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Cavin-3 is a tumor suppressor protein that inhibits Akt signaling, suppresses Warburg metabolism, promotes apoptosis, and protects against cachexia.

The spindle assembly protein Bub3 recruits the checkpoint kinase Bub1 to kinetochores by binding to phosphorylated MELT repeats in the kinetochore subunit Knl1.

Structural analyses of the centriole proteins CPAP and STIL identify domains that are critical for centriole formation and provide a structural explanation for a mutation that causes human microcephaly.

Cells repair damage to their outer membranes not by patching them as previously thought, but by using proteins called caveolins to remove the damaged regions by endocytosis.

The motor domains of dynein are sufficient to crosslink microtubules and slide them antiparallel to each other.

The proteins Bax and Bak, which increase the permeability of the mitochondrial membrane during apoptosis, are also crucial for generating a mitochondrial membrane pore that is specifically involved in necrosis.

A cell-free system combined with cell-based assays elucidate the biochemical mechanism of signal transduction mediated by the mitochondrial protein MAVS and delineates the role of ubiquitin E3 ligases in antiviral innate immune responses.

Long and short variants of a protein called UNC-13, assisted by another called Tomosyn, regulate the timing of synaptic vesicle release in C. elegans.