Mutants and molecular dockings reveal that the primary L-thyroxine binding site in human serum albumin is not the one which can cause familial dysalbuminemic hyperthyroxinemia

Computer modeling; Genetic variants; High-affinity binding site; Human serum albumin; L-thyroxine; Site-directed mutagenesis; Binding Sites; Serum Albumin; Thyroxine; Hyperthyroxinemia, Familial Dysalbuminemic; Molecular Docking Simulation; Molecular Dynamics Simulation; Mutation; Biophysics; Biochemistry; Molecular Biology