Cereblon-based small-molecule degraders rely on the sequential action of ubiquitin-conjugating enzymes UBE2G1 and UBE2D3 to assemble K48-linked polyubiquitin chains on cereblon neomorphic substrates, resulting in their proteasomal degradation.
The presynaptic scaffolding protein Bassoon is involved in regulating neurotransmitter release by controlling synaptic vesicle pool size and vesicular protein turnover through increased ubiquitination and Parkin-dependent autophagy.
The glial developmental factor, Daam2, promotes glioma tumorigenesis by degrading the VHL tumor suppressor, illustrating how dysregulation of gliogenic factors can impact tumor suppressor activity and promote glioma tumorigenesis.
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.
Engineered E3 ubiquitin ligases are utilized to elucidate mechanisms underlying ubiquitin regulation of membrane proteins, and to achieve robust post-translational functional knockdown of ion channels.
Under normal nutritional conditions, G-protein coupled receptors can control autophagy by regulating the degradation of key autophagic regulator Atg14L through ZBTB16-mediated ubiquitination and proteasome degradation.