Fraser N W, Sehgal P B, Darnell J E
Nature. 1978 Apr 13;272(5654):590-3. doi: 10.1038/272590a0.
Exposure of HeLa cells to 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazde (DRB) late in the course of adenovirus 2 infection results in the inhibition of virus-specific RNA synthesis from all parts of the previously identified, very long (approximately 28 kilobases) late transcriptional unit, except for the first approximately 400-800 nucleotides. It is suggested that DRB acts not as an inhibitor of RNA chain initiation, but rather causes "premature" chain termination close to the promoter. A practical aspect of these findings may be that RNA sequences near promoter sites that are responsible for mRNA formation can be isolated from DRB-treated cells.
在腺病毒2感染过程后期,将HeLa细胞暴露于5,6-二氯-1-β-D-呋喃核糖基苯并咪唑(DRB)中,会抑制病毒特异性RNA合成,该合成来自先前鉴定的非常长(约28千碱基)的晚期转录单位的所有部分,但第一个约400 - 800个核苷酸除外。有人提出,DRB并非作为RNA链起始的抑制剂,而是在靠近启动子处导致“过早”的链终止。这些发现的一个实际应用可能是,可以从经DRB处理的细胞中分离出负责mRNA形成的启动子位点附近的RNA序列。