The mechanism of HTLV-1 LTR activation by TPA varies in different human T-cell lines: role of specific PKC isoforms.
We demonstrate here that TPA activates HTLV-1 LTR expression in Jurkat and H9 T-cell lines, by strictly different mechanisms. In Jurkat cells this activation is exerted by a PKCalpha- and PKCvarepsilon-antagonized mechanism which operates through an Sp1 binding site residing within the Est responsive region 1 of the LTR. On the other hand, in H9 cells TPA activates the LTR by two consecutive mechanisms; the first depends on PKCeta activity and is exerted through the 21 bp repeats of the LTR, whereas the second is analogous to that observed in Jurkat cells, except that it is antagonized by PKCdelta.
Chamias
Rachel
R
The Shraga Segal Department of Microbiology and Immunology, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, Israel.
Huleihel
Mahmoud
M
Aboud
Mordechai
M
D015368:Human T-lymphotropic virus 1 / Q000235:genetics*; D006801:Humans; D007527:Isoenzymes / Q000378:metabolism*; D011493:Protein Kinase C / Q000378:metabolism*; D012091:Repetitive Sequences, Nucleic Acid; D013601:T-Lymphocytes / Q000187:drug effects* / Q000201:enzymology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology*
D007527:Isoenzymes; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate