Dorn P L, Derse D
Biological Carcinogenesis Development Program, National Cancer Institute Frederick Cancer Research Facility, Maryland 21701-1013.
J Virol. 1988 Sep;62(9):3522-6. doi: 10.1128/JVI.62.9.3522-3526.1988.
Deletion analysis of the equine infectious anemia virus long terminal repeat revealed that sequences responsive to virus-specific transactivation are located within the region spanning the transcriptional start site (-31 to +22). In addition, an active exon of a trans-acting factor (tat) was identified downstream of pol and overlapping env (nucleotides 5264 to 5461). Activation by tat is accompanied by an increase in the steady-state levels of mRNA directed by the equine infectious anemia virus long terminal repeat.
马传染性贫血病毒长末端重复序列的缺失分析表明,对病毒特异性反式激活有反应的序列位于跨越转录起始位点(-31至+22)的区域内。此外,在pol下游且与env重叠(核苷酸5264至5461)的位置鉴定出一个反式作用因子(tat)的活性外显子。tat介导的激活伴随着马传染性贫血病毒长末端重复序列指导的mRNA稳态水平的增加。