LNCIB Laboratorio Nazionale Consorzio Interuniversitario Biotecnologie AREA Science Park, Trieste, Italy.
Autophagy. 2009 Aug;5(6):858-9. doi: 10.4161/auto.8822. Epub 2009 Aug 21.
We unveiled novel p65/RelA consensus sites in the promoter of the beclin 1 gene and demonstrate that p65/RelA positively modulates canonical autophagy in various human cell lines both under basal conditions and upon induction by ceramide. Interestingly, we find that T cell receptor-dependent activation of Jurkat cells triggers an increase in the binding of p65/RelA to the beclin 1 promoter accompanied by enhanced autophagy, suggesting that p65/RelA could regulate T-cell activation and homeostasis through autophagy.
我们在 beclin 1 基因启动子中发现了新的 p65/RelA 共识结合位点，并证实 p65/RelA 在各种人源细胞系中正向调节经典自噬，无论是在基础条件下还是在用神经酰胺诱导时都是如此。有趣的是，我们发现 Jurkat 细胞中 T 细胞受体依赖性激活会触发 p65/RelA 与 beclin 1 启动子结合增加，同时伴随着自噬增强，这表明 p65/RelA 可以通过自噬来调节 T 细胞激活和稳态。
