Fig 1: FGFR1c kinase (FGFR1K) and phosphorylation sites.(A) FGFR1c consists of three domains: extracellular receptor domain (D1, D2, D3), transmembrane domain (TM) and kinase domain (N lobe and C lobe). The kinase domain posesses seven tyrosine autophosphorylation sites, including Y653 and Y654 in the active loop (A-loop). The kinase domain (residues 458-765; FGFR1K) were constructed and recombined expressed for functional studies. (B) Surface representation of inactive (left, PDB ID: 3KY2) and active (right, PDB ID: 3GQI) conformations of the FGFR1 kinase domain. The A-loop is shown as a cartoon representation in green, and Y653 and Y654, which are unphosphorylated and phosphorylated in the respective inactive and active forms, are highlighted as yellow sticks.
Fig 2: Treatment with an fibroblast growth factor receptor 1 (FGFR1) inhibitor blocked the effects of palmatine (PAL) in IR HepG2 cells. (A) glucose uptake by IR HepG2 cells after FGFR1 inhibitor treatment. (B) the relative mRNA level of glucose transporter type 1 (GLUT-1) in IR HepG2 cells treated with the FGFR1 inhibitor. (C) quantitative analysis of the expression levels of p-FGFR1 and FGFR1 (p-FGFR1/total FGFR1), p-FRS2 and FRS2 (p-FRS2/total FRS2), p-AKT and AKT (p-AKT/total AKT), and p-AMPK and AMPK (p-AMPK/total AMPK) by western blot. Data are presented as means ± SD, n = 9. *p < 0.05, **p < 0.01, versus the model group; ## p < 0.01, versus the untreated group.
Fig 3: Autophosphorylation kinetics of FGFR1K in solution and on NTA(Ni)-nanodiscs.The relative phosphorylation levels of the total tyrosine phosphorylation (A), p-Y653 (B), and p-Y654 (C) of FGFR1K in solution (black lines) and on NTA(Ni)-nanodiscs (red lines) at indicated time points were calculated based on western blotting data (Fig. S6). The increment fold of phosphorylation at specific time point is defined by the intensity of the western blotting band relative to that of the starting point. Specific antibodies of phospho-tyrosine, FGFR1 p-Y653, and FGFR1 p-Y654 were used for western blotting analysis. n > 3; *p < 0.05, **p < 0.01, and ***p < 0.001.
Fig 4: EGFR/MET participated in regulation of phosphorylation of hetero-RTKs.A Western Blot was used to observe phosphorylation of RTKs in HCCLM3, MHCC97H and PLC/PRF/5 cell lines with Lenvatinib or Sorafenib added. B Western blot was used to determine the effect of down-regulation of EGFR/MET on hetero-RTKs, including: Phosphorylation of EGFR, MET, Her3, RON, IR/IGF-1R and RET in HCC cell lines with EGFR/MET inhibitor added. C Phosphorylation of EGFR, Her3, RON, IR/IGF-1R and RET in HCC cell lines with MET knock-down. D Phosphorylation of FGFR1, VEGFR2 and PDGFRβ with ligand stimulated in HCC cell lines with EGFR/MET inhibitor added. E Phosphorylation of FGFR1, VEGFR2 and PDGFRβ with ligand stimulated in HCC cell lines with MET knock-down. F Phosphorylation of RTKs in PLC/PRF/5 cell line with EGFR or MET knock-down.
Fig 5: The effect of JinQi Jiangtang tablet (JQJTT) on the fibroblast growth factor receptor 1 (FGFR1) pathway in mice with streptozotocin (STZ)-induced diabetes. (A) The fasting blood glucose level in each group. (B) The relative mRNA level of glucose transporter type 1 (GLUT-1) in the livers of mice in each group. (C) The protein expression levels of p-FGFR1 and FGFR1 (p-FGFR1/total FGFR1) and those of p-FRS2 and FRS2 (and p-FRS2/total FRS2) as quantified using western blot. Data are presented as means ± SD, n = 12. *p < 0.05, **p < 0.01, versus the model group.
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