[7] Subsequently, βTrCP was shown to regulate multiple cellular processes by mediating the degradation of various targets.

In response to genotoxic stress, it contributes to turn off CDK1 activity by mediating the degradation of CDC25A in collaboration with Chk1,[9][14] thereby preventing cell cycle progression before the completion of DNA repair.

[19][20][21] At the same time, βTrCP mediates the degradation of the pro-apoptotic protein BimEL to promote cell survival.

[22] βTrCP also associates with phosphorylated IkappaBalpha and beta-catenin destruction motifs, probably functioning in multiple transcriptional programs by regulating the NF-kappaB and the WNT pathways.

Elevated levels of βTrCP expression have been found in colorectal,[36] pancreatic,[37] hapatoblastoma,[38] and breast cancers.