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c-Jun 对软骨细胞中 CTRP3 转录激活的调控。

Regulation of the transcriptional activation of CTRP3 in chondrocytes by c-Jun.

机构信息

Department of Biochemistry, School of Medicine, Dongguk University, 707 Sukjang-dong, Gyeongju 780-714, Republic of Korea.

出版信息

Mol Cell Biochem. 2012 Sep;368(1-2):111-7. doi: 10.1007/s11010-012-1349-0. Epub 2012 May 30.

Abstract

Although C1qTNF-related protein 3 (CTRP3) is highly expressed in cartilage and is involved in the proliferation and migration of chondrocytes, the molecular mechanism governing the transcriptional regulation of CTRP3 in chondrocytes is largely unknown. Here, we demonstrated the mechanism of transcriptional activation of the CTRP3 gene in chondrogenic cells. We observed that c-Jun stimulated CTRP3 promoter activity in ATDC5 cells. Deletion analysis of the CTRP3 promoter showed that the c-Jun-responsive region is localized at the position between -359 and -176. Mutation of the AP-1 binding site in this region eliminated c-Jun-mediated CTRP3 promoter activity. A promoter enzyme immunoassay and a chromatin immunoprecipitation assay showed that c-Jun binds directly to the AP-1 binding site at the region -184/-177 of the mouse CTRP3 promoter. Thus, these results demonstrated that c-Jun is a cis-acting element for CTRP3 regulation in chondrogenic cells.

摘要

虽然 C1qTNF 相关蛋白 3(CTRP3)在软骨中高度表达,并参与软骨细胞的增殖和迁移,但调控软骨细胞中 CTRP3 转录的分子机制在很大程度上仍是未知的。在这里,我们证明了在软骨细胞中 CTRP3 基因的转录激活机制。我们观察到 c-Jun 在 ATDC5 细胞中刺激 CTRP3 启动子活性。CTRP3 启动子的缺失分析表明,c-Jun 反应区位于 -359 到 -176 之间的位置。该区域中 AP-1 结合位点的突变消除了 c-Jun 介导的 CTRP3 启动子活性。启动子酶免疫测定和染色质免疫沉淀测定表明,c-Jun 直接结合到位于小鼠 CTRP3 启动子 -184/-177 区域的 AP-1 结合位点。因此,这些结果表明 c-Jun 是调控软骨细胞中 CTRP3 的顺式作用元件。

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