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• W3085483453 endingPage "102971" @default.
• W3085483453 startingPage "102971" @default.
• W3085483453 abstract "• First synthetic gene network of multiple cell fates induced by DNA damage based on the U87 glioblastoma cell line. • The model describes cell fate determination for three phenotypes: apoptosis, senescence and autophagy. • The model was generalized to describe other three different cell lines: MCF-7, A549 and U2OS. • For p53-deficient cell lines the model contemplates the alternative AMPK pathway which compensates this deficiency. • The approach is useful for designing experiments of loss and gain of function perturbations to induce a specific phenotype. How a cell determines a given phenotype upon damaged DNA is an open problem. Cell fate decisions happen at cell cycle checkpoints and it is becoming clearer that the p53 pathway is a major regulator of cell fate decisions involving apoptosis or senescence upon DNA damage, especially at G1/S. However, recent results suggest that this pathway is also involved in autophagy induction upon DNA damage. To our knowledge, in this work we propose the first model of the DNA damage-induced G1/S checkpoint contemplating the decision between three phenotypes: apoptosis, senescence, and autophagy. The Boolean model is proposed based on experiments with U87 glioblastoma cells using the transfection of miR-16 that can induce a DNA damage response. The wild-type case of the model shows that DNA damage induces the checkpoint and the coexistence of the three phenotypes (tristable dynamics), each with a different probability. We also predict that the positive feedback involving ATM, miR-16, and Wip1 has an influence on the tristable state. The model predictions were compared to experiments of gain and loss of function in other three different cell lines (MCF-7, A549, and U2OS) presenting agreement. For p53-deficient cell lines such as HeLa, H1299, and PC-3, our model contemplates the experimental observation that the alternative AMPK pathway can compensate this deficiency. We conclude that at the G1/S checkpoint the p53 pathway (or, in its absence, the AMPK pathway) can regulate the induction of different phenotypes in a stochastic manner in the U87 cell line and others." @default.
• W3085483453 created "2020-09-21" @default.
• W3085483453 creator A5000081923 @default.
• W3085483453 creator A5033025455 @default.
• W3085483453 creator A5049678192 @default.
• W3085483453 date "2020-12-01" @default.
• W3085483453 modified "2023-10-17" @default.
• W3085483453 title "Towards DNA-damage induced autophagy: A Boolean model of p53-induced cell fate mechanisms" @default.
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• W3085483453 doi "https://doi.org/10.1016/j.dnarep.2020.102971" @default.
• W3085483453 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32987354" @default.
• W3085483453 hasPublicationYear "2020" @default.
• W3085483453 type Work @default.
• W3085483453 sameAs 3085483453 @default.

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