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Arch Biochem Biophys. 2004 Nov 1;431(1):71-8.

Requirement of c-jun transcription factor on the mouse mast cell protease-6 expression in the mast cells.

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  • 1Department of Immunology, Chonbuk National University Medical School, Jeonbuk, Republic of Korea.

Abstract

Mast cell tryptases may be a key mediator in mast cell-mediated inflammatory reactions, and these expressions can be regulated by microenvironmental factors of tissues, particularly stem cell factor. In the present study, we investigated whether the transcription of mouse mast cell protease-6 (mMCP-6) gene was caused by SCF-mediated c-jun. We observed that mMCP-6 mRNA was expressed by overexpression of c-jun in the immature mast cell line in which both mMCP-6 and c-kit receptor are negative. The c-jun increased synergistically the luciferase activity of mMCP-6 promoter through the direct interaction with mi transcription factor (MITF). The synergic effect of c-jun with MITF was abolished by deletion of sequence between nt -171 and -151 in the mMCP-6 promoter. Furthermore, the level of mMCP-6 mRNA in mast cells was attenuated by the introduction of dominant negative c-jun (TAM-67) and the treatment of Jun N-terminal kinase inhibitor, SP600125. These results show that c-jun might play a role in regulating the transcription of mMCP-6 gene in mast cells stimulated by SCF.

PMID:
15464728
[PubMed - indexed for MEDLINE]
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