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Fig. 5 | Acta Neuropathologica Communications

Fig. 5

From: DNA hypomethylator phenotype reprograms glutamatergic network in receptor tyrosine kinase gene-mutated glioblastoma

Fig. 5

mTORC2-driven global DNA hypomethylation reprograms glutamatergic network in GBM. A Heatmap of the DNA methylation profile (Infinium HumanMethylation 850 K BeadChip) in U87-EGFRvIII cells with shScramble or shRictor. DMP, differential methylation probes; KD, knockdown; SD, standard deviation. B Differential DNA-methylated regions (DMRs) in U87-EGFRvIII cells with shScramble or shRictor, including CpG-islands. ExonBnd, exon boundaries; IGR, intergenic region; TSS, transcription start sites; UTR, untranslated region. C GO term analyses on David_RHyper10perGenes on mTORC2 inhibition.”Chemical synaptic transmission (GO:0007268)” suggest that mTORC2-dependent hypomethylator could regulate the expression of genes related to EAA metabolism. D mRNA expression of glutamate transporters (SLC1A1, SLC1A3, SLC1A6) in Rictor knockdown U87-EGFRvIII GBM cells. E Measurement of EAA (glutamate and aspartate) indicated that Rictor knockdown reduced intracellular glutamate (Glu) and aspartate (Asp) in U87-EGFRvIII GBM cells. Conc, concentration

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Acta Neuropathologica Communications

ISSN: 2051-5960

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