Tangier disease is caused by mutations in ATP binding cassette transporter A1( ABCA1). ABCA1 interacts with lipid-free apolip oproteins, promoting phospholipid and cholesterol efflux from cells and giving r ise to HDL...Tangier disease is caused by mutations in ATP binding cassette transporter A1( ABCA1). ABCA1 interacts with lipid-free apolip oproteins, promoting phospholipid and cholesterol efflux from cells and giving r ise to HDL particles. ABCA1 may act as a phospholipid translocase facilitating p hospholipid binding to apoA-I. ABCA1 gene expression is upregulated in cholester ol-loaded cells as a result of activation of LXR/RXR-mediated gene transcription . LXR and RXR coordinately induce a battery of genes mediating cellular choleste rol efflux, centripetal cholesterol transport, and cholesterol excretion in bile . Small-molecule activators of LXR/RXR or other stimulators of macrophage or int estinal cholesterol efflux hold great promise as future treatments for atheroscl erosis.展开更多
文摘目的本研究旨在建立一种实时荧光定量PCR方法,用于检测猕猴三磷酸腺苷结合盒转运蛋白G2(adenosine triphosphate-binding cassette transporter protein G2,ABCG2)mRNA的基因转录水平。方法使用NCBI上GenBank数据库猕猴(Macaca mulatta)的ABCG2核苷酸序列号NM_001032919.1及内参GAPDH核苷酸序列号NM_001195426.1,借助Primer premier 5.0软件设计PCR引物。提取猕猴新鲜肾组织的总RNA,并反转录合成cDNA。接着,利用PCR引物进行实时荧光定量PCR扩增,并根据反应体系中荧光的变化情况定量分析ABCG2的mRNA相对表达水平。结果PCR产物测序结果显示,扩增的ABCG2和GAPDH核苷酸序列与NCBI上猕猴的序列同源性分别为90.91%和91.14%。ABCG2和GAPDH的扩增效率均达到80%~120%,实时荧光定量PCR标准曲线的熔解曲线为单峰,R2接近1。结论本研究建立的检测猕猴ABCG2 mRNA实时荧光定量检测方法,为研究高尿酸血症的发病机制以及新药开发奠定基础。
文摘Tangier disease is caused by mutations in ATP binding cassette transporter A1( ABCA1). ABCA1 interacts with lipid-free apolip oproteins, promoting phospholipid and cholesterol efflux from cells and giving r ise to HDL particles. ABCA1 may act as a phospholipid translocase facilitating p hospholipid binding to apoA-I. ABCA1 gene expression is upregulated in cholester ol-loaded cells as a result of activation of LXR/RXR-mediated gene transcription . LXR and RXR coordinately induce a battery of genes mediating cellular choleste rol efflux, centripetal cholesterol transport, and cholesterol excretion in bile . Small-molecule activators of LXR/RXR or other stimulators of macrophage or int estinal cholesterol efflux hold great promise as future treatments for atheroscl erosis.
