Proteins can fold deeper inside ribosomes with an enlarged exit tunnel.

The human cytomegalovirus (HCMV) interactome systematically characterises high-confidence viral-viral and viral-host protein interactions in HCMV-infected cells, facilitating multiple novel insights into HCMV and herpesviral function.

ULK3 is a kinase in the abscission checkpoint that temporarily inactivates ESCRT-III proteins via phosphorylation, which is required to delay cytokinesis in response to defects in mitosis.

The first structures of Kaposi’s sarcoma-associated herpesvirus ORF68 and Epstein–Barr virus BFLF1, conserved and essential proteins required in herpesviruses, reveal new insights into viral genome packaging.

A combination of cryo-electron microscopy, structure prediction, and evolutionary analyses reveal several functional states of the dynamic protein translocation machinery at the mammalian endoplasmic reticulum.

The interaction of SecA with its substrate proteins is regulated by its evolutionarily conserved C-terminal tail, which autoinhibits SecA unless SecA binds to the ribosome.

A set of ER-localized membrane proteins whose loss causes developmental diseases in humans, assemble with Sec61 into a translocon that facilitates the biogenesis of hundreds of different multi-pass membrane proteins.

CRISPR genome editing technology can efficiently introduce mutations into lytic and latent HSV genomes to block lytic replication and reactivation of latent herpes simplex virus genome though differential mechanisms.

Interactions were visualized between the nuclear egress complex from herpes simplex virus and a capsid protein that could promote nucleocytoplasmic translocation of the capsid in infected cells.

CDKG1 is a D-cyclin dependent retinoblastoma related protein kinase whose abundance scales with cell size and controls cell division cycle number during multiple fission.