Molybdän – vom Grundstoffwechsel zur Neurobiologie und Blutdruckregulation

Four molybdenum(Mo)-dependent enzymes are known in humans, each harboring a pterin-based Mo cofactor (Moco), which is synthesized by a conserved biosynthetic pathway. A deficiency in Moco results in a lethal neurodegenerative disorder, for which a therapy has been developed. Moco biosynthesis and enzymes present the origin of various cellular functions ranging from synaptogenesis to nitric oxide synthesis. Understanding this complex interplay aims to translate into new diagnostics and therapies.