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- W2334157044 abstract "It was revealed by our previous research that sodium selenite repressed autophagy accompanied by the induction of apoptosis in human leukemia NB4 cells. The inhibition of autophagy exerted a facilitative effect on apoptosis. In the present study, we further explored the mechanisms underlying the switch from autophagy to apoptosis and elucidated p53 played a key role. Selenite induced phosphorylation of p53 at the vital site Ser15 via p38MAPK and ERK. Subsequently p53 dissociated with its inhibitory protein mouse double minute 2 (MDM2). Meanwhile, the nucleolar protein B23 transferred from the nucleolus to the nucleoplasm and associated with MDM2, probably stabilizing p53. The active p53 participated in the decrease of autophagic protein Beclin-1 and LC-3, as well as activation of apoptosis-related caspases. Furthermore, in p53 mutant U937 leukemia cells, selenite could not elicit such a switch from autophagy to apoptosis, laying emphasis on the crucial role p53 played in this process." @default.
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- W2334157044 date "2014-07-28" @default.
- W2334157044 modified "2023-10-11" @default.
- W2334157044 title "Activation of p53 by Sodium Selenite Switched Human Leukemia NB4 Cells From Autophagy to Apoptosis" @default.
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- W2334157044 doi "https://doi.org/10.3727/096504014x14024160459087" @default.
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