人cidec基因启动子的克隆及PPARγ上调其活性大小比较研究  

Cloning of Human cidec Gene Promoter and Up-regulation of its Activity by PPARγ

作　　者：郭冬妹[1,2] 刘小花[2] 彭家和[2] 杨星勇[1] 江渝[2] 

机构地区：[1]重庆师范大学生命科学学院,重庆401331 [2]第三军医大学基础部生物化学与分子生物学教研室,重庆400038

出　　处：《重庆师范大学学报（自然科学版）》2015年第5期148-151,共4页Journal of Chongqing Normal University:Natural Science

基　　金：国家自然科学基金(No.81270363;No.81070228)

摘　　要：人诱导细胞死亡的DFF45样效应因子C(Cell death-inducing DNA fragmentation factor 45-like c,cidec)可调节脂肪代谢,与动脉粥样硬化有密切联系,研究显示该因子表达受到过氧化物酶体增殖物激活受体γ(Peroxisome proliferatoractivated receptor gamma,PPARγ)的调节,但其中的表达机制还不清楚。从人肝癌细胞HepG2中扩增cidec基因启动子不同长短片段,分别克隆到虫荧光素酶报告基因载体中;cidec基因启动子片段重组报告基因质粒转染HepG2细胞,经PPARγ激动剂罗格列酮(Rosiglitazone,ROZ)处理后,检测荧光素酶活性。结果发现,cidec基因启动子(-1 800^+150bp)加ROZ前后均无明显变化,而cidec基因启动子(-2 289^+150bp)质粒荧光素酶活性明显增加,且加ROZ后活性显著升高(p<0.05)。这表明激活PPARγ可能通过cidec基因启动子的-2 289^-1 800bp区域PPARγ结合元件而上调该基因转录活性。Human cell death-inducing DNA fragmentation factor 45-like c （cidec） can regulate fat metabolism, is closely related toatherosclerosis. Some research shows that it was affected by Peroxisome proliferator-activated receptor gamma （PPAR）. So far,the expression of cidec gene mechanism is not clear. In this study from human liver cancer cell HepG2 amplification of cidec genepromoter fragment, and cloned into the luciferase reporter gene vector insect. A cidec gene promoter fragment reorganization reportgene plasmid transfection HepG2 cells, PPARy agonist activity. The result found that report gene carrier to build successful cidecgene promoter. Report gene assay show that cidec gene promoter -- 1 800∽＋ 150 bp had no obvious change add rosiglitazone（ROZ）. But the promoter --2 289∽＋150 bp plasmid luciferase activity increased significantly, and significantly increased addROZ. The result show that activation of PPAR）＇ may pass cidec gene promoter --2 289 ∽＋ 1 800 bp area PPAR）＇ combination com-ponents and increase the gene transcriptional activity.

关 键 词：诱导细胞死亡的DFF45样效应因子C 过氧化物酶体增殖物激活受体Γ 罗格列酮 启动子 

分 类 号：Q523[生物学—生物化学]