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Repressive PER2:CRY1:CK1δ complexes assembling in the cytosol enter the nucleus, where PER2 hyperphosphorylation eventually disrupts the complex, causing PER2 to relocalize to the cytoplasm, allowing nuclear accumulation of CRY1.

A generic strategy for producing functional snake venom metalloproteinases opens the field to reproducible mechanistic studies and inhibitor discovery.

Cellular sensitivity to cell death stimuli depends on cell-size-dependent proteome changes - specifically, cell size can modulate ferroptosis susceptibility through changes in glutathione biosynthetic enzymes, ferritin, and cathepsin B concentrations.

Empirical substitution matrices from experimental measurements on 31,614 variants accurately predict cellular protein abundance changes using only amino-acid substitution and whether the site is buried or exposed.