Thébault Sabine, Basbous Jihane, Hivin Patrick, Devaux Christian, Mesnard Jean-Michel
Laboratoire Infections Rétrovirales et Signalisation Cellulaire, CNRS/UM I UMR 5121/IFR 122, Institut de Biologie, 4 Bd Henri IV, CS 89508, 34960 Montpellier Cedex 2, France.
FEBS Lett. 2004 Mar 26;562(1-3):165-70. doi: 10.1016/S0014-5793(04)00225-X.
Human T-cell leukemia virus type I (HTLV-I) bZIP factor (HBZ) is a viral basic leucine zipper protein that was originally described as a partner of cAMP response element binding protein-2 and as a repressor of HTLV-I viral transcription. In addition, HBZ is able to interact with the activator protein-1 (AP-1) transcription factors c-Jun and JunB, the interaction with c-Jun leading to a transcriptional repression of AP-1-regulated genes. Here we show that HBZ also interacts with JunD in vitro and in vivo, and that this association occurs via the bZIP domain of the two proteins. Moreover, we show that HBZ can activate JunD-dependent transcription and that its amino-terminus is required.
人类I型T细胞白血病病毒（HTLV-I）碱性亮氨酸拉链因子（HBZ）是一种病毒碱性亮氨酸拉链蛋白，最初被描述为环磷酸腺苷反应元件结合蛋白2的伴侣以及HTLV-I病毒转录的抑制因子。此外，HBZ能够与激活蛋白-1（AP-1）转录因子c-Jun和JunB相互作用，与c-Jun的相互作用导致AP-1调控基因的转录抑制。在此我们表明，HBZ在体外和体内也与JunD相互作用，并且这种关联通过两种蛋白的碱性亮氨酸拉链结构域发生。此外，我们表明HBZ可以激活JunD依赖的转录，并且其氨基末端是必需的。
