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目的线粒体融合基因2是一个新发现的负调控血管平滑肌细胞增殖的基因,在原发性高血压患者血管平滑肌细胞中低表达,但其调控机制还不明确。本研究通过生物信息学方法研究线粒体融合基因2的转录和调控机制。方法通过使用在线软件,对线粒体融合基因2上游5’端的启动子分布、转录因子及其结合位点、CpG岛、TATA box分析、保守区域等进行分析。同时对该区SNP的分布及其功能进行研究。结果线粒体融合基因2上游5’端存在5个启动子,但是起核心作用的可能只有2个;有2个保守区域,存在69个转录因子结合位点,后者主要与炎症反应、氧化应激、细胞增殖与分化和MAPK、STAT信号传导通路相关;一个CpG岛;15个TATA box,有8个处于-2000 bp以内;32个SNP位点,其中9个处于核心启动子区,5个可能会影响线粒体融合基因2的转录。结论线粒体融合基因2上游5’端-400 bp以内可能存在着核心启动子,该启动子区存在着一些重要的与线粒体融合基因2功能相关的转录因子。同时,启动子区存在的大量SNP可能会影响基因的转录调控。
Objective Mitochondrial fusion gene 2 is a newly discovered gene that negatively regulates the proliferation of vascular smooth muscle cells and is lowly expressed in vascular smooth muscle cells of patients with essential hypertension. However, its regulatory mechanism is unclear. In this study, we investigated the transcriptional and regulatory mechanisms of mitochondrial fusion 2 by bioinformatics methods. Methods Using online software, we analyzed the promoter distribution, transcription factor and binding site, CpG island, TATA box analysis and conserved region in the upstream 5 ’of mitochondrial fusion gene 2. At the same time, the distribution and function of SNP in this area were studied. Results There were 5 promoters upstream of 5 ’end of mitochondrial fusion gene 2, but only 2 of them could play a central role. There were 2 conserved regions and 69 transcription factor binding sites, which were mainly related to inflammation, oxidative stress , One of CpG islands and 15 TATA boxes, 8 of which were within -2000 bp; 32 SNP sites, of which 9 were in the core promoter region and 5 were possible Will affect the transcription of mitochondrial fusion gene 2. Conclusion The core promoter may exist within -400 bp upstream of the mitochondrial fusion gene 2, and there are some important transcription factors related to mitochondrial fusion gene 2 function in this promoter region. In the meantime, a large number of SNPs present in the promoter region may affect the transcriptional regulation of the gene.