人免疫缺陷病毒基因转录的CD30诱导由TRAF2介导。
CD30 induction of human immunodeficiency virus gene transcription is mediated by TRAF2.
作者信息
Tsitsikov E N, Wright D A, Geha R S
机构信息
Division of Immunology, Children's Hospital, Department of Pediatrics Harvard Medical School, Boston, MA 02115, USA.
出版信息
Proc Natl Acad Sci U S A. 1997 Feb 18;94(4):1390-5. doi: 10.1073/pnas.94.4.1390.
Abstract
CD30 is a member of the tumor necrosis factor receptor (TNFR) superfamily expressed on activated T and B lymphocytes and natural killer cells. Ligation of CD30 was previously shown to induce NF-kappaB activation and HIV expression in chronically infected T lymphocytes. In this study, we report that two members of the TNFR-associated factor (TRAF) family of proteins, TRAF1 and TRAF2, independently bind to the intracellular domain of CD30 (CD30IC). Transient overexpression of TRAF2, but not TRAF1, induced NF-kappaB activation and HIV-1-long terminal repeat-driven transcription in the T cell line, KT3. Moreover, dominant negative mutants consisting of the TRAF domain of TRAF1 and TRAF2 inhibited CD30 induction of NF-kappaB activation and HIV-1 transcription. These results suggest that CD30 ligation may enhance the expression of HIV via TRAF-2-mediated activation of NF-kappaB.
摘要
CD30是肿瘤坏死因子受体（TNFR）超家族的成员，在活化的T和B淋巴细胞以及自然杀伤细胞上表达。先前已证明CD30的连接可诱导慢性感染的T淋巴细胞中的NF-κB活化和HIV表达。在本研究中，我们报告TNFR相关因子（TRAF）蛋白家族的两个成员TRAF1和TRAF2独立结合至CD30的胞内结构域（CD30IC）。TRAF2而非TRAF1的瞬时过表达在T细胞系KT3中诱导了NF-κB活化和HIV-1长末端重复序列驱动的转录。此外，由TRAF1和TRAF2的TRAF结构域组成的显性负性突变体抑制了CD30诱导的NF-κB活化和HIV-1转录。这些结果表明，CD30连接可能通过TRAF-2介导的NF-κB活化增强HIV的表达。
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本文引用的文献
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CD30 contains two binding sites with different specificities for members of the tumor necrosis factor receptor-associated factor family of signal transducing proteins.CD30含有两个结合位点，对信号转导蛋白的肿瘤坏死因子受体相关因子家族成员具有不同的特异性。
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The CD40L promoter contains nuclear factor of activated T cells-binding motifs which require AP-1 binding for activation of transcription.CD40L启动子包含活化T细胞核因子结合基序，这些基序需要AP-1结合以激活转录。
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