E3 ubiquitin ligase Bre1-induced H2B monoubiquitination is epigenetically important for recruiting replication factor Mcm10 and cohesion establishment factors Ctf4, Ctf18 and Eco1 to early replication origins to establish sister chromatid cohesion.
CRISPR/Cas9 genome-wide screens using sterol-sensitive endogenous HMG-CoA reductase (HMGCR) reporter identify the sterol-responsive RNF145 and gp78 as independently responsible for sterol-accelerated degradation of HMGCR, the rate-limiting enzyme of cholesterol biosynthesis.
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.
A cell-free system combined with cell-based assays elucidate the biochemical mechanism of signal transduction mediated by the mitochondrial protein MAVS and delineates the role of ubiquitin E3 ligases in antiviral innate immune responses.
The endoplasmic reticulum E3 ubiquitin ligase Doa10 and the mitochondrial AAA-ATPase Msp1 govern targeting fidelity of outer mitochondrial tail-anchored proteins by controlling cytoplasmic concentration and extracting mistargeted and orphan species.