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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．突变受体的发现为研究ＰＢＲ的结构和功能提供了理想的分子和细胞模型
PBR cDNAs of three human peripheral benzodiazepine receptors were amplified and cloned by RT-PCR. Sequencing showed that the 442 bp fragment lacked the 84 bp coding sequence compared with the reported one, and its transcription level was higher than that of the normal PBR. This sequence encodes a mutant receptor protein that is structurally related to PBR but lacks 28 amino acid residues. This aberrant transcript may be transcribed by alternative splicing and present only in Chinese human hepatocellular carcinoma BEL7402 cell line, indicating PBR gene expression is cell-specific and heterogeneous. The discovery of mutant receptors provides the ideal molecular and cellular model for studying the structure and function of PBR