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. Author manuscript; available in PMC: 2017 Mar 1.
Published in final edited form as: Hepatology. 2015 Dec 11;63(3):731–744. doi: 10.1002/hep.28252

Figure 3. MLK3 mediates CXCL10 trafficking by a JNK dependent mechanism.

Figure 3

(A) Huh7 cells were co-transfected with green fluorescent protein (GFP)-tagged C-X-C ligand chemokine 10 (CXCL10) and red fluorescent protein (RFP)-tagged cluster of differentiation (CD) 63. Co-localization of both CXCL10 and CD63 on the cell surface and in the extracellular vesicles, in response to LPC treatment with or without one of the MLK3 inhibitors URMC099, and CLFB1134, was assessed respectively by total internal reflectance microscopy (TIRF) and confocal microscopy. (B) CXCL10 protein levels in whole Huh7 cell lysate, treated with either vehicle, or 20 μM lysophosphatidylcholine (LPC) with or without 40 μM of the C-JUN N-terminal kinase (JNK), inhibitor SP600125 (SP) and in extracellular vesicles (EVs) derived from Huh 7 cells under the conditions above were assessed by western blot. Tumor susceptibility gene 101 (TSG101) was employed as an EV marker, and actin as a loading control. (*Irrelevant bands omitted).