Fig. 1: Low κB-Ras expression in PDAC patient samples. | Nature Communications

Fig. 1: Low κB-Ras expression in PDAC patient samples.

From: κB-Ras and Ral GTPases regulate acinar to ductal metaplasia during pancreatic adenocarcinoma development and pancreatitis

Fig. 1

a Signalling scheme of Ras effector pathways and control of Ral activity through κB-Ras proteins. G12D mutation in Ras leads to GTP-locked and thus constitutively active Ras. Ras-GTP can trigger activity of the MAPK, the PI3K/Akt and the Ral pathway. κB-Ras:Ral-GAP complexes limit Ral GTPase activity through increasing the low intrinsic GTP hydrolysis rate of RalA and RalB, and thus promoting the GDP-bound OFF state. Raf Rapidly Acc fibrosarcoma kinase, Erk extracellular signal-regulated kinase, PI3K phosphatidylinositol-3-kinase, GAP GTPase-activating protein, GEF guanine nucleotide exchange factor. b Immunohistochemical staining of human PDAC samples showing weak (left) and strong (right) κB-Ras expression. Upper panel scale bar: 100 µm; lower panel scale bar: 40 µm. c Statistical analysis revealed a significant association between histological tumour grade and expression levels of κB-Ras (Fisher’s exact test, p = 0.0216). Numbers of patients are given on the graph (high grade n = 23 and low grade n = 33 patients).

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