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Identification of a ferrireductase required for efficient transferrin-dependent iron uptake in erythroid cells

In that sense, the presence of the M105I mutation in a TPR module could affect -SNAP half-life, thus contributing to protein hypomorphism observed in several organs of the hyh mutant mouse 8,14,19,20,25 Supporting this, the M105 amino acid residue is highly conserved across various species 14,15

Gholizadeh-Hashjin A, Monajjemzadeh F, Ghafourian T, Hamishehkar H, Nokhodchi A

Should this pharmacological profile be confirmed in late-stage clinical studies, optimized FGF21 analogs have the potential to not only resolve liver pathology, but also to reduce risk of cardiovascular morbidity and mortality, and incidence of organ damage associated with inadequate glycemic control