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Mammalian cellular iron homeostasis and the maturation of the cytosolic iron sulfur cluster proteins are dependent on the mitochondrial protein import machinery.

Pulse electron paramagnetic resonance on intact Escherichia coli reveals a substrate-induced structural transition in BtuB, the vitamin B₁₂ transporter, which is not seen in reconstituted membranes and indicates a mechanism of transport.

In vivo studies reveal that mitochondrial Complex I deficiencies induce iron misregulation and liver iron overload that may contribute to neurodegeneration in mitochondrial disease mice, and that iron restriction is effective in reducing disease progression.

The heme and HRI-mediated eIF2aP–ATF4 integrated stress response in erythropoiesis has a major global impact, especially under the stress condition of iron deficiency.

An ECF-type transporter serves as broad-spectrum heme iron scavenger and allows an opportunistic pathogen to use multiple eukaryotic hemoproteins to overcome nutritional iron-limitation.

Recent reports on the ability of biological molecules to sense magnetic fields are found to be inconsistent with basic physical principles.

Six-transmembrane epithelial antigen of the prostate isoform 1 (STEAP1) can establish a physiologically relevant electron transfer chain and STEAP2 can transfer electrons via a diffusible FAD mechanism.

Nuclear receptor NHR-14 regulates the subcellular localization of the zinc transcription factor PQM-1 to coordinate innate immunity with iron sequestration during pathogen infection in C. elegans..

Crystallography and single particle cryo-EM reveal hexameric and pentameric structures of the ExbBD energizer in the Ton system and oligomeric transition, which provides a unique working mechanism and a new vision of dynamic membrane biology.

In Drosophila, the loss of Frataxin causes iron accumulation in the nervous system, which in turn enhances sphingolipid synthesis and activation of PDK1 and Mef2, which leads to neurodegeneration.