IndraLab
Statements
reach
"The elevated ubiquitylation and decreased steady-state levels of CCND1 seen after USP22 depletion suggest that deubiquitylation of CCND1 by USP22 may protect it from proteasomal degradation.Levels of both USP22 and CCND1 are elevated in human cancer, raising the possibility that elevated USP22 might protect CCND1 from degradation."
reach
"Collectively these findings support a model in which elevated expression of USP22 contributes to the aggressive growth of cancer cells in part via its ability to deubiquitylate and stabilize the rate-limiting cyclin CCND1, thereby promoting the G1–S transition.The identification of the USP22-CCND1 enzyme–substrate relationship may explain the previously reported phosphorylation-independent ubiquitylation and degradation of CCND1 (50)."