Axonal metabolic flux analysis demonstrates that expression of NMNAT1 blocks axonal degeneration in cultured mouse neurons not by altering NAD+ synthesis, but rather by inhibiting injury-induced, SARM1-dependent NAD+ consumption.

An in-depth metagenomic analysis of possibly the most abundant and widespread microbial lineage in the surface ocean teases apart evolutionary processes that maintain its genomic heterogeneity and biogeography.

Genetic and biochemical analyses reveal a virulence mechanism employed by V. dahliae that involves inhibition of the transcription factor activity of CBP60g and SARD1.

Genetic and biochemical analysis reveals that MAPK signaling promotes axon degeneration by modulating the turnover of axon-protective proteins.

A new study has identified the proteins that adapt COPII vesicles to the needs of starving cells.

A cell-free biochemical assay for protein lipidation identifies the ER–Golgi intermediate compartment as a key early station in the formation of an autophagosome.

Evidence that certain proteins can be transported between Golgi via structures that resemble COPI vesicles suggests that these vesicles could also be involved in the transport of proteins from the cis to the trans face of the Golgi.

COPII vesicles regulate the metabolism of cholesterol through the selective transport of secretory proteins.

Building on previous work (Nogueira et al., 2014), we describe a mechanism for the generation of a mega-carrier for the export of bulky procollagen from the endoplasmic reticulum.