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Fig. 11

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ZDB-IMAGE-210902-113
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Figures for Jia et al., 2021
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Fig. 11

Graphical abstract for FGF-2-dependent regulation of sVEGFR1 splice variants in endothelial cells and its contribution to angiogenesis and lung tumorigenesis. In endothelial cells, FGF-2 stimulates a SRPK1/SRSF1/SRSF3 signaling pathway that controls VEGFR1 splicing in favor of sVEGFR1 splice variants, in particular sVEGFR1-ex12 (variant 4), that contribute to FGF-2 pro-angiogenic functions. In squamous lung carcinoma patients (LUSC), elevated sVEGFR1-ex12 usage value correlates with FGF-2/FGFR1 mRNA levels and with poor prognosis, thereby supporting a role of the FGF-2/FGFR1/sVEGFR1-ex12 signaling network in both physiological and pathological angiogenesis

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