E3 ubiquitin-protein ligase (CHFR) that functions in the antephase checkpoint by actively delaying passage into mitosis in response to microtubule poisons. It acts in early prophase before chromosome condensation, when the centrosome move apart from each other along the periphery of the nucleus. CHFR is probably involved in signaling the presence of mitotic stress caused by microtubule poisons by mediating the 'Lys-48'-linked ubiquitination of target proteins, leading to their degradation by the proteasome. Marked reduction of CHFR expression was detected in primary tumors and decreased CHFR expression was linked to promoter hypermethylation. Restoration of CHFR expression by treatment with the microtubule stress agent nocodazole and the methyltransferase inhibitor 5-aza-2'-deoxycytidine has been reported.