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Fig. 4 | Acta Neuropathologica Communications

Fig. 4

From: Novel targetable FGFR2 and FGFR3 alterations in glioblastoma associate with aggressive phenotype and distinct gene expression programs

Fig. 4

Signaling pathway activation and feedback inhibition. a WB with indicated antibodies of total protein lysates (50 µg protein) from LMS4, DIS6, and normal white matter control (NWM) fresh frozen autopsy samples. Molecular weight markers are indicated. For FGFR2, an autopsy HG glioma control with FGFR2 overexpression run on the same blot is shown for comparison. The blots performed for phosphorylation detection yielding negative results are not shown but the result is indicated with (P-) in red, following the corresponding protein. b Heatmap of semiquantitative WB, as shown quantified and normalized in Additional file 1: Fig. S8. White, green and blue shades indicate lack of expression, similar expression to control, and decreased expression, respectively. Incremental red or blue shades indicate incrementally increased or decreased expression, respectively. The maximum of a protein expression increase is shown as red or orange based on comparison with other glioblastoma samples. c Structural alterations induced by SERPINE1/PAI-1 R210H mutation. Surface 3D representations of active PAI-1 with wild-type R210 residue in green and mutant H210 residue in orange. The reactive center loop (RCL) of PAI-1, which is the binding site of uPA, is shown in magenta. Note significant surface change induced by the side chain of H210 mutant in the vicinity of RCL. Protein Data Base of the crystal structure accession number: 3r4I. d, e Fold-expression heatmaps of the ECM remodeling fibrin cluster and MAPK/PI3K inhibitor genes. CNs for RTK inhibitor genes were identical in all F48 tumors, except for SPRY4 and DUSP5 that showed normal 2-copy complement in DIS6 and loss of one copy in the HG F2↑ and F2T2↑ tumors

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