Vps34-PIK-III

VPS34:0.018μM|PI3Kδ:1.2μM

DFX诱导的NCOA4依赖的FTH1和FTL的周转在加入PIK-III后被阻断，这表明是一个自噬依赖的过程[2]。

VPS34的酶功能对哺乳动物细胞中的LC3脂质化是必要的，而PIK-III是一种强效的自噬和LC3脂质化抑制剂。在H4细胞中，PIK-III抑制自溶体的形成，并且在基础条件下以及使用mTOR抑制剂AZD8055诱导自噬时增加LC3的胞质信号。在CCCP诱导的线粒体自噬模型中，PIK-III抑制了线粒体的清除。PIK-III处理导致H4和PSN1细胞中LC3-I水平的增加。在Panc10.05细胞中，PIK-III同时增加LC3-II和LC3-I的水平，暗示了一种细胞类型特异性反应[1]。

H2O:< 1 mg/mL (insoluble or slightly soluble);DMSO:60 mg/mL (187.88 mM);Ethanol:59 mg/mL (184.74 mM)

To determine whether inhibition of VPS34 function impacts autophagy,LC3 and known autophagy substrates such as damaged mitochondria or the autophagy cargo receptor p62 are monitored. H4 cells expressing mCherry–GFP–LC3 are treated overnight with the indicated compounds, fixed, stained with Hoechst 33342 and imaged by automated acquisition. HeLa cells expressing GFP–Parkin are treated with PIK-III for 12 h followed by the addition of CCCP for 12 h, fixed, stained for endogenous Tom20 and imaged. (Only for Reference)