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The MIDAS domain of Mdn1, an ATP-driven mechanoenzyme involved in ribosome biogenesis, forms catch bonds with two different ubiquitin-like domain-containing ribosomal assembly factors.

Biophysical experiments, pulse-chase assays, and molecular dynamics simulations reveal how the proteasome targeting signal Fat10 can modulate the structure of substrate proteins to potentially regulate their degradation by the proteasome.

Maintenance of ubiquitin homeostasis is essential for proper control of the size of postsynaptic density and the growth of specialized membrane structure.

Genetic and biochemical analyses show that Chlamydia protects secreted effectors necessary for its exit from infected cells, preventing them from undergoing ubiquitination and degradation.

The E3 ubiquitin ligase complex linear ubiquitin chain assembly complex (LUBAC) forms a branched chain on linear ubiquitin chains depending on the RING-in-between-RING-type E3 ligase heme-oxidized IRP2 ubiquitin ligase 1 (HOIL-1L).

The structure of human PINK1 explains structural regulation and clarity on the impact of loss of function disease-associated mutations, which may stimulate future drug discovery efforts for both familial and idiopathic Parkinson's disease.

The cooperative action of PAF15 deubiquitylation by USP7 and its dissociation from chromatin by ATAD5 regulates proper PAF15Ub2 signaling termination, which is important for replication and maintenance of DNA methylation.

A nuclear Non-stop identity complex (NIC) supervises enterocyte (EC) identity, preserves tissue homeostasis, and prevents premature aging by maintaining EC-specific gene expression, silencing non-relevant programs, and safeguarding large-scale nuclear organization.

METRIS is a method that reports a mechanical readout of protein-protein interactions and due to its unique properties, it will allow many protein-protein interactions to be quantitatively measured easily that are currently laborious to measure with conventional methods.

Stimulation of cells with a mitochondria-depolarizing mitogen reveals a requirement for UBQLN1 expression in maintaining protein synthesis levels during cell cycle entry.