HIC-5: A Mobile Molecular Scaffold Regulating the Anchorage Dependence of Cell Growth
Figure 2
A mobile HIC-5/PINCH scaffold regulating cyclin D1 subcellular localization in response to adhesion status. Cyclin D1 is retained in the nucleus in adherent cells such as mouse primary fibroblasts, C3H10T1/2 fibroblasts, and mammary epithelial NMuMG cells by the CRM1-dependent nuclear export of HIC-5 with the aid of PINCH, which counteracts the nuclear export of cyclin D1. The higher affinity of HIC-5 for CRM1 favours the export of HIC-5. In detached cells, the nuclear export of HIC-5 is inhibited by elevated levels of ROS, and cyclin D1 is actively transported out of the nucleus, which results in a decrease in its nuclear localization (see further details in [24]).
