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. Author manuscript; available in PMC: 2010 Sep 16.
Published in final edited form as: Sci Signal. 2010 Jan 26;3(106):ra7. doi: 10.1126/scisignal.2000514

Fig. 6. Schematic model for RACK1 acting as a crucial regulatory adaptor within the IRE1α signaling platform in pancreatic β-cells.

Fig. 6

RACK1 is constitutively associated with PP2A under normal physiological conditions. It interacts with IRE1α in response to acute glucose stimulation, thereby directing PP2A to exert a feedback “brake” control on IRE1α phosphorylation as well as IRE1α-dependent upregulation of insulin biosynthesis. Conversely, ER stress or prolonged exposure to high glucose causes RACK1 to dissociate from PP2A, resulting in disruption of this tripartite regulatory module. In this scenario, the retained phosphorylation of RACK1-associated IRE1α may exert altered functional outputs during the cellular UPR.