REGULATION OF THE HUMAN INTERLEUKIN-2 RECEPTOR ALPHA-CHAIN PROMOTER - ACTIVATION OF A NONFUNCTIONAL PROMOTER BY THE TRANSACTIVATOR GENE OF HTLV-1
REGULATION OF THE HUMAN INTERLEUKIN-2 RECEPTOR ALPHA-CHAIN PROMOTER - ACTIVATION OF A NONFUNCTIONAL PROMOTER BY THE TRANSACTIVATOR GENE OF HTLV-1
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DOI：
10.1016/0092-8674(87)90754-9
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发表时间：
1987-04-10
期刊：
影响因子：
64.5
通讯作者：
LEONARD, WJ
中科院分区：
文献类型：
--
作者：
CROSS, SL;FEINBERG, MB;LEONARD, WJ
我们已经表征了人IL-2受体α链（IL 2 R α）的调节区。启动子延伸至-327的5 ″缺失构建体指导HTLV-1感染的T细胞中的CAT表达，其表达IL 2 R α。组成型，以及在表达IL 2 R α的Jurkat细胞中。只有在感应之后。-267和-265的缺失仅在HTLV-I转化的T细胞中有活性，但它们在Jurkat细胞中的活性通过共转染表达HTLV-I反式激活蛋白（tat-I）的构建体而恢复。然而，HTLV-1感染的人骨肉瘤细胞不表达IL 2 R α。CAT结构。因此，细胞类型特异性因子是IL 2 R α所必需的。表达，以及tat-I与IL 2 R α的特定区域之间的直接或间接相互作用。启动子可能导致调节改变。在某些条件下，Tat-I还增强IL 2-CAT表达，提示HTLV-I诱导的白血病发生可能是自分泌或旁分泌机制。
We have characterized regulatory regions of the human IL-2 receptor alpha chain (IL2R.alpha.) promoter. 5'' deletion constructs extending to -327 directed CAT expression in HTLV-I-infected T cells, which express IL2R.alpha. constitutively, and in Jurkat cells, which express IL2R.alpha. only after induction. Deletions to -267 and -265 were active only in HTLV-I-transformed T cells, but their activity in Jurkat cells was restored by cotransfection of a construct expression the HTLV-I transactivator protein (tat-I). However, HTLV-I-infected human osteosarcoma cells do not express IL2R.alpha.-CAT constructs. Thus cell-type-specific factors are required for IL2R.alpha. expression, and direct or indirect interaction(s) between tat-I and a specific region of the IL2R.alpha. promoter may cause altered regulation. Tat-I also augments IL2-CAT expression under some conditions, suggesting possible autocrine or paracrine mechanisms for HTLV-I-induced leukemogenesis.