Iron is a crucial transition metal for virtually all life. Two major destinations of iron within
mammalian cells are the cytosolic iron-storage protein, ferritin, and mitochondria. In …

Mitochondria play a key role in iron metabolism in that they synthesize heme, assemble iron–
sulfur (Fe/S) proteins, and participate in cellular iron regulation. Here, we review the latter …

Iron/sulfur centers are key cofactors of proteins intervening in multiple conserved cellular
processes, such as gene expression, DNA repair, RNA modification, central metabolism and …

Fe–S clusters are partners in the origin of life that predate cells, acetyl-CoA metabolism,
DNA, and the RNA world. The double helix solved the mystery of DNA replication by base …

Building iron-sulfur (Fe-S) clusters and assembling Fe-S proteins are essential actions for
life on Earth. The three processes that sustain life, photosynthesis, nitrogen fixation, and …

In eukaryotes, sulfur is mobilized for incorporation into multiple biosynthetic pathways by a
cysteine desulfurase complex that consists of a catalytic subunit (NFS1), LYR protein …

Reduced levels of the protein frataxin cause the neurodegenerative disease Friedreich's
ataxia. Pathology is associated with disruption of iron–sulfur cluster biosynthesis …

Maturation of iron–sulphur (Fe/S) proteins involves complex biosynthetic machinery. In vivo
synthesis of [2Fe–2S] clusters on the mitochondrial scaffold protein Isu1 requires the …

Friedreich's ataxia is a severe neurodegenerative disease caused by the decreased
expression of frataxin, a mitochondrial protein that stimulates iron–sulfur (Fe-S) cluster …

Iron–sulfur clusters are ubiquitous protein cofactors with critical cellular functions. The
mitochondrial Fe–S assembly complex, which consists of the cysteine desulfurase NFS1 …