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. Author manuscript; available in PMC: 2014 Aug 1.
Published in final edited form as: Cancer Res. 2013 May 30;73(15):4770–4780. doi: 10.1158/0008-5472.CAN-13-0384

Figure 6. Ablation of FABP5 diminishes ErbB2-induced proliferative signaling and attenuates the transcriptional activity of PPAR □In vivo.

Figure 6

a)-c) Upper panels: immumoblots demonstrating phosphorylation status of ERK (a), phosphorylation status of AKT (b), and expression level of CNX26 (c) in tumors of three individual M5+/+, M5+/−, and M5−/− mice. Lower panels: quantitation of immunoblots. Data are mean±S.D. p values for differences between denoted groups and respective M mice were calculated by a two-tail Student's t-test. d) Levels of mRNA for the direct PPAR~target gene VEGFa in tumors of three individual M5+/+, M5+/−, and M5−/− mice. Mean±S.D. p values vs. M5+/+ tumors are shown. e) Left: immunoblots of PDPK1, encoded by the direct PPAR~target gene pdpk1, and PTEN, whose expression is suppressed by PPARβ/δ, in tumors of three individual M5+/+, M5+/−, and M5−/− mice. Right: quantitation of immunoblots. Mean±S.D. *p vs. respective M mice, and **p vs. M5+/− mice are shown.