SODIUM-BUTYRATE ACTIVATES HUMAN-IMMUNODEFICIENCY-VIRUS LONG TERMINAL REPEAT - DIRECTED EXPRESSION
SODIUM-BUTYRATE ACTIVATES HUMAN-IMMUNODEFICIENCY-VIRUS LONG TERMINAL REPEAT - DIRECTED EXPRESSION
复制标题
DOI：
10.1016/s0006-291x(87)80217-6
复制
发表时间：
1987-11-13
影响因子：
3.1
通讯作者：
SRINIVASAN, A
中科院分区：
文献类型：
--
作者：
BOHAN, C;YORK, D;SRINIVASAN, A
为了研究丁酸钠对人类免疫缺陷病毒(HIV)长末端重复序列(LTR)定向表达的影响，我们构建了HIV分子克隆的LTR序列与氯霉素乙酰转移酶(CAT)基因融合的嵌合表达载体(Pl，tr-CAT)。我们在转基因的组织培养细胞中使用瞬时表达分析来监测LTR的活性。当细胞感染丁酸盐后，pLTR-CAT表达被激活。丁酸诱导的增加幅度在8 mM浓度下是线性的，并且与所使用的目标启动子不同。与标记基因相连的重组质粒可能是研究各种化学和生物来源的药物对HIV影响的有用模型。
To study the effect of sodium butyrate on human immunodeficiency virus (HIV) long terminal repeat (LTR)-directed expression, we constructed a chimeric plasmid (pL,TR-CAT) in which the LTR sequences derived from a molecular clone of HIV were fused to the chloramphenicol acetyltransferase (CAT) gene. We used transient expression assays in transfected tissue culture cells to monitor the activity of the LTR. The expression of the pLTR-CAT plasmid was activated when the cells were exposed to butyrate after transfection. The magnitude of butyrate induced increase was linear up to an 8 mM concentration and was different with regard to the target promoters used. Recombinant plasmids linked to marker genes may be useful models for studying the effects on HIV of various agents of chemical and biological origin.