Autophagic cargo receptors recruit the E3-like enzyme for Atg8 lipid conjugation to the cargo and thereby promote local formation of Atg8-positive autophagosomal membranes.

Group II introns can target mRNA, causing inhibition of gene expression, as a potential driver for evolution to the spliceosome.

Three complementary computational approaches reveal a set of putative causes of initiation of pan-USA waves of influenza.

Analyses using His6-HA-SUMO1 and SUMO1 KO mice indicate that SUMO1 modification of synaptic proteins is either absent or cannot be detected in brain and cultured neurons.

Structural studies reveal the mechanism by which a HECT E3 ubiquitin ligase carries out E2-to-E3-to-substrate ubiquitin transfer and prioritizes target lysines for ubiquitination.

Human cullin-RING ligases are buffered to a much greater extent than had been previously appreciated, and the roles of ubiquitin chain extension enzymes are far more nuanced at physiological concentrations.

An in vivo disulfide crosslinking assay shows preferential disassembly of nucleosomes with two H2A.Z histones by transcription machinery in yeast and conjugation to one or two ubiquitin moieties in human cells.

Legionella effector RavZ evades host autophagy by extracting LC3-PE from the membrane before deconjugation.

An ensemble of the ubiquitin-activating enzyme UBA6 and ubiquitin-conjugating enzyme/ubiquitin-ligase BIRC6 mediates ubiquitination of LC3, targeting the latter for proteasomal degradation and thus attenuating autophagic degradation of cellular substrates.

Expression of a Dravet syndrome-associated mutation in inhibitory neurons disrupts activity of brainstem respiratory neurons and diminishes respiratory behavior in conjunction with seizures and premature death.