Molecular characterization of a β-thalassemia intermedia patient presenting inferior vena cava thrombosis: interaction of the β-globin erythroid Krüppel-like factor binding site mutation with Hb E and α(+)-thalassemia.
Molecular analysis of globin gene expression in different thalassaemia disorders: individual variation of β(E) pre-mRNA splicing determine disease severity.
Markedly, however, no significant differences were observed between suppression of hepcidin as mediated by media from the culture of erythroblasts from normal controls and beta0-thalassemia/Hb E patients Discussion: Previous studies investigating the suppression of hepcidin expression in beta0-thalassemia/Hb E disease have used patient-derived serum samples, which are complex fluids with contributions from multiple cell types.