Figure 7. Proposed model for the regulation of CAR by the ubiquitin-proteasome system.

An equilibrium between a stable CAR cytoplasmic complex (at top left) and a weaker associated complex exists (at top right), and HSP70 functions to favor the stable cytoplasmic complex. Activator treatment signals for ubiquitination of CCRP, resulting in its degradation by the proteasome. This results in the release of CAR from the cytosolic complex, followed by translocation into the nucleus.