βTrCP has also emerged as an important player in protein translation, cell growth and survival. In response to mitogens, PDCD4, an inhibitor of the translation initiation factor eIF4A, is rapidly degraded in a βTrCP- and S6K1-dependent manner, allowing efficient protein translation and cell growth. βTrCP also cooperates with mTOR and CK1α to induce the degradation of DEPTOR (an mTOR inhibitor), thereby generating an auto-amplification loop to promote the full activation of mTOR. At the same time, βTrCP mediates the degradation of the pro-apoptotic protein BimEL to promote cell survival. 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. Interactions BTRC (gene) has been shown to interact with: FBXW11 DLG1 IκBα NFKB2 RELA SKP1A CDC34 CUL1 β-catenin WEE1 EMI1 Cdc25A Claspin REST PDCD4 DEPTOR Clinical Significance βTrCP behaves as an oncoprotein in some tissues. Elevated levels of βTrCP expression have been found in colorectal, pancreatic, hapatoblastoma, and breast cancers. References Further reading