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. Author manuscript; available in PMC: 2015 Jun 4.
Published in final edited form as: Oncogene. 2014 Feb 10;33(49):5626–5636. doi: 10.1038/onc.2013.506

Fig. 2. MAF is regulated by NF1 through a RAS/MAPK/AP-1 pathway.

Fig. 2

(A) RT-PCR analysis showing mRNA expression of S462TY MPNST cells treated with the MEK inhibitor PD0325901 or vehicle control for 24 hours, relative to β-actin, with corresponding protein levels below. (B) Luciferase reporter assays for AP-1 response after transfecting full length human NF1 (NF1), dominant negative H-Ras (RasN17), the NF1 gap-related domain (GRD), an N-terminal NF1 fragment (NF1 N-term), a C-terminal NF1 fragment (NF1 c-term), or active RasG12V (RasV12) into MPNST cells. (C) Luciferase reporter assay for MAF response to dominant negative aFOS transfected into MPNST cell lines. (D) Model showing that NF1 loss through Ras activation promotes ERK activation and AP-1, thereby suppressing MAF expression.