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Multimodal spectroscopy (smFRET, EPR, SAXS, and SANS) and integrative structural modeling reveal large-scale domain rearrangements in human guanylate binding protein 1 (hGBP1) that are driving forces for the formation of oligomers that enable its biological function in innate immune defense.

Analysis of the tumor microenvironment reveals that pancreatic tumors experience metabolic stress caused by immune cell degradation of the amino acid arginine, and that pancreatic cancers cope by synthesizing arginine to provide access this amino acid despite low tumor availability.

A new role for Endonuclease G with respect to the generation of mtDNA deletions is identified, which is dependent on the formation of G4 DNA within human mitochondria.

Definition of the mitoribosome interactome revealed inner membrane proteins and elucidated new assembly factors of the cytochrome c reductase and cytochrome c oxidase.

5-Hydroxymethylcytosine-mediated active DNA demethylation occurs in postmitotic neurons, and is required for their terminal differentiation and function.

GTPBP7, NSUN4, and MTERF4 facilitate maturation of the peptidyl transferase center of the mitochondrial ribosome.

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.

A spectroscopic analysis of the sarco(endo)plasmic reticulum Ca²⁺-ATPase (SERCA)-phospholamban membrane complex reveals the importance of the relative transmembrane orientation for inhibition or activation of the ATPase.

A human experimental model for physiological glucocorticoid exposure and glucocorticoid withdrawal identifies a multi-omic cluster, including microRNA miR-122-5p and metabolites, associated with glucocorticoid-responsive genes.

During times of mitochondrial impairment, non-imported mitochondrial precursor proteins are targeted to the nucleus for proteasome-dependent degradation.