HTLV-1 Basic Leucine-Zipper Factor, HBZ, Interacts With MafB and Suppresses Transcription Through a Maf Recognition Element
HTLV-1 Basic Leucine-Zipper Factor, HBZ, Interacts With MafB and Suppresses Transcription Through a Maf Recognition Element
复制标题
DOI：
10.1002/jcb.22687
复制
发表时间：
2010-09-01
影响因子：
4
通讯作者：
Shimotohno, Kunitada
中科院分区：
文献类型：
--
作者：
Ohshima, Takayuki;Mukai, Risa;Shimotohno, Kunitada
HTLV-1 感染会导致成人 T 细胞白血病 (ATL)。开发还是ATL。被认为与细胞基因转录控制的破坏有关。 HTLv-1 巴斯克白细胞拉链 (bZIP) 因子 HBZ 由原病毒的互补链编码。我们之前报道过 HBZ 与 c-Jun 相互作用并抑制其转录活性为了鉴定与 HBZ 相互作用的细胞因子，我们使用全长 HBZ 作为禁令和已识别的人进行了酵母双杂交筛选。通过每个 bZIP 结构域，HBZ 与 MafB 形成异源二聚体 荧光素酶分析显示，通过 Maf 识别元件 (MARE) 的转录显着减少，其方式依赖于 bZIP 结构域或 HBZ。事实上，细胞中产生或全长的 HBZ 降低了 MARE-hound MafB 蛋白，表明 HBZ 消除了 MafB 的 DNA 结合活性。此外，HBZ 降低了 MafB 的稳态水平，并且通过蛋白酶体抑制剂处理恢复了该水平。这些结果表明 HBZ 对功能障碍有抑制作用，这可能在 HTLV-1 大鼠发病机制中具有重要作用 J. Cell。生物化学。 111. 187-194, 2010。(C) 2010 Wiley-Liss, Inc
HTLV-1 infection causes adult T-cell leukemia (ATL). The development or ATL. is thought to be associated with disruption of transcriptional control of cellular genes. HTLv-1 bask leucme-zipper (bZIP) factor, HBZ, is encoded by the complementary strand of the provirus. We previously reported that HBZ interacts with c-Jun and suppresses its transcriptional activity To identify the cellular factor(s) that Interact with HBZ, we conducted a yeast two-hybrid screen using full-length HBZ as ban and Identified Man). HBZ heterodimenzes with MafB via each bZIP domain Luciferase analysis revealed a significant decrease in transcription through Maf recognition element (MARE) in a manner dependent on the bZIP domain or HBZ. Indeed, production or full-length HBZ in cells decreased the MARE-hound MafB protein, indicating that HBZ abrogates the DNA-binding activity of MafB In addition HBZ reduced the steady-state levels of MafB and the levels were restored by treatment with a proteasome inhibitor These results suggest a suppressive effect or HBZ on Malfunction, which may have a significant role in HTLV-1 ratted pathogenesis J. Cell. Biochem. 111. 187-194, 2010. (C) 2010 Wiley-Liss, Inc