Transactivation of the c-myc Gene by HTLV-1 tax is Mediated by NFkB
The human T cell leukemia virus type I is the causative agent of adult T cell leukemia (Hinuma et al. 1981) and B cell chronic lymphocytic leukemia (Mann et al. 1987). Its genome encodes a 40 kD protein called tax (Lee et al. 1984) that is important for the immortalization of cells (Siekevitz et al. 1987a). Stimulation of genes by tax protein is mediated by indirect mechanisms involving the activation of several cellular transcription factors, including NFkB and CREB. We have recently demonstrated that the murine c-myc gene has two elements that bind and are transactivated by the transcription factor NFkB (Duyao et al. 1990; Kessler et al., 1990). They are located —1101/-1081 bp and +440/+459 bp with respect to the P1 promoter and thus were called upstream regulatory element or URE and internal regulatory element or IRE, respectively. Expression of the c-myc gene has been implicated in both induction of proliferation of quiescent mammalian cells and in immortalization and transformation of cells. Thus here we have tested whether tax can transactivate the c-myc gene through induction of NFkB. The studies were performed in collaboration with Miriam Siekevitz, Christopher Bartholomew and John Cleveland.
KeywordsCell Chronic Lymphocytic Leukemia Chloramphenicol Acetyl Transferase Cellular Transcription Factor Chloramphenicol Acetyl Transferase Activity Upstream Regulatory Element
Unable to display preview. Download preview PDF.