Structural and functional asymmetry of RING trimerization controls priming and extension events in TRIM5α autoubiquitylation

Abstract

TRIM5α is an E3 ligase that inhibits retroviral replication. Here, the authors delineate the biochemical mechanism that accelerates N terminal autoubiquitylation of TRIM5α upon its association with the retroviral capsid and, thus, enables recognition of an infection-associated molecular pattern.