Cyclin D1 protein stability is regulated by ubiquitin-proteasome mechanism mediated by multiple E3 ligases, including newly identified Keap1, DDB2, and WSB2.

Human cullin-RING ligases are buffered to a much greater extent than had been previously appreciated, and the roles of ubiquitin chain extension enzymes are far more nuanced at physiological concentrations.

Using IGF2BP1-PLK1 axis as an example, targeting oncogenic signaling represents a direction treatment for HCC patients with high FBXO45 expression.

SPOP-dependent degradation of interferon regulatory factor 1 curtails cell-intrinsic innate immunity, thereby contributing to immune resolution.

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.

MARCH5 mediates a pathway driving MCL1 degradation in response to cellular stress, which sensitizes to BH3 mimetic drugs targeting BCLXL and provides a broadly effective therapeutic strategy for solid tumors.

Aberrant neddylation of non-cullin substrates disrupts normal cell cycle progression.

Expression of plant immune genes is controlled by the opposing actions of ubiquitin ligases and deubiquitinases that modify the master coactivator NPR1, thereby regulating its intrinsic transcriptional activity.

By joining the Skp1-Cul1-Rbx1 SCF complex, Fbxo21 interacts with ASK1 and mediates Lys29-linkage of ASK1, leading to type I IFN production.

Simultaneous phosphorylation of multiple substrate motifs drives switch-like target recognition and monoubiquitylation by an E3 ligase during metazoan development.