Obesity is a leading cause of preventable illness and death worldwide. Genome-wide association studies have shown a strong correlation of a single nucleotide polymorphism in the first intron of the FTO gene with increased body mass index and obesity risk. Mouse model studies demonstrated that FTO is functionally involved in energy homeostasisand affects the whole body metabolism, establishing a mechanistic link between FTO and obesity. FTO protein was predicted and biochemically confirmed to belong to the AlkB family of Fe2+/2-oxoglutarate-dependent oxidative DNA/RNA demethylases. A link between FTO demethylase activity and increased fat mass was suggested by the observation that the single mutation Ile367Phe in mouse FTO protein with an impaired activity resulted in a lean phenotype of mouse. You can see here a the crystal structure of human FTO with an N-terminally truncated 31 residues (FTOΔ31) bound by the mononucleotide 3-meT, which was used as an FTO substrate in previous studies (PDB code: 3LFM)

#molecularart ... #immolecular ... #obesity ... #FTO ... #crystal ... #substrate ... #xray

Structure rendered with @proteinimaging and depicted with @corelphotopaint.