β-catenin gets jaded and von Hippel-Lindau is to blame

Numerous studies have pointed to interactions between the tumor suppressor von Hippel-Lindau (VHL) and the oncogenic Wnt–β-catenin signaling cascade; however, the mechanism of this crosstalk has remained elusive. Among other roles, VHL can promote the stabilization of Jade-1. Now, recent findings provide compelling evidence that Jade-1 ubiquitylates β-catenin, leading to its degradation. Thus, the loss of VHL, as seen in clear cell renal cell carcinoma, could lead to tumor formation through β-catenin de-repression.