Hooper W C, Rudolph D L, Lairmore M D, Lal R B
Hematologic Diseases Branch, National Center for Infectious Diseases, Centers for Disease Control, Public Health Service, U.S. Department of Health and Human Services, Atlanta, Georgia 30333.
Biochem Biophys Res Commun. 1991 Dec 31;181(3):976-80. doi: 10.1016/0006-291x(91)92032-f.
To better understand the transcriptional regulation of human T-lymphotropic viruses, expression of the nuclear proto-oncogenes, jun-B and c-jun were examined in cell lines infected with HTLV-I/II. Constitutive high levels of jun-B and c-jun expression were observed in HTLV-I (MT-2, Hut-102, IR, FS, SP) and HTLV-II infected cell lines (Mo-T, PAN). In contrast, the uninfected cell lines (Jurkat, Hut-78) expressed only basal levels of jun. This expression of jun was not dependent upon IL-2, as both IL-2 dependent (IR, FS, SP, and Pan) and IL-2 independent (MT-2, Hut-102, Mo-T) cell lines constitutively expressed transcripts for jun-B and c-jun. These data demonstrate that deregulated expression of nuclear protooncogenes such as jun may lead to cellular proliferation and the protein products of these nuclear oncogenes may potentially serve as transcriptional activators of HTLV-LTR by complexing with other nuclear proteins.
为了更好地理解人类嗜T淋巴细胞病毒的转录调控，我们检测了感染HTLV-I/II的细胞系中核原癌基因jun-B和c-jun的表达。在HTLV-I（MT-2、Hut-102、IR、FS、SP）和HTLV-II感染的细胞系（Mo-T、PAN）中观察到jun-B和c-jun的组成性高水平表达。相比之下，未感染的细胞系（Jurkat、Hut-78）仅表达基础水平的jun。jun的这种表达不依赖于IL-2，因为IL-2依赖型（IR、FS、SP和Pan）和IL-2非依赖型（MT-2、Hut-102、Mo-T）细胞系均组成性表达jun-B和c-jun的转录本。这些数据表明，诸如jun等核原癌基因的失调表达可能导致细胞增殖，并且这些核癌基因的蛋白质产物可能通过与其他核蛋白复合而潜在地作为HTLV-LTR的转录激活因子。
