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TRIM13 regulates ubiquitination and turnover of NEMO to suppress TNF induced NF-κB activation

机译：TRIM13调节NEMO的泛素化和转换以抑制TNF诱导的NF-κB活化

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摘要

The NF-κB family of transcription factors is activated in response to various intracellular or extracellular stimuli and its dysregulation leads to pathological conditions like infection, cancer, neurodegenerative disorders. The post-translational modification by ubiquitination regulates various steps of NF-κB pathway. In the current study, we have described the role of TRIM13, an endoplasmic reticulum (ER) membrane anchored E3 ligase in regulation of NF-κB. The expression of TRIM13 represses TNF induced NF-κB while the knockdown has the opposite effect. The E3 ligase activity and ER localization is essential for NF-κB suppression whereas TRIM13 regulated autophagy is not essential. TRIM13 interacts with NEMO and modulates its ubiquitination and turnover, hence may regulate IKK complex activity. TRIM13 mediated NF-κB repression is essential for negative regulation of clonogenic ability of the cells. This study for the first time demonstrated the role of TRIM13, ER resident RING E3 ligase as a novel regulator of NEMO ubiquitination, negative regulator of NF-κB signaling and its role as a tumor suppressor.
机译：转录因子NF-κB家族可响应各种细胞内或细胞外刺激而被激活，其失调可导致诸如感染，癌症，神经退行性疾病等病理状况。通过泛素化的翻译后修饰调节NF-κB途径的各个步骤。在当前的研究中，我们已经描述了内质网（ER）膜锚定的E3连接酶TRIM13在调节NF-κB中的作用。 TRIM13的表达抑制TNF诱导的NF-κB，而敲低具有相反的作用。 E3连接酶活性和ER定位对于NF-κB抑制至关重要，而TRIM13调控的自噬并不是必需的。 TRIM13与NEMO相互作用并调节其泛素化和周转，因此可能调节IKK复合物的活性。 TRIM13介导的NF-κB抑制对于细胞克隆能力的负调控至关重要。这项研究首次证明了TRIM13（ER驻留RING E3连接酶）作为NEMO泛素化的新型调节剂，NF-κB信号传导的负调节剂的作用及其作为肿瘤抑制因子的作用。

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