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. 2006 Oct 9;26(24):9338–9351. doi: 10.1128/MCB.01032-06

FIG. 6.

FIG. 6.

Absence of Irs-1 increases tumor cell survival. (A) Aliquots of tumor extracts from PyV-MT and PyV-MT::Irs1−/− transgenic mammary tumors containing equivalent amounts of total protein were immunoblotted with antibodies specific for phosphoserine-209 of eIF4E (eIF4E S209), total eIF4E, phosphothreonine-308 of Akt (Akt T308), phosphoserine-473 of Akt (Akt S473), total Akt, phosphoserine-9 of GSK-3β (GSK3β S9), total GSK-3β, or β-actin. For densitometry, n = 12 for each genotype except for GSK-3β (n = 11). The relative levels of phosphorylation are shown in the graphs to the right of each immunoblot pair. (B and C) Terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling analysis of PyV-MT and PyV-MT::Irs1−/− transgenic mammary tumors. (B) Representative images from PyV-MT and PyV-MT::Irs1−/− mammary tumors stained with Apoptag reagent are shown (magnification, ×400). (C) The percentages of ApopTag-positive nuclei in the tumor sections were determined using the following formula: number of ApopTag-positive nuclei/total nuclei (P < 0.01). n = 20 fields (4 random fields from 5 tumors) for each group (PyV-MT or PyV-MT::Irs1−/− mice). WT, PyV-MT mice; Irs1−/−, PyV-MT::Irs1−/− mice.