Inactivation of the Fto gene protects from obesity

By Julia Fischer, Linda Koch, Christian Emmerling, Jeanette Vierkotten, Thomas Peters, Jens C. Brüning, U. Rüther. Nature, 2009

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Meclofenamic acid selectively inhibits FTO demethylation of m6A over ALKBH5 (2014, background): “to influence human obesity and energy utilization (20,21).”
Rethinking m6A Readers, Writers, and Erasers (2017, background): “These mice are largely normal except for alterations in dopaminergic neurotransmission, lean body mass, and alterations in metabolic rate (Fischer et al. 2009, Hess et al. 2013).”
Comprehensive Analysis of mRNA Methylation Reveals Enrichment in 3' UTRs and Near Stop Codons (2012, neutral): “The fat mass and obesity-associated (FTO) gene is a major regulator of metabolism and energy utilization (Church et al., 2009, 2010; Fischer et al., 2009).”
Regulation of disease-associated gene expression in the 3D genome (2016, positive): “Variants in introns of FTO , a gene that can influence body mass in mice 148 , were found to be located within enhancers that regulate not FTO but the physically contacted IRX3 and IRX5 genes, ~0.5–1 Mb away from the identified variants 149,150 .”
RNA N6-methyladenosine methylation in post-transcriptional gene expression regulation (2015, background): “In contrast, FTO is most highly expressed inmouse brains, and FTO-deficient mice mainly suffer from early mortality and reduced body mass (Gerken et al. 2007; Fischer et al. 2009).”