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. Author manuscript; available in PMC: 2008 May 30.
Published in final edited form as: Hepatology. 2008 Apr;47(4):1191–1199. doi: 10.1002/hep.22159

Fig. 2. Activation of Ras and JAK/STAT pathways in GNMT-mutant mice liver.

Fig. 2

(A) Representative Western blot analysis of Ras downstream effectors (pRAF, pMEK1/2, and pERK1/2). Phosphorylation of RAF, MEK1/2, and ERK1/2 was markedly increased in liver tumors from GNMT-knockout (GNMT-KO) mice as compared with wild-type (WT) animals. One representative data set is shown out of 4 experiments performed. (B) Ras activity, assessed by immunoprecipitation with anti-pan Ras antibody and probed with anti-RAF-1 antibody, was markedly increased in livers from 3-month-old GNMT mice and in liver tumors from 8-month-old GNMT-mutant mice. Four animals from each subgroup were analyzed (WT mice, open bars; GNMT-KO mice, filled bars). (C) Representative Western blot analysis of JAK/STAT downstream effectors (pJAK1/2, pSTAT1, pSTAT3, cyclin D1 and D2, and Bcl-xL). Phosphorylation of JAK1/2, STAT1, and STAT 3 and protein levels of the JAK/STAT target genes, including the proliferation proteins cyclin D1 and cyclin D2 and the antiapoptotic protein Bcl-xL, were markedly increased in liver tumors from GNMT-KO mice. One representative data set is shown of 4 experiments performed. Unless otherwise indicated, animals were all 8 months old.