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. Author manuscript; available in PMC: 2015 Aug 14.
Published in final edited form as: Dig Liver Dis. 2014 Sep 29;47(1):62–67. doi: 10.1016/j.dld.2014.09.002

Fig. 5.

Fig. 5

Working model. As shown in the upper panel, in the absence of ligand, PPAR recruits NM23-H2 as a corepressor to inhibit proliferation and carcinogenesis. As shown in the lower panel, corepressors are released in the presence of ligand. In the absence of NM23-H2, PPAR transcriptional activity is enhanced. Increased PPAR transcriptional activity activates the PI3K/AKT signalling pathway to promote cholangiocarcinogenesis. PPAR, peroxisome proliferator-activated receptor; NM23-H2, nucleoside diphosphate kinase alpha; PI3K, phosphoinositide 3-kinase; Akt, protein kinase B.