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. Author manuscript; available in PMC: 2014 Dec 12.
Published in final edited form as: Nature. 2014 May 21;510(7504):283–287. doi: 10.1038/nature13320

Extended Data Figure 3. Smyd3 deletion inhibits pancreatic tumorigenesis.

Extended Data Figure 3

a, Analysis of pancreatic tumorigenesis at 6 months in Kras and Kras;Smyd3 mutant mice. Representative serial histology section (HE), IHC for pERK1/2 and the PanIN marker MUC5. b, Pancreatic cancer phenotypes in Kras;p53 and Kras;p53;Smyd3 mutant mice. Representative IHC for pERK1/2. Arrowheads indicate areas with intact acinar cells. c, Quantitation of intact normal acinar area (Amylase positive area) in Kras;p53 and Kras;p53;Smyd3 mutant mice. Data are represented as mean +/− SEM. ***: p-value<0.001 (two-tailed unpaired Student's t-test). d, Representative HE and pERK1/2 IHC images of lung sections from Kras and Kras;Smyd3 mutant mice 12, 16 and 20 weeks after Ad-Cre infection. pERK1/2 is a marker of Ras activity and advanced tumors. e, f IHC analysis of SMYD3 expression in the PDAC (e) and LAC (h) mouse models. Arrowheads indicate cytoplasmic localization of SMYD3. Scale bars, 50 μm. g, h, Immunoblot analysis with the indicated antibodies probing (g) pancreatic adenocarcinoma or (h) lung adenocarcinoma tumor lysates dissected from Kras and Kras;Smyd3 mutant mice. Active Ras corresponds to Ras protein in the GTP-bound state pulled down with the RAF Ras-Binding Domain (RBD) (see Methods). *Tubulin loading control as in Figure 1j and 2f, respectively.