Matches in SemOpenAlex for { <https://semopenalex.org/work/W2904453831> ?p ?o ?g. }
- W2904453831 abstract "Injured peripheral sensory neurons switch to a regenerative state after axon injury, which requires transcriptional and epigenetic changes. However, the roles and mechanisms of gene inactivation after injury are poorly understood. Here, we show that DNA methylation, which generally leads to gene silencing, is required for robust axon regeneration after peripheral nerve lesion. Ubiquitin-like containing PHD ring finger 1 (UHRF1), a critical epigenetic regulator involved in DNA methylation, increases upon axon injury and is required for robust axon regeneration. The increased level of UHRF1 results from a decrease in miR-9. The level of another target of miR-9, the transcriptional regulator RE1 silencing transcription factor (REST), transiently increases after injury and is required for axon regeneration. Mechanistically, UHRF1 interacts with DNA methyltransferases (DNMTs) and H3K9me3 at the promoter region to repress the expression of the tumor suppressor gene phosphatase and tensin homolog (PTEN) and REST. Our study reveals an epigenetic mechanism that silences tumor suppressor genes and restricts REST expression in time after injury to promote axon regeneration." @default.
- W2904453831 created "2018-12-22" @default.
- W2904453831 creator A5001384115 @default.
- W2904453831 creator A5009564247 @default.
- W2904453831 creator A5010966735 @default.
- W2904453831 creator A5034527807 @default.
- W2904453831 creator A5048486234 @default.
- W2904453831 creator A5089361096 @default.
- W2904453831 date "2018-12-10" @default.
- W2904453831 modified "2023-10-13" @default.
- W2904453831 title "Epigenetic regulator UHRF1 inactivates REST and growth suppressor gene expression via DNA methylation to promote axon regeneration" @default.
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- W2904453831 doi "https://doi.org/10.1073/pnas.1812518115" @default.
- W2904453831 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6310844" @default.
- W2904453831 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30530687" @default.
- W2904453831 hasPublicationYear "2018" @default.