Citation: 'complementary binding sites' in the IUPAC Compendium of Chemical Terminology, 3rd ed.; International Union of Pure and Applied Chemistry; 2006. Online version 3.0.1, 2019. 10.1351/goldbook.C01201 • License: The IUPAC Gold Book is licensed under Creative Commons Attribution-ShareAlike CC BY-SA 4.0 International for individual terms.
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Potential therapeutic targeting of BKCa channels in glioblastoma treatment
This review summarizes current insights into the role of BKCa and mitoBKCa channels in glioblastoma biology, their potential classification as oncochannels, and the emerging pharmacological strategies targeting these channels, emphasizing the translational challenges in developing BKCa‐directed therapies for glioblastoma treatment.
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AutoDockFR: Advances in Protein-Ligand Docking with Explicitly Specified Binding Site Flexibility
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Pharmacologic ascorbate (vitamin C) increases ROS, disrupts cellular metabolism, and induces DNA damage in CRPC cells. These effects sensitize tumors to PARP inhibition, producing synergistic growth suppression with olaparib in vitro and significantly delayed tumor progression in vivo. Pyruvate rescue confirms ROS‐dependent activity.
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