Figure 6

PSTi8 competes with PST on GRP78 receptor binding. Molecular docking (a) PST (yellow) is docked in the active site of human GRP78 (blue): the residues of PST in red are showing hydrogen bond with the residues of human GRP78 (green). (b) The superimposed image of PSTi8 (purple) and PST in the active site of human GRP78. (c) PSTi8 is docked in the active site of human GRP78: the residues of PSTi8 in red are showing hydrogen bond with the residues of human GRP78. (d) Competitive binding between different concentrations of PST and Sulphorhodamine labelled PSTi8 (150 nM) in HepG2 cells. (e) Competitive binding between different concentrations of PSTi8 and Sulphorhodamine labelled PST (25 nM) in HepG2 cells. (f) GRP78 ATPase activity in presences of PST (1 µM) with different dose of PSTi8 (0, 1, 2.5, 5 µM). Western blot analysis (g) Effect of PSTi8 (800 nM) on PST (100 nM) inhibited tunicamycin (5 mg/ml) stimulated GRP78 expression in HepG2 cells. α, control vs tunicamycin; β, Tunicamycin vs Tunca. + PST; γ, Tunica. PST vs Tunica. +PST + PSTi8 and δ, control vs PSTi8. *P < 0.05; **P < 0.01; ***P < 0.001, NS, Non-significant. Error bar indicate mean ± s.e.m.