期刊
JOURNAL OF IMMUNOLOGY
卷 164, 期 2, 页码 855-860出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.164.2.855
关键词
-
类别
The microphthalmia (mi) locus encodes a member of the basic-helix-loop-helix-leucine zipper (bHLH-Zip) protein family of transcription factors (MITF). We have reported that expression of several genes was impaired in cultured mast cells (CMCs) of mi/mi mice due to a defective transactivation ability of mutant MITF (mi-MITF). We also found that mi/mi CMCs did not express a receptor (MC1R) for alpha-melanocyte-stimulating hormone. The overexpression of the wild-type (+/+) MITF but not mi-MITF normalized the expression of the MC1R in mi/mi CMCs, indicating the involvement of +-MITF in the MC1R gene expression. Next, we analyzed the promoter region of the MC1R gene by the transient cotransfection assay. The luciferase construct under the control of the MC1R promoter and the cDNA-encoding +-MITF or mi-MITF were cotransfected into NIH/3T3 fibroblasts, The cotransfection of +-MITF but not mi-MITF increased the luciferase activity. There were five CANNTG moths recognized by bHLA-Zip-type transcription factors in the cloned promoter region. We found +-MITF bound two of five CANNTG motifs, and both moths were essential for the transactivation of the MC1R gene by +-MITF. These results indicated that +-MITF directly transactivated the MC1R gene through these two motifs.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据