The autophagy process is initiated by the engulfing of large sections of a cytoplasm by a crescent-shaped phagophore that elongates into an autophagosome
, which subsequently fuses with a lysosome, causing its contents to be degraded by lysosomal hydrolases (Chang et al.
reported that expanded polyglutamine- (polyQ-) induced ER stress activates autophagosome
formation with LC3 conversion from LC3-I to -II via the PERK-eIF2[alpha] pathway .
cells that cannot form autophagosome
, the GAS could survive and proliferate, and was ultimately released from the cells.
Autophagy induction and autophagosome
clearance in neurons: Relationship to autophagic pathology in Alzheimer's disease.
Three well-established methods were adopted to detect autophagosome
formation to determine whether diosgenin induces autophagy in CML cells (Mizushima et al.
a)-(b) Analysis of the mitophagy biomarker (BNIP3) and autophagosome
regulators (beclin1 and LC3-II) by western blot (a) and densitometry (b).
The mechanisms of this suppression might be that the engulfment of defective mitochondria by autophagosomes
limited the release of proapoptotic proteins such as cytochrome c and apoptosis-inducing factors into the cytosol.
p62/SQSTM1 and HDAC6 interact with Ambra1 and Beclin1, prompting the accumulation of the autophagosome
to mitochondria [213, 214]; interestingly, studies in p62 knockout mice showed that p62 also mediates mitochondrial perinuclear clustering .
The mTOR pathway, a major negative regulator of autophagy, phosphorylates Atg13 and reduces Atg13-ULK1 interaction, thereby inhibiting the formation of a trimeric complex required for autophagosome
formation (Yang et al.
TFEB overexpression in cultured cells significantly increases the number of autophagosomes
and induces lysosomal biogenesis [9, 10].
accumulation can be detected with a fluorescence microscope.
In the current study, we found that [alpha]-TOS produced early induction of autophagy manifested by increased beclin-1 protein level and an early increase in the expression of LC3B protein, responsible for the completion of the autophagosome
formation, which recovered after prolonged incubation to control value.