Fig 1: The predicted conformation docking of doxorubicin (DOX), Chloroquine (CQ), and tioconazole (TIC) in complex with ATG4B, PI3Ka isoform and, PI3K? isoform. The binding models obtained from the docking simulation analysis of TIC (A), CQ (B), DOX (C) selected drugs against ATG4B (PDB 2Z0D) (I), PI3Ka (p110alpha/p85) catalytic subunit (PDB 2RD0) (II) and PI3K? kinase (PDB 1E8X) (III). The ligands (drugs) are represented as an orange stick, and the active site residues in the expanded panels are represented in blue sticks while interacting residues are in lines and labeled with their three-letter code. Structures of all proteins are shown as cyan-colored ribbon surface model, and H-bonds and hydrophobic interactions are shown by a blue line and dashed-gray line, respectively.
Fig 2: The disparity of apoptotic, anti-apoptotic, autophagy markers. Bar diagrams showing apoptotic markers as caspase-3, caspase-8, P53 (A), Bcl2, KI-67 as proliferation markers (B), ATG4B (C) and ATG5 (D) as autophagic markers of MCF-7 cells (I) and MCF-7 Xenograft mice (II) treated with single or combinatorial treatments. The data are presented as mean ± SE of at least three independent experiments. # p < 0.05, ## p < 0.01, ### p < 0.001, #### p < 0.0001 compared with control (untreated group). + p < 0.05, ++ p < 0.01, +++ p < 0.001, ++++ p < 0.0001 compared with the DOX treated group.
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