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Upon AMPK activation by acute glucose restriction, Atg14p shifts its distribution from ER exit sites to liquid-ordered membrane domains on the vacuolar surface where, together with Atg6p, it facilitates LD-specific autophagy (i.e., microautophagy of lipid droplets) for energy production and long-term survival of starved cells.

The remarkable lifelong stability of mechanotransducing stereocilia of the inner ear hair cells depends on the activity of the transduction ion channels located at the tips of these mechanosensory projections.

The first inhibitor identified against an iso-enzyme that initiates O-glycosylation in the Golgi complex promises new therapeutic approaches for cancer and chronic kidney disease.

A few SNARE complexes suffice to fuse membranes, but many more are needed to dilate the nascent fusion pore by molecular crowding for efficient neurotransmitter or hormone release during exocytosis.

Both cooperative and competitive associations of actin binding proteins with actin filaments help drive the self-organization of functionally diverse F-actin networks in fission yeast.

One minute biotinylation with APEX2 peroxidase in living cells identifies established and new components of mitochondrial and ER membranes; dataset intersection and overexpression screen identifies SYNJ2BP overexpression as inducing mitochondria-rough ER contacts.

Palmitoylation recruits the phosphatase SCP1 to endothelial cell membranes where it negatively regulates Akt kinase activity, resulting in suppressed angiogenesis and decreased tumorigenesis.

Two seemingly distinct cellular stress response pathways that contribute to neurodegeneration after axonal insults are now revealed to be under the control of a single master regulator of the neuronal injury response, the kinase DLK.

The ATP7A interactome is the first comprehensive view of putative Menkes disease neurodegeneration mechanisms.

Phosphorylation of ezrin involves an unusual mechanism requiring coincident binding to PIP2 and involvement of the non-catalytic domain to gain access to the phosphorylation site thereby restricting selective phosphorylation to the plasma membrane.