
Recruitment of LC3 to damaged Golgi apparatus | Cell Death
2018年10月22日 · LC3 is a protein that can associate with autophagosomes, autolysosomes, and phagosomes. Here, we show that LC3 can also redistribute toward the damaged Golgi apparatus where it clusters with...
The ER–Golgi intermediate compartment is a key membrane
2013年8月6日 · We developed a systematic membrane isolation scheme to identify the endoplasmic reticulum–Golgi intermediate compartment (ERGIC) as a primary membrane source both necessary and sufficient to trigger LC3 lipidation in vitro. Functional studies demonstrate that the ERGIC is required for autophagosome biogenesis in vivo.
布雷菲德菌素A对HepG2细胞自噬的诱导作用 - RCEES
结果表明,BFA可引起HepG2细胞内自噬特征蛋白LC3-Ⅱ、Atg5、Beclin-1的蛋白表达水平明显增加;同时引起HepG2细胞活性降低、细胞数量减少、细胞核固缩和变形。
Nature | 陈志坚团队首次系统性揭示cGAS-STING在细胞自噬中的功能
2019年3月13日 · 使用ER-Golgi转运抑制剂BFA或者GCA,可以同时抑制IRF3的激活和细胞自噬。 敲除COPII家族的蛋白,显著抑制cGAMP诱导的TBK1-IRF3激活和细胞自噬。 这些结果表明, STING的膜转运过程是激活其下游信号通路的重要步骤。
布雷菲德菌素A对HepG2细胞自噬的诱导作用 - 百度学术
为探讨新型抗癌药物布雷菲德菌素A(BFA)诱导肝癌细胞发生自噬性死亡的作用机制,以HepG2细胞作为研究对象,将细胞分成阴性对照组,不同浓度BFA组和阳性对照组(雷帕霉素),采用MTT法测定HepG2细胞活性;采用免疫荧光法检测细胞内自噬标志蛋白LC3的表达和细胞核形态学 ...
NF-κB pathway link with ER stress-induced autophagy and apoptosis in ...
We found that BFA significantly increased autophagy in tumor cells and induced TC-1 tumor cell death in a dose-dependent manner. BFA increased punctate staining of LC3 and the number of autophagosomes observed by TEM in TC-1 and HeLa cells. The autophagic flux …
Golgi-associated LC3 lipidation requires V-ATPase in ... - Nature
2016年8月11日 · AMDE-1-induced LC3 lipidation was colocalized with the Golgi complex, and was inhibited by the disturbance of Golgi complex. The integrity of the Golgi complex was also required for multiple...
NF-κB通路与内质网应激诱导的宫颈癌细胞自噬和细胞凋亡相关 …
2017年1月1日 · BFA增加了TC-1和HeLa细胞中LC3的点状染色以及通过TEM观察到的自噬体的数量。还评估了自噬通量。阻滞溶酶体中LC3降解的Bafilomycin导致LC3I和LC3II积累。BFA通过激活caspase-12 / caspase-3途径启动TC-1肿瘤细胞的凋亡。
Golgi-associated LC3 lipidation requires V-ATPase in ... - PubMed
2016年8月11日 · AMDE-1-induced LC3 lipidation was colocalized with the Golgi complex, and was inhibited by the disturbance of Golgi complex. The integrity of the Golgi complex was also required for multiple other agents to stimulate noncanonical LC3 lipidation.
Regulation of autophagic flux by MSNs-BFA. (a) LC3
The LC3 level of cells treated with MSNs-BFA is even higher than that of cells treated with BFA alone, which is attributed to accumulation of autolysosomes by BFA induction and the...