Society for Biochemistry and Molecular Biology
%X 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.
%K JNK
%K Leukotactin-1
%K Macrophage
%K Mycobacterium tuberculosis
%K p38 MAPK
%U http://www.jbmb.or.kr/jbmb/pdf.php?data=MTMwMTIyMTdAcGRmX3JhaW50cmFjZV9sZWV5c0AlNUI0NS0xMCU1RDEyMTAyOTIxMjJfJTI4NTgzLTU4OCUyOUJNQl8xMi0xMjAucGRm