Int J Mol Med 2008,
PMID: 19020776
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
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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.