The
cullin family of
ubiquitin ligases can potentially assemble hundreds of RING-type E3 complexes (CRLs) by utilizing different substrate receptors that share common interaction domains.
Cullin receptors dictate substrate specificity, and
cullin-mediated substrate degradation controls a wide range of cellular processes, including proliferation, differentiation, and apoptosis. Dysregulation of
cullin activity has been shown to contribute to
oncogenesis through the accumulation of
oncoproteins or the excessive degradation of
tumor suppressors. In this review, we will discuss
cullin complexes and their substrates, the regulatory pathways that affect
cullin activity, and the mechanisms by which
cullins may facilitate or inhibit
carcinogenesis.