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A chemical screen identifies DHODH inhibitors as robust activators of mitochondrial respirasome assembly. Lipidomics reveal that peroxisomal-derived ether phospholipids accumulate in mitochondria during nucleotide deprivation to drive proliferation.
Acyl protein thioesterase APT2 interacts with membranes via its charged β-tongue, becomes palmitoylated by ZDHHC3/7 and deforms the bilayer to extract substrate acyl chains. APT2 deacylation leads to its membrane release and degradation.
TfuA, YcaO and thiol donor protein, ThiS, collaborate in peptide backbone thioamidation of McrA and during the biosynthesis of certain ribosomally synthesized and post-translationally modified peptide (RiPP) natural products.
Fusion of a split form of the protein O-GlcNAcase with nanobodies enables the targeted removal of O-GlcNAc protein modifications, providing a tool for probing the functional roles of specific O-GlcNAc modifications in a cellular context.
Kinetic modulatory profiling identifies regulators of ferroptosis, including the FDA-approved drug bazedoxifene, which acts in an off-target manner as a radical trapping antioxidant while mTOR inhibitors increased resistance to ferroptosis.
An agarose hydrogel mimicking cytoskeleton stabilizes protein liquid droplets and enables precise quantification of protein percentage in phase-separated droplets and in the dispersed phases as well as intramolecular distances via NMR and EPR.
The mutanofactin family of lipopeptide natural products, produced by strains of cariogenic Streptococcus mutans, promotes biofilm formation via increased cell-surface hydrophobicity and binding to extracellular DNA.
High mobility and nuclear translocation of the PKA catalytic subunit, PKAcat, relays signals induced by endosomal cAMP generated through endocytosis and signaling from the G-protein-coupled receptor β2-adrenergic receptor.
Combined use of a DNA-barcoded nucleosome library and a humanized yeast library allows the identification of histone globular domain mutations that affect histone exchange and nucleosome sliding processes, as well as cancer-associated gene pathways.
Plants utilize naturally produced ROS in shoot apical stem cells as a developmental signal to trigger phase separation of TMF. The resulting transcriptional condensates repress expression of the floral identity gene to precisely time flowering.
High-performance engineered myosins robustly change speed or direction in response to an optical signal. In living cells, these motors localize to the tips of protrusions when illuminated and deliver molecular cargos.
Hydrogen peroxide and peroxiredoxin oxidation levels oscillate during the yeast metabolic cycle, while the absence of peroxiredoxins or the use of thiol oxidants and reductants disrupts metabolic cycling and its coupling with cell division.
A synthetic protein quality control system (ProQC) uses RNA hybridization to enhance translation of full-length proteins in coupled transcription–translation systems to optimize production of biosynthetic enzymes for metabolic engineering efforts.
An engineered Pichia pastoris strain enables the synthesis of tryptophan C-mannosylated proteins, and selected monoclonal antibodies provide tools for detecting these modified proteins and studying their functions.
Ca2+-independent phospholipase A2β cleaves an oxidized form of phosphatidylethanolamine (PE) involved in ferroptosis such that increases in PE sensitize cells to ferroptosis. A mutant allele of the enzyme links neurodegeneration and ferroptosis.
A computational design strategy guided by biophysical principles enables engineering of split protein systems to tune their degree of interfacial destabilization, and thus reconstitution propensity, while preserving stability and catalytic activity.
Dissection of the allosteric coupling in the cyclin-dependent kinase Cdk2 shows that this allostery explains how the kinase is activated by cyclin binding and phosphorylation and how it differentiates between Cdk2 and Cdk4 inhibitors.
A systems-based approach to profile glucocorticoid (GC) receptor ligands in a broad range of assays representing different phenotypic responses linked these to transcriptional profiles and led to separation of GC therapeutic effects from side effects.