Gene interactions and pathways from curated databases and text-mining
Int J Mol Med 2008, PMID: 19020776

LC3-I conversion to LC3-II does not necessarily result in complete autophagy.

Giménez-Xavier, Pol; Francisco, Roser; Platini, Francesca; Pérez, Ricardo; Ambrosio, Santiago

Autophagy was induced in human neuroblastoma SH-SY5Y cells by two different procedures: deprivation of fetal serum in culture medium, or treatment with dopamine. 3-methyladenine prevented autophagy in the two procedures. Although it is usually considered that the conversion of soluble LC3-I to lipid bound LC3-II is associated with the formation of autophagosomes, the inhibition of autophagy with 3-methyladenine prevented this transformation in serum-deprived but not in dopamine-treated cells. While the PI3K-mTOR pathway was inhibited by serum deprivation, dopamine increased the phosphorylation of Akt but inhibited mTOR activity in a similar way to rapamycin. Dopamine and rapamycin increased LC3-II levels by a mechanism not prevented by 3-methyladenine. The activation of LC3-I to LC3-II may then be necessary but not sufficient to trigger cell autophagy. Thus, the increase in LC3-II, as the main biochemical parameter for autophagy at present, should be considered with caution.

Diseases/Pathways annotated by Medline MESH: Neuroblastoma
Document information provided by NCBI PubMed

Text Mining Data

Akt ⊣ mTOR: " While the PI3K-mTOR pathway was inhibited by serum deprivation, dopamine increased the phosphorylation of Akt but inhibited mTOR activity in a similar way to rapamycin "

Manually curated Databases

No curated data.