Structural studies reveal the mechanism by which a HECT E3 ubiquitin ligase carries out E2-to-E3-to-substrate ubiquitin transfer and prioritizes target lysines for ubiquitination.

Smurf1 and Smurf2 have essential functions in the mammalian Shh signaling pathway, binding to and ubiquitylating Patched1, leading to its endocytosis and subsequent degradation in lysosomes.

Notch ligands expressed in the same cell as the Notch receptor are crucial to prevent accidental, ligand-independent Notch activity.

TRIM23 plays a critical role in the switching from early to late adipogenic enhanceosomes by stabilizing the PPARγ protein.

Dual FAK/PYK2 kinase inhibition disrupts GSK3β phosphorylation and may present a new treatment for colorectal cancer in patients carrying APC mutations.

Proteasome-mediated degradation of the TATA-box binding protein (TBP) during terminal differentiation is regulated by the E3 ligase Huwe1 and the deubiquitinase USP10.

Yersinia pseudotuberculosis and enteropathogenic Escherichia coli promote pathogenicity by deamidating the ubiquitin-like protein NEDD8 to block ubiquitin-dependent trafficking of Perforin-2, which is an effector of innate immunity.

The ubiquitin ligase ROQUIN cross-talks with cellular metabolic signals to generate protective T cell-dependent antibody responses.

Building on previous work (Materne et al., 2015), it is shown that the ubiquitylation of histone H2B represses cell differentiation by opposing chromatin remodeling at the promoter of the master regulator of gametogenesis, ste11

PTRF (Cavin-1) mediates metabolism-regulated ribosomal transcription in mature adipocytes, independent of its role in caveolae formation.