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- W205586457 endingPage "356" @default.
- W205586457 startingPage "323" @default.
- W205586457 abstract "The β thalassemias and related disorders are characterized by a quantitative reduction in the production of β-globin chains of HbA. More than 200 β thalassemia alleles have now been characterized (http://globin.cse.psu.edu) involving mutations affecting any of the steps in the transcription of the β-globin gene, posttranscriptional processing of its pre-mRNA, or the translation of its mRNA into protein. The vast majority of simple β thalassemias are caused by point mutations within the gene or its immediate flanking sequences, although small deletions involving the β gene may also occur. If β-chain production is totally abolished by the mutation it is referred to as β0 thalassemia, whereas reduced output of β-chains (of normal structure) produces β+ thalassemia, with the mildest forms sometimes referred to as β++ or “silent” β thalassemia. These common forms of β thalassemias are inherited as haploinsufficient mendelian recessives." @default.
- W205586457 created "2016-06-24" @default.
- W205586457 creator A5055644792 @default.
- W205586457 creator A5076081716 @default.
- W205586457 date "2009-08-17" @default.
- W205586457 modified "2023-10-13" @default.
- W205586457 title "The Molecular Basis of β Thalassemia, δβ Thalassemia, and Hereditary Persistence of Fetal Hemoglobin" @default.
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