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. 2014 Mar 18;9(3):e91921. doi: 10.1371/journal.pone.0091921

Figure 7. ABCB11 canalicular trafficking model based on experimental observations in sandwich-cultured mouse hepatocytes.

Figure 7

Taurocholate, cAMP and AICAR enhanced ABCB11 trafficking to the canalicular membrane of hepatocytes. Canalicular delivery of ABCB11 was greatly reduced in the LKB1-decficient cell. The accelerating effects of taurocholate and AICAR were prevented by the disruption of LKB1. In contrast, addition of cAMP augmented ABCB11 trafficking even in the LKB1-deficient cells. Activation of Epac by CTP-cAMP also led to enhanced canalicular trafficking, however, its effect was LKB1-dependent. Specific activation of PKA by 6-Bnz-cAMP results in increased canalicular trafficking of ABCB11 independently of LKB1. The accelerating effect of cAMP was blocked by specific inhibition of PKA in LKB1-deficient cells, suggesting a PKA-dependent regulatory pathway in control of ABCB11 trafficking. PP2C – Protein phosphatase 2C, the major phosphatase dephosphorylating phospho-AMPK.