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Korean Society for Biochemistry and Molecular Biology (생화학분자생물학회)
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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

  • Cho, Jang-Eun (Department of Biomedical Laboratory Science, Daegu Health College) ;
  • Park, Sang-Jung (Department of Biomedical Laboratory Science, College of Health Scineces, Yonsei University) ;
  • Cho, Sang-Nae (Department of Microbiology, Yonsei University College of Medicine) ;
  • Lee, Hye-Young (Department of Biomedical Laboratory Science, College of Health Scineces, Yonsei University) ;
  • Kim, Yoon-Suk (Department of Biomedical Laboratory Science, College of Health Scineces, Yonsei University)
  • Received : 2012.06.05
  • Accepted : 2012.07.11
  • Published : 2012.10.31
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Abstract

Leukotactin(Lkn)-1 is a CC chemokine and is upregulated in macrophages in response to Mycobacterium tuberculosis (MTB) infection. We investigated whether mitogen-activated protein kinases (MAPKs) are involved in MTB-induced expression of Lkn-1. The up-regulation of Lkn-1 by infection with MTB was inhibited in cells treated with inhibitors specific for JNK (SP600125) or p38 MAPK (SB202190). Since the up-regulation of Lkn-1 by MTB has been reported to be mediated by the PI3-K/PDK1/Akt signaling, we examined whether JNK and/or p38 MAPK are also involved in this signal pathway. MTB-induced Akt phosphorylation was blocked by treatment with JNK- or p38 MAPK-specific inhibitors implying that p38 and JNK are upstream of Akt. In addition, treatment with the PI3-K-specific inhibitor inhibited MTB-stimulated activation of JNK or p38 MAPK implying that PI3-K is upstream of JNK and p38 MAPK. These results collectively suggest that JNK and p38 MAPK are involved in the signal pathway responsible for MTB-induced up-regulation of Lkn-1.

Keywords

References

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