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. 2014 Jul 21;111(31):11455–11460. doi: 10.1073/pnas.1404267111

Fig. 3.

Fig. 3.

PRL inhibits immune induction of MAP3K-dependent pathways including PI3K/AKT/mTORC1 by accelerating degradation of trafasome. (A) PRL constrains mTORC1 members mTOR and 4E-BP1 in parallel with AKT. (B) MAP3K inhibitor 5(Z)-7-oxozeaenol, but not Ras inhibitor manumycin, mirrors PRL in disruption of p38 MAPK, AKT, and NF-κB p65/RelA phosphorylation. (C, Upper) Western blot demonstrates that prior PRL accelerates degradation of IRAK1 following IL-1β challenge in AML12 cells. (Lower) TRAF6 immunoprecipitation (IP) followed by immunoblot (IB) shows nondegrading ubiquitination by PRL alone, and accelerated degradation of IRAK1 and TRAF6 following IL-1β challenge.