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SARS-CoV-2 infection reduces the intracellular levels of a human tRNA modification enzyme and alters host tRNA modification profiles.

Signal-peptide cleavage of HIV-1 envelope glycoprotein is delayed because of alpha-helical structure covering the cleavage site, effecting early cleavage alters the folding pathway and resulting in localized misfolding and reduced viral fitness.

Cell cycle asynchrony regulates apical cell shape to drive cell division orientation in the apical plane.

The protease γ-secretase generates amyloid-beta peptides using a mechanism that is driven by the stabilization of an enzyme-substrate scisson complex.

Mutational analysis and biochemical experiments suggest that the conserved β-hairpin-like membrane-reentrant loop of RseP - an S2P family intramembrane cleaving protease - helps to discriminate substrates by directly interacting with their transmembrane segments.

Proteolytic activation of a sodium-permeable channel that aids in gas exchange and fluid homeostasis likely evolved at the water to land transition in vertebrates.

Endoproteolytic cleavage of the ribosomal precursor protein FUBI-eS30 is required for efficient maturation of small ribosomal subunits in the cytoplasm of human cells and involves the nucleolar deubiquitinase USP36.

An analysis of innate immunity reveals why dengue viruses do not reach high titers in primate laboratory models, even though they emerged through zoonotic transmission from primate reservoirs.

Whereas SARS-CoV-2 utilizes cathepsins to enter most cell lines, human airway organoids revealed that entry into relevant cells is dependent on serine proteases, which can be targeted for treatment.

Matrix metalloprotease (MMP)-14 cleaves Tie2 at three distinct sites within the fibronectin type-III (FN3) domain and its pharmacological blockade inhibits Tie2 pathological shedding to exert barrier protective effects.