Ron R. Kopito

This study identifies UBE3C and NRF1-dependent proteasomal pathways that regulate acute protein aggregate turnover in response to misfolded protein accumulation.

This study identifies how BoHV-1 UL49.5 protein hijacks the C-degron pathway to promote TAP degradation via the CRL2 E3 ligase.

The paper identifies molecular machinery underlying CFTR-F508del ERAD and shows correctors stabilize RNF5-resistant folding states.

The paper shows that mutant huntingtin aggregates spread between neurons via phagocytic glia in Drosophila, requiring the Draper receptor and synaptic dysfunction.