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首页> 外文期刊>Molecular and Cellular Biology >Induction of nuclear factor kappaB by the CD30 receptor is mediated by TRAF1 and TRAF2.
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Induction of nuclear factor kappaB by the CD30 receptor is mediated by TRAF1 and TRAF2.

机译：CD30受体对核因子κB的诱导是由TRAF1和TRAF2介导的。

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CD30 is a lymphoid cell-specific surface receptor which was originally identified as an antigen expressed on Hodgkin's lymphoma cells. Activation of CD30 induces the nuclear factor kappaB (NF-kappaB) transcription factor. In this study, we define the domains in CD30 which are required for NF-kappaB activation. Two separate elements of the cytoplasmic domain which were capable of inducing NF-kappaB independently of one another were identified. The first domain (domain 1) mapped to a approximately 120-amino-acid sequence in the membrane-proximal region of the CD30 cytoplasmic tail, between residues 410 and 531. A second, more carboxy-terminal region (domain 2) was identified between residues 553 and 595. Domain 2 contains two 5- to 10-amino-acid elements which can mediate the binding of CD30 to members of the tumor necrosis factor receptor-associated factor (TRAF) family of signal transducing proteins. Coexpression of CD30 with TRAF1 or TRAF2 but not TRAF3 augmented NF-kappaB activation through domain 2 but not domain 1. NF-kappaB induction through domain 2 was inhibited by coexpression of either full-length TRAF3 or dominant negative forms of TRAF1 or TRAF2. In contrast, NF-kappaB induction by domain 1 was not affected by alterations in TRAF protein levels. Together, these data support a model in which CD30 can induce NF-kappaB by both TRAF-dependent and -independent mechanisms. TRAF-dependent induction of NF-kappaB appears to be regulated by the relative levels of individual TRAF proteins in the cell.
机译：CD30是淋巴样细胞特异性表面受体，最初被鉴定为霍奇金淋巴瘤细胞上表达的抗原。 CD30的激活诱导核因子kappaB（NF-kappaB）转录因子。在这项研究中，我们在CD30中定义了NF-κB激活所需的域。鉴定了能够彼此独立地诱导NF-κB的胞质结构域的两个独立元件。在残基410和531之间，第一个结构域（结构域1）映射到CD30细胞质尾部膜近端区域中大约120个氨基酸的序列。第二个更羧基末端的区域（结构域2）被鉴定为残基553和595。域2包含两个5至10个氨基酸的元件，它们可以介导CD30与信号转导蛋白的肿瘤坏死因子受体相关因子（TRAF）家族成员的结合。 CD30与TRAF1或TRAF2共同表达，但不通过TRAF3增强通过结构域2而不是结构域1的NF-kappaB激活。全长TRAF3或TRAF1或TRAF2的显性阴性形式的共表达抑制了通过结构域2的NF-kappaB诱导。相反，域1诱导的NF-κB不受TRAF蛋白水平变化的影响。这些数据共同支持了一个模型，其中CD30可以通过TRAF依赖性和非依赖性机制诱导NF-κB。依赖TRAF的NF-κB诱导似乎受细胞中单个TRAF蛋白的相对水平调节。

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