The COPII coat protein, in association with p24 machinery molecules, actively excludes misfolded and resident proteins from endoplasmic reticulum-derived transport vesicles.
Secretion of the inflammatory cytokine TNF requires a protein called iTAP/FrmD8, which controls the cell surface stability of the TNF shedding machinery, iRhom2 and TACE/ADAM17.
The molecular microenvironment of coronaviral replicase complexes provides functional and spatial links between conserved cellular processes and viral RNA synthesis, and highlights potential targets for the development of novel antivirals.
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.
A fear conditioning-induced miRNA acts in a negative feedback loop that targets vesicle exocytosis and neurotransmitter receptor trafficking, and inhibits memory formation.
The retrograde vesicular trafficking GARP complex, which is mutated in a neurodegenerative disease, is important for sphingolipid homeostasis in yeast and mammalian cells.
Zebrafish mutants and human endothelial cell experiments reveal that GIPC family endocytic adaptors bind to the Semaphorin receptor PLEXIND1, a critical regulator of vascular development, to negatively modulate its signaling.
Lumen formation by single epithelial cells depends on FGF-signalling-dependent expression of a spectraplakin, which can be functionally replaced by Tau.
Regulation of cellular properties such as ligand secretion and migratory ability through changes in the cytoskeleton mediated by a Wnt5a–Ror2–Vangl2 axis is a major determinant of alveolar formation.
β-adrenergic receptors at the Golgi apparatus activate a local signaling pathway, not accessed by cell surface receptors, to drive cardiac hypertrophy and could represent a target for heart failure therapy.
