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Ferredoxins are universal electron donors. A study focusing on the two human mitochondrial ferredoxins reveals the existence of unique cellular functions and partners for each protein.
Studies of the microbiome–host interaction are uncovering the metabolic mutual crosstalk between host tissues and gut microbiota. Hepatic glutamine synthetase takes part in this interaction by metabolizing a bacterial substance and producing a molecule with interesting clinical potential.
Ferroptosis is a mechanism of cell death that has possible roles in numerous diseases. Two new studies have identified hydropersulfides as potent inhibitors of O2-dependent membrane damage and destruction, and as potential regulators of ferroptosis.
Mitochondrial ferredoxins FDX1 and FDX2 are assigned to specifically donate electrons to steroidogenesis, Fe–S protein biogenesis, heme a formation or lipoylation. The proteins’ functions can be swapped by mutually exchanging short peptide segments.
Glutamine synthetase is the only enzyme that synthesizes glutamine in mammals. In vivo metabolomics showed that glutamine synthetase utilizes methylamine to produce N5-methylglutamine, whose levels correlate with tumor burden in a β+catenin+mutant liver cancer model.
YcaO enzymes carry out diverse tailoring reactions of peptide-derived natural products, such as formation of rings and incorporation of sulfur, but YcaO enzymes also catalyze peptide proteolysis using adenosine 5′-triphosphosphate as a co-factor.
Metabolic rewiring of activated macrophages promotes glycolysis and contributes to bacterial killing. A new study shows that reactive nitrogen species, released during macrophage activation, induce a profound inhibitory signal that facilitates metabolic reprogramming by modification of lipoate.
A combined structural and biochemical analysis reveals that TRIM7 E3 ligase targets viral proteins for degradation by recognizing their C-terminal glutamine (C-Gln) via its PRY-SPRY domain, providing mechanistic insight into the C-degron pathway.
Base editor technology combined with a fluorescent reporter of DNA methyltransferase activity enable in situ mutational scanning of DNMT3A, revealing a requirement of DNA binding by the PWWP histone reader domain for full activity.
By designing a fluorescent protein with a well characterized non-native ensemble, which captures the structural modulation of a substrate by the Hsp70/DnaJ/NEF system, Tiwari et al. resolved the individual steps of the disaggregation unfolding mechanism of Hsp70.
Reactive nitrogen species can cause profound inhibition of α-ketoacid dehydrogenase complexes via covalent S-modifications of the E2 subunit’s catalytic lipoic arm. The enzymes’ substrate, CoA, can mediate targeted delivery of such modifications.
Tan et al. reveal that a class of lipids, 3-sulfogalactosyl diacylglycerols, decrease in the central nervous system with aging. 3-sulfogalactosyl diacylglycerols are present in the human brain and suppress inflammation suggesting these lipids may play a role in age-related diseases and inflammation.
