期刊
MOLECULAR AND CELLULAR BIOCHEMISTRY
卷 323, 期 1-2, 页码 69-79出版社
SPRINGER
DOI: 10.1007/s11010-008-9965-4
关键词
ADAMTS; NFAT; VIVIT; Chondrocyte; Protein transduction domain; Arthritis
类别
资金
- Japan Society for the Promotion of Science (JSPS) [20659232, 20390399]
- Japan Science and Technology Corporation (JST)
- Grants-in-Aid for Scientific Research [20390399, 20659232] Funding Source: KAKEN
ADAMTS9 is a member of the disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) genes, with aggrecan-degrading activity. It has also been characterized to be reactive and highly activated ADAMTS by IL-1 beta in both chondrosarcoma cells and human chondrocytes (Demircan et al. Arthritis Rheum 52:1451-1460, 2005). In order to understand the regulation of ADAMTS9 gene expression a functional 3.0 kb human ADAMTS9 promoter has been cloned and characterized. A sequence analysis of the promoter revealed the presence of putative binding sites for Nuclear Factor of Activated T cells (NFAT), which is commonly found in the ADAMTS4 and ADAMTS5 promoters. NFATc1 was up-regulated in an activated form by IL-1 beta in human chondrocytes. The IL-1 beta inducible ADAMTS9 expression was inhibited by NFAT inhibitors, FK506 and 11Arg (11R)-VIVIT. Furthermore, direct binding of NFATc1 on distal and proximal promoters of ADAMTS9 was demonstrated by a chromatin immunoprecipitation assay. Promoter-reporter assays supported those results. These findings may provide a better understanding of the regulation of ADAMTS9 expression induced by inflammatory cytokines.
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