NIK expression stimulated G6PD phosphorylation

Our findings establish NIK as a pivotal regulator of T cell metabolism in anti-tumor immunity and highlight a posttranslational mechanism of metabolic regulation involving the G6PD-NADPH redox system. CoIP assays revealed a strong physical interaction between NIK and G6PD in both T cells and transiently transfected 293 cells, suggesting G6PD to be a direct target of NIK. Using a phosphoprotein gel analysis approach, we demonstrated that NIK expression stimulated G6PD phosphorylation. To further study the mechanism, we performed mass spectrometry identify phosphorylation sites of G6PD stimulated by NIK本研究证实NIK（核因子κB诱导激酶）是抗肿瘤免疫过程中T细胞代谢的关键调控因子，并揭示了一条涉及G6PD（葡萄糖-6-磷酸脱氢酶）-NADPH氧化还原系统的代谢调控翻译后修饰机制。免疫共沉淀（Co-immunoprecipitation, CoIP）实验结果表明，在T细胞与瞬时转染的293细胞中，NIK与G6PD之间存在强烈的物理相互作用，提示G6PD为NIK的直接靶标。我们采用磷酸化蛋白质凝胶分析方法，证实NIK的表达可诱导G6PD发生磷酸化修饰。为进一步阐明该调控机制，我们通过质谱技术鉴定了NIK诱导的G6PD磷酸化位点。