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. Author manuscript; available in PMC: 2014 Jan 8.
Published in final edited form as: Cell Metab. 2012 Dec 27;17(1):113–124. doi: 10.1016/j.cmet.2012.12.001

Figure 1. AMPKα1 cooperates with Myc to promote lymphomagenesis.

Figure 1

A) Kaplan-Meier curves showing latency to tumor development in Eμ-Myc transgenic mice deficient (α1−/−, red), heterozygous (α1+/−, blue) or wild-type (α1+/+, black) for AMPKα1. B) Kaplan-Meier curves showing latency to tumor development in chimeric mice reconstituted with Eμ-Myc/α+/+ (α1+/+, black) or Eμ-Myc/α1−/− (α1−/−, red) HSCs (n=5 per group). C) Representative histological sections of Eμ-Myc/α+/+ and Eμ-Myc/α1−/− lymphomas stained for the proliferation marker Ki-67. D) Competition assay of Eμ-Myc lymphoma cells expressing GFP and control (Ctrl) or AMPKα1-specific (α1) shRNAs. Data are expressed as the fold enrichment in GFP+ to GFP− cells after 6 days of growth. E) Viability of control (Ctrl) or AMPKα1 shRNA-expressing Eμ-Myc lymphomas cells after 24h treatment with 2-deoxyglucose (2-DG, 15 mM). F) Immunohistochemical analysis of representative Eμ-Myc/α+/+ and Eμ-Myc/α1−/− lymphomas stained with antibodies to detect TORC1 activity (total and phospho-ribosomal S6 (pS6, S240/244), or total and phospho-4EBP1 (p4EBP1, S37/46)). G) Immunoblot analysis of primary Eμ-Myc/α+/+ or Eμ-Myc/α1−/− lymphomas. Whole cell lysates prepared from sorted primary lymphoma cells were analyzed by immunoblot using the indicated antibodies. Each lane represents an independent tumor. Lysates from non-transformed B cells isolated from Eμ-Myc-negative mice are shown. **, p<0.01; ***, p<0.001.