A molecular model of the assembled COPI coat, determined by cryo-electron tomography of an in vitro reconstituted budding reaction, reveals details of interactions mediating coat assembly and shows the binding site of ArfGAP2.

Cryo-EM structures reveal the structural dynamics of ArfA*RF2-mediated rescue of stalled ribosomes.

PRUNE2/PCA3 axis dysregulation is an early, rather than late, event in prostate cancer tumorigenesis.

Pathogenic activating mutations in PIK3CA or NRAS were the most common genetic findings in a lymphatic malformation patient cohort and an N-of-1 trial of the PI3Kα inhibitor alpelisib in a patient with a PIK3CA mutation confirmed these findings are actionable.

Cryo-electron tomography of COPI vesicles in the Golgi reveals coat structure, disassembly dynamics, cargo binding, and morphological variability.

A peptide motif targeting tumor-infiltrating macrophage in triple-negative breast cancer delays tumor growth and favors an antitumor immune response.

The ability of COPI to bind polyubiquitin is a key determinant for SNARE incorporation into intracellular vesicles and for maintenance of a functional Golgi complex.

Erythroid-enriched BMP2K kinase, in addition to its predicted function in endocytosis, regulates distribution and abundance of COPII assemblies and autophagic degradation through opposing actions of its two splicing variants.

A mechanistic mathematical model informed by standard‐of‐care imaging and pathology predicts tumor responses to immunotherapy a priori on a per-patient basis.

Advances in imaging techniques have shed new light on the structure of vesicles formed by COPI protein complexes.