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- W2214441024 abstract "Despite the widespread interest in direct neuronal reprogramming, the mechanisms underpinning fate conversion remain largely unknown. Our study revealed a critical time point after which cells either successfully convert into neurons or succumb to cell death. Co-transduction with Bcl-2 greatly improved negotiation of this critical point by faster neuronal differentiation. Surprisingly, mutants with reduced or no affinity for Bax demonstrated that Bcl-2 exerts this effect by an apoptosis-independent mechanism. Consistent with a caspase-independent role, ferroptosis inhibitors potently increased neuronal reprogramming by inhibiting lipid peroxidation occurring during fate conversion. Genome-wide expression analysis confirmed that treatments promoting neuronal reprogramming elicit an anti-oxidative stress response. Importantly, co-expression of Bcl-2 and anti-oxidative treatments leads to an unprecedented improvement in glial-to-neuron conversion after traumatic brain injury in vivo, underscoring the relevance of these pathways in cellular reprograming irrespective of cell type in vitro and in vivo." @default.
- W2214441024 created "2016-06-24" @default.
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- W2214441024 date "2016-03-01" @default.
- W2214441024 modified "2023-10-18" @default.
- W2214441024 title "Identification and Successful Negotiation of a Metabolic Checkpoint in Direct Neuronal Reprogramming" @default.
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- W2214441024 doi "https://doi.org/10.1016/j.stem.2015.12.003" @default.
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