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14 天
《Cell Death & Disease 》靶向 USP35:恶性黑色素瘤免疫治疗的新曙光
敲低 USP35 可促进内源性 MAVS 的泛素化。 USP35 调节 MAVS-TBK1-IRF3 信号通路:建立 USP35 敲低或敲除细胞系后发现,敲低或敲除 USP35 可显著增强 VSV 刺激后 TBK1 和 IRF3 的磷酸化水平,而过表达 Myc-USP35 则抑制这种激活。这表明 USP35 负向调节 MAVS 活性,从而抑制 I 型干扰 ...
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