CCAAT/enhancer-binding proteins modulate human T cell leukemia virus type 1 long terminal repeat activation
CCAAT/enhancer-binding proteins modulate human T cell leukemia virus type 1 long terminal repeat activation
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DOI：
10.1016/j.virol.2005.12.024
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发表时间：
2006-05-10
期刊：
影响因子：
3.7
通讯作者：
Wigdahl, Brian
中科院分区：
文献类型：
--
作者：
Grant, Christian;Nonnemacher, Michael;Wigdahl, Brian
CCAAT/增强子结合蛋白（C/EBP）碱性区/亮氨酸拉链（bZIP）转录因子与cAMP-responsive element binding protein 2 （CREB-2）形成异源二聚体，CREB-2是一种参与调节人T细胞白血病病毒1型（HTLV-1）长末端重复序列（LTR）的基础和税基介导的转激活的转录因子。在单核-巨噬细胞谱系的细胞中（被认为作为辅助靶细胞在HTLV-1发病机制中发挥作用），C/EBP家族的几个成员高水平表达，可能对HTLV-1LTR的基础和税收介导的转激活都有功能影响。过表达C/EBPO、C/EBP6或C/EBPE可增强HTLV-1LTR的基础激活，而过表达C/EBP α和C/EBP可抑制Tax对LTR的反激活。税收介导的HTLV-1LTR转激活的抑制与共激活因子无关，不需要C/EBP与税收响应元件结合，并且可能涉及与CREB因子的异源二聚化。(c) 2006爱思唯尔公司版权所有。
CCAAT/enhancer-binding protein (C/EBP) basic region/leucine zipper (bZIP) transcription factors have been shown to form heterodimers with cAMP-responsive element binding protein 2 (CREB-2), a transcription factor involved in regulating basal and Tax-mediated transactivation of the human T cell leukemia virus type 1 (HTLV-1) long terminal repeat (LTR). In cells of the monocyte-macrophage lineage (proposed to play a role in HTLV-1 pathogenesis as an accessory target cell), several members of the C/EBP family are expressed at high levels and may have functional impact on both basal and Tax-mediated transactivation of the HTLV-1LTR. Basal activation of the HTLV-1LTR was enhanced by overexpression of C/EBPO, C/EBP6, or C/EBPE, whereas transactivation of the LTR by Tax was inhibited by overexpression of C/EBP alpha and C/EBP. Inhibition of Tax-mediated transactivation of the HTLV-1LTR was co-activator-independent, did not require C/EBP binding to the Tax-responsive elements, and may involve heterodimerization with CREB factors. (c) 2006 Elsevier Inc. All rights reserved.