Fig. 5: Signaling connections involved in autophagy pathways sensitive to cyclinB1 silencing in CNE-1 and CNE-2 cells. | Cell Death & Disease

Fig. 5: Signaling connections involved in autophagy pathways sensitive to cyclinB1 silencing in CNE-1 and CNE-2 cells.

From: Downregulation of G2/mitotic-specific cyclinB1 triggers autophagy via AMPK-ULK1-dependent signal pathway in nasopharyngeal carcinoma cells

Fig. 5

Silencing of cyclinB1 elevated the reactive oxygen species levels. This in turn directly activated AMPKα by phosphorylating at Thr172 and then activated ULK1 by phosphorylating at Ser555 leading to autophagy. Activated AMPKα also phosphorylated beclin-1 at Ser93 site, which further enhanced the activity of PI3K compound. Moreover, elevated ATG4a cleaved the C-terminal part of MAP1LC3 allowing the release of (LC3-I). Then a subpopulation of LC3-I was subsequently converted into a LC3-II. Additionally, p62 bound autophagosomal membrane protein LC3/Atg8, delivering p62-containing protein aggregated to the autophagosome, which led to a decline in p62 level. Arrows represented promotion events, blunt arrows indicated suppression events

Back to article page