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
Keywords: HSA; Human serum albumin; rHSA; Recombinant HSA; Alb; Albumin; Alb A; Normal (wild-type) albumin isolated from serum; proAlb; Proalbumin; Tr1-Tr4; L-thyroxine binding sites; Human serum albumin; L-thyroxine; High-affinity binding site; Genetic variants;