Reoxygenation of anoxic cardiac tissue promotes massive endocytosis that is triggered by release of coenzymeA from mitochondria, followed by palmitoylation of membrane proteins, sarcolemma vesiculation, and transfer of sarolemma vesicles to large endosomes and vacuoles.

Mitochondria can trigger massive endocytosis by releasing coenzyme A into the cytoplasm and thereby promoting the addition of fatty acids to surface membrane proteins.

The protein-lipid modification palmitoylation targets the kinase LIMK1 to dendritic spines to ensure precise control of the size of individual spines in response to synaptic activation.

There are at least two separate pathways for AMPA receptor recycling, which are regulated by synaptic activity.

Lamellipodin, an important regulator of cytoskeletal and assembly cell migration, enhances the activity of Ena/VASP family actin polymerases by clustering them on leading-edge membranes and tethering them to actin filaments.

The C. elegans ninein homolog NOCA-1 is important for the assembly of non-centrosomal microtubule arrays required for embryo production, nuclear positioning and larval development.

The ciliary G-protein Arl13B – which is often mutated in Joubert syndrome – is the Guanine nucleotide exchange factor for the G-protein Arl3 and exclusively localizes to cilia.

Palmitate turnover is controlled by distinct enzyme families with different specificities.

Molecular engineering can generate light-sensitive NMDA receptors with specific subunit combinations.