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首页> 外文期刊>Molecular and Cellular Biology >STAP-2 Negatively Regulates both Canonical and Noncanonical NF-κB Activation Induced by Epstein-Barr Virus-Derived Latent Membrane Protein 1
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STAP-2 Negatively Regulates both Canonical and Noncanonical NF-κB Activation Induced by Epstein-Barr Virus-Derived Latent Membrane Protein 1

机译：STAP-2负调节由爱泼斯坦-巴尔病毒衍生的潜在膜蛋白1诱导的规范性和非规范性NF-κB激活。

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The signal-transducing adaptor protein 2 (STAP-2) is a recently identified adaptor protein that contains a pleckstrin homology (PH) and Src homology 2 (SH2)-like domains, as well as a proline-rich domain in its C-terminal region. In previous studies, we demonstrated that STAP-2 binds to MyD88 and IKK-α or IKK-β and modulates NF-κB signaling in macrophages. In the present study, we found that ectopic expression of STAP-2 inhibited Epstein-Barr virus (EBV) LMP1-mediated NF-κB signaling and interleukin-6 expression. Indeed, STAP-2 associated with LMP1 through its PH and SH2-like domains, and these proteins interacted with each other in EBV-positive human B cells. We found, furthermore, that STAP-2 regulated LMP1-mediated NF-κB signaling through direct or indirect interactions with the tumor necrosis factor receptor (TNFR)-associated factor 3 (TRAF3) and TNFR-associated death domain (TRADD) proteins. STAP-2 mRNA was induced by the expression of LMP1 in human B cells. Furthermore, transient expression of STAP-2 in EBV-positive human B cells decreased cell growth. Finally, STAP-2 knockout mouse embryonic fibroblasts showed enhanced LMP1-induced cell growth. These results suggest that STAP-2 acts as an endogenous negative regulator of EBV LMP1-mediated signaling through TRAF3 and TRADD.
机译：信号转导衔接子蛋白2（STAP-2）是最近发现的衔接子蛋白，在其C末端包含pleckstrin同源（PH）和Src同源2（SH2）样结构域，以及富含脯氨酸的结构域地区。在以前的研究中，我们证明了STAP-2与MyD88和IKK-α或IKK-β结合并调节巨噬细胞中的NF-κB信号传导。在本研究中，我们发现STAP-2的异位表达抑制了爱泼斯坦-巴尔病毒（EBV）LMP1介导的NF-κB信号传导和白介素6的表达。实际上，STAP-2通过其PH和SH2样结构域与LMP1结合，并且这些蛋白质在EBV阳性人B细胞中彼此相互作用。此外，我们发现STAP-2通过与肿瘤坏死因子受体（TNFR）相关因子3（TRAF3）和TNFR相关死亡域（TRADD）蛋白的直接或间接相互作用来调节LMP1介导的NF-κB信号传导。 STAP-2 mRNA是由人B细胞中LMP1的表达诱导的。此外，在EBV阳性人B细胞中STAP-2的瞬时表达降低了细胞的生长。最后，STAP-2基因敲除小鼠胚胎成纤维细胞显示增强的LMP1诱导的细胞生长。这些结果表明，STAP-2通过TRAF3和TRADD充当EBV LMP1介导的信号转导的内源性负调节剂。

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