Department of Anatomy, Cell and Developmental Biology, Eötvös Loránd University, Budapest, Hungary.
Autophagy. 2012 Dec;8(12):1875-6. doi: 10.4161/auto.21544.
Recent publications showed that the kinase MTOR localizes to lysosomes and its activation depends on amino acids inside the lysosomal lumen, implying that autophagic protein degradation is a positive regulator of MTOR in this setting. Since decreased MTOR activity results in autophagy induction, drug treatments that block autolysosomal degradation (a commonly used technique to estimate autophagic flux) may actually interfere not only with lysosomal breakdown, but also increase autophagosome generation through impaired MTOR signaling.
最近的出版物表明，激酶 MTOR 定位于溶酶体，其激活依赖于溶酶体腔内的氨基酸，这意味着在这种情况下，自噬蛋白降解是 MTOR 的正向调节剂。由于 MTOR 活性的降低会导致自噬的诱导，因此，阻断自溶酶体降解的药物治疗（一种常用于估计自噬通量的常用技术）实际上不仅可能干扰溶酶体的降解，而且还可能通过受损的 MTOR 信号转导增加自噬体的产生。
