Tumor necrosis factor receptor-associated factor (TRAF)2 represses the T helper cell type 2 response through interaction with NFAT-interacting protein (NIP45).
Tumor necrosis factor receptor-associated factor (TRAF)2 represses the T helper cell type 2 response through interaction with NFAT-interacting protein (NIP45).
复制标题
肿瘤坏死因子受体相关因子（TRAF）2通过与NFAT相互作用蛋白相互作用（NIP45）来抑制T辅助细胞2型反应。
DOI：
10.1084/jem.194.1.89
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发表时间：
2001-07-02
影响因子：
15.3
通讯作者：
Glimcher, L H
中科院分区：
文献类型：
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作者：
Lieberson, R;Mowen, K A;McBride, K D;Leautaud, V;Zhang, X;Suh, W K;Wu, L;Glimcher, L H
最近，我们发现了一种新的蛋白NIP45（活化T细胞核因子[NFAT]-相互作用蛋白），它大大增加了白细胞介素(IL)-4基因的转录。将NIP45与NFAT和T辅助细胞2型（Th2）特异性转录因子c-Maf一起提供给通常难以产生IL-4的细胞，如B细胞或Th1克隆，可导致大量IL-4分泌至接近原代Th2细胞产生的水平。在旨在进一步了解NIP45活性的研究中，我们发现了IL-4基因调控的一个新方面。我们提供的证据表明，肿瘤坏死因子受体相关因子（TRAF）蛋白家族的成员，通常被称为转导肿瘤坏死因子受体超家族信号的适配器蛋白，有助于抑制IL-4基因的转录，并且这种作用是通过它们与NIP45的相互作用介导的。
Recently we have identified a novel protein NIP45 (nuclear factor of activated T cells [NFAT]-interacting protein) which substantially augments interleukin (IL)-4 gene transcription. The provision of NIP45 together with NFAT and the T helper cell type 2 (Th2)-specific transcription factor c-Maf to cells normally refractory to IL-4 production, such as B cells or Th1 clones, results in substantial IL-4 secretion to levels that approximate those produced by primary Th2 cells. In studies designed to further our understanding of NIP45 activity, we have uncovered a novel facet of IL-4 gene regulation. We present evidence that members of the tumor necrosis factor receptor–associated factor (TRAF) family of proteins, generally known to function as adapter proteins that transduce signals from the tumor necrosis factor receptor superfamily, contribute to the repression of IL-4 gene transcription and that this effect is mediated through their interaction with NIP45.