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The spider venom peptide Pn3a recognizes a pharmacophore unique to Ca_V3.3 amongst T-type calcium channels, underscoring its potential as a novel molecular tool for the study of Ca_V3.3-mediated currents in native cells.

Sequence-variant analogs of mitochondria-targeted tetrapeptides have distinct patterns of membrane-bound conformations, effects on membrane properties, and abilities to protect mitochondria subject to stress, illuminating how side chain variation can be leveraged in the development of more effective therapeutic compounds.

Manganese drives the activation of the ‘target of rapamycin complex 1’ and uncouples sensing and response to nutrient availability.

By using mass spectrometry, we determined the global levels of various DNA modifications across species and tissues.

Inhibition of GOT2 drives growth inhibitory reductive stress that can be rescued by electron acceptors in vitro, whereas GOT2 inhibition in endogenous or transplanted tumor models is tolerated without consequence, highlighting the importance of context when studying tumor metabolism.

A combination of single-molecule and in vivo FRET showed how drugs affect conformation of mGluR2 at different domains.

Cryo-EM shows a 5’ DNA site on the RFC clamp loader, in addition to the 3’ site, and biochemical study shows the 5’ site facilitates PCNA loading onto gaps, consistent with genetics indicating the 5’ DNA site facilitates gap repair.

Biochemical studies in combination with computational modeling and molecular dynamics simulations reveal that the lipid bilayer promotes intramembrane proteolysis by stabilizing the enzyme-substrate complex and the protease active site.

Mg²⁺-dependent JAK1-mediated phosphorylation sensitizes TRPV2 activity and thermo-threshold, which is counterbalanced by PTPN1-mediated dephosphorylation, highlighting a role of phosphorylation homeostasis in setting the basal activity of TRPV2.

Distinct surfaces of an interbacterial competition cell wall toxin mediate interactions with different cellular binding partners, resulting in an inherent evolutionary trade-off across the toxin superfamily.