Journal
BMB REPORTS
Volume 45, Issue 10, Pages 583-588Publisher
KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
DOI: 10.5483/BMBRep.2012.45.10.120
Keywords
JNK; Leukotactin-1; Macrophage; Mycobacterium tuberculosis; p38 MAPK
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Funding
- Korean Health 21 R&D Project, Ministry of Health & Welfare, Republic of Korea [A010381]
- Korea Health Promotion Institute [A010381] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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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 INK (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 INK 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 INK are upstream of Aid. In addition, treatment with the PI3-K-specific inhibitor inhibited MTB-stimulated activation of INK or p38 MAPK implying that PI3-K is upstream of INK and p38 MAPK. These results collectively suggest that INK and p38 MAPK are involved in the signal pathway responsible for MTB-induced up-regulation of Lkn-1. [BMB Reports 2012; 45(10): 583-588].
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