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作 者:徐国恒[1] 胡本荣[1] 罗超权[1] 陈汝筑[1] 邱鹏新[1]
出 处:《生物化学杂志》1997年第4期423-427,共5页
摘 要:用RT-PCR方法扩增并克隆了三种人外周型苯二氮卓受体PBRcDNA,测序表明,442bp片段与文献报道相比缺失84bp编码序列,其转录水平高于正常PBR.该序列编码一个与PBR结构相关但缺失了28个氨基酸残基的突变受体蛋白.这一异常转录本可能是通过选择性剪接方式转录产生并只存在于中国人肝癌BEL7402细胞系,表明PBR基因表达具有细胞特异性和异质性.Three of the human peripheral benzodiazepine receptor cDNA were detected and cloned via RT PCR method.One of these,a 442 bp amplification product has a 84 bp deletion and its transcript amount was higher than that of the native PBR.This abnormal transcript probably occurs through alternative splicing at transcriptional level,and it presents only in the human hepatoma BEL 7402 cell line.The results suggest that the expression of the PBR gene has cellular specificity and heterogenicity,which probably regulate the cellular function of the PBR at molecular level.The finding of the mutant PBR can provide a molecular and cellular model usefully to study the structure and function of the PBR.
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