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Nitric oxide inhibits FTO demethylase activity to regulate N6-methyladenosine mRNA methylation [MDA-MB-231-RNASeq]

GSE236270 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2024/06/30 Platform GPL24676
Summary
Here we show that nitric oxide (NO) is a potent inhibitor of FTO demethylase activity by directly binding to the catalytic iron center, which causes global m6A hypermethylation of mRNA in cells and results in gene-specific enrichment of m6A on mRNA of NO-regulated transcripts. Both cell culture and tumor xenograft models demonstrated that endogenous NO synthesis can regulate m6A-mRNA levels and transcriptional changes of m6A-associated genes. These results build a direct link between NO and m6A-mRNA regulation and reveal a novel signaling mechanism of NO as an endogenous regulator of the epitranscriptome.
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Also filed as BioProject PRJNA989607 and SRA study SRP446826. Searching any of these in the dataset finder brings you back here.

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