The Shraga Segal Department of Microbiology and Immunology, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, Israel.
Leuk Res. 2010 Jan;34(1):93-9. doi: 10.1016/j.leukres.2009.03.032. Epub 2009 Apr 29.
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.
我们在这里证明，TPA 通过严格不同的机制激活 Jurkat 和 H9 T 细胞系中的 HTLV-1 LTR 表达。在 Jurkat 细胞中，这种激活是通过一种 PKCalpha 和 PKCvarepsilon 拮抗的机制发挥作用的，该机制通过 LTR 的 Est 反应区 1 内的 Sp1 结合位点发挥作用。另一方面，在 H9 细胞中，TPA 通过两种连续的机制激活 LTR；第一种依赖于 PKCeta 活性，并通过 LTR 的 21 个碱基重复发挥作用，而第二种类似于在 Jurkat 细胞中观察到的机制，只是它被 PKCdelta 拮抗。
