TY -的A2 Khanna Savita AU -李,温家宝AU -杨,越盟- Ba,非盟-李、Shupeng盟——陈郝AU -侯,小燕盟- Ma,灵灵盟——他,Pengcheng盟——江,Lei AU - Li Longxuan盟——他,Rongrong盟——张Liangqing盟——冯,Du PY - 2017 DA - 2017/10/03 TI -微- 93调节低氧诱导自噬通过瞄准ULK1 SP - 2709053六世- 2017 AB -核心自噬激酶的表达,Unc51-like激酶1 (ULK1),由starvation-induced自噬调控转录和转译。然而,ULK1如何监管在缺氧原因还不是很清楚。以前,我们表明,ULK1表达式是缺氧引起的压力。在这里,我们报告一个新的ULK1-modulating微rna, mir - 93;的转录与翻译负相关ULK1缺氧条件下。mir - 93目标ULK1在缺氧条件下,降低其蛋白质含量。mir - 93还能抑制低氧诱导自噬通过防止LC3-I LC3-II过渡和P62退化;这些过程的超表达是相反的一个内生mir - 93抑制剂。ULK1没有mir - 93反应元素的表达,恢复的低氧诱导自噬抑制mir - 93。最后,我们发现mir - 93对细胞生存能力和细胞凋亡的影响在非癌症细胞系和肿瘤细胞。 We found that miR-93 sustains the viability of MEFs (mouse embryonic fibroblasts) and inhibits its apoptosis under hypoxia. Thus, we conclude that miR-93 is involved in hypoxia-induced autophagy by regulating ULK1. Our results provide a new angle to understand the complicated regulation of the key autophagy kinase ULK1 during different stress conditions. SN - 1942-0900 UR - https://doi.org/10.1155/2017/2709053 DO - 10.1155/2017/2709053 JF - Oxidative Medicine and Cellular Longevity PB - Hindawi KW - ER -