Honkakoski P, Moore R, Washburn K A, Negishi M
Pharmacogenetics Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.
Mol Pharmacol. 1998 Apr;53(4):597-601. doi: 10.1124/mol.53.4.597.
By extending previous studies of the phenobarbital (PB)-responsive 132-base pair (bp) enhancer sequence in the CYP2B10 gene, we have delimited a 51-bp enhancer element that is fully inducible by PB in mouse primary hepatocytes. Sixteen structurally unrelated phenobarbital-type inducers activated the 51-bp enhancer element in transient transfection assays. The results thus indicate that most PB-type inducers, if not all inducers, increase the transcription of the CYP2B10 gene by activating this 51-bp element, now designated PB-responsive enhancer module or PBREM.
通过扩展先前对CYP2B10基因中苯巴比妥（PB）反应性132碱基对（bp）增强子序列的研究，我们确定了一个51 bp的增强子元件，该元件在小鼠原代肝细胞中可被PB完全诱导。在瞬时转染实验中，16种结构不相关的苯巴比妥型诱导剂激活了51 bp的增强子元件。因此，结果表明，大多数PB型诱导剂（如果不是所有诱导剂）通过激活这个现在称为PB反应性增强子模块或PBREM的51 bp元件来增加CYP2B10基因的转录。
