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. 2021 Sep 10;6(1):209–222. doi: 10.1002/hep4.1724

FIG. 5.

FIG. 5

SLC45A2‐AMACR activates ERK kinase in vitro and in vivo. (A) GST‐SLC45A2‐AMACR (GST‐SLAM) enhanced the kinase activity of recombinant ERK2 on basic myelin protein. The kinase activity is calculated as percentage recombinant ERK2 kinase activity without any added GST recombinant protein component in a kinase assay. Standard deviations are indicated. (B) SLC45A2‐AMACR activates the kinase cascade of ERK in vivo. Overexpression of SLC45A2‐AMACR but not its mutant with a deletion of the ERK binding motif enhanced the activation of ERK1/2 kinase activity and its cascade signaling molecules MEK and mTOR in HUH7 cells (lanes 1‐4). Knockout of SLC45A2‐AMACR deactivates the ERK kinase cascade in H1299 and HuH7 cells (lanes 5‐8). (C) Rescue of H1299KO2 cells with SLC45A2‐AMACR‐FLAG reactivates ERK kinase cascades but not with the SLC45A2‐AMACR mutant that lacks the ERK binding motif or the mutant that lacks the SLC45A2 domain. (D) Diagram of SLC45A2‐AMACR signaling cascade; green line shows the SLC45A2 domain, red line shows the AMACR domain.