ArticleProceedings of the National Academy of Sciences of the United States of America2026
Phosphorylation and DNA damage resolution coordinate SOX2-mediated reprogramming in vivo.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Article
- in vivo Reprogramming of NG2 Glia Improves Bladder Function After Spinal Cord Injury.bioRxiv : the preprint server for biology · 2025Article
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3 authors.
Funding
Abstract
The stem cell factor SOX2 can reprogram resident glial cells into neurons in the adult mammalian central nervous system, but the molecular mechanisms underlying this process remain poorly understood. Here, we show that both SOX2 phosphorylation and the PRKDC-dependent nonhomologous end joining (NHEJ) pathway are essential for SOX2-mediated in vivo glia-to-neuron reprogramming. A phospho-mimetic SOX2 mutant significantly enhances reprogramming output without altering neuronal fate. Conversely, loss of PRKDC or knockdown of core NHEJ components KU80 and LIG4 abolishes reprogramming. Notably, p53 knockdown restores reprogramming in PRKDC-deficient mice, likely by overcoming DNA damage-induced cell-cycle arrest. These findings demonstrate that SOX2-driven glial reprogramming requires both precise posttranslational regulation and effective DNA damage repair and suggest that targeting these pathways could enhance regenerative strategies in the CNS.
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