论文部分内容阅读
人心血管内皮细胞中的一氧化氮合酶(Nitric oxide synthase,NOS),又称为内皮型一氧化氮合酶(EndothelialNOS,eNOS),该基因定位于人类第12号染色体,由26个外显子组成,它以L-精氨酸为底物生成一氧化氮(NO)而发挥生物学作用。在eNOS结构基因的-103bp有Sp1位点,这个位点和位于-230bp的GAGA区是激活eNOS启动子的重要顺式作用元件。eNOS结构基因的Sp1位点对转录是必需的,而GATA-2转录因子是激发eNOS转录的重要细胞因子。溶血磷脂胆碱、氧化的低密度脂蛋白、Statin、TGF-β、TNF-α和雌激素均可影响eNOS基因表达。eNOS与小凹蛋白、GPCR、Hsp90、钙/钙调素等调节蛋白之间的相互作用对翻译后的eNOS活性均有影响。eNOS可通过促进NO的生成,减少心、脑血管疾病的发生。
Nitric oxide synthase (NOS) in human cardiovascular endothelial cells, also known as endothelial nitric oxide synthase (eNOS), is located on human chromosome 12 and consists of 26 exosomes Exon, which uses L-arginine as a substrate for the production of nitric oxide (NO) and play a biological role. The -103bp Sp1 site of the eNOS structural gene and this site and the GAGA region at -230bp are important cis-acting elements that activate the eNOS promoter. The Sp1 site of the eNOS structural gene is essential for transcription, whereas the GATA-2 transcription factor is an important cytokine that elicits eNOS transcription. Lysophosphatidylcholine, oxidized low-density lipoprotein, Statin, TGF-β, TNF-α and estrogen all affect eNOS gene expression. The interaction between eNOS and regulatory proteins such as caveolin, GPCR, Hsp90 and calcium / calmodulin exerts effects on post-translational eNOS activity. eNOS can reduce the occurrence of cardiovascular and cerebrovascular diseases by promoting the production of NO.