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Fig. 1 Constitutive NF-κB activation in the lentivirus-induced GBM mouse model. Constitutive NF-κB activation in the lentivirus-induced GBM mouse model.

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Presentation on theme: "Fig. 1 Constitutive NF-κB activation in the lentivirus-induced GBM mouse model. Constitutive NF-κB activation in the lentivirus-induced GBM mouse model."— Presentation transcript:

1 Fig. 1 Constitutive NF-κB activation in the lentivirus-induced GBM mouse model.
Constitutive NF-κB activation in the lentivirus-induced GBM mouse model. (A) Heat map of the RNA-Seq analysis of NF-κB target genes (list of 150 genes; comparing normal brain tissue (NBT; n = 3), HRas-shp53–induced GBM tumors (n = 5), and 005 tumors (n = 3). (B) qRT-PCR analysis of six representative NF-κB target genes in NBT and tumor samples. (C) Immunofluorescence staining of CD44 (red) and Nestin (white) in tumor sections shows MES subtype (left) and nuclear p65 (white) staining, and IL-6 (red) confirms NF-κB activation in these tumors (right). Arrows point to p65 staining in the nucleus of cells. N, normal tissue; T, tumor; PLAU, plasminogen activator, urokinase; SERPINE1, serpin peptidase inhibitor, clade E (nexin, plasminogen activator inhibitor type 1), member 1; CCL2, chemokine (C-C motif) ligand 2; DAPI, 4′,6-diamidino-2-phenylindole. Dinorah Friedmann-Morvinski et al. Sci Adv 2016;2:e Copyright © 2016, The Authors

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