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Beta thalassemia is a hereditary disease affecting hemoglobin. As with about half of all hereditary diseases, [ 19 ] an inherited mutation damages the assembly of the messenger-type RNA (mRNA) that is transcribed from a chromosome .
Hemoglobin A2 (HbA 2) is a normal variant of hemoglobin A that consists of two alpha and two delta chains (α 2 δ 2) and is found at low levels in normal human blood.Hemoglobin A2 may be increased in beta thalassemia or in people who are heterozygous for the beta thalassemia gene.
Alpha thalassemia is caused by deficient production of the alpha globin component of hemoglobin, while beta thalassemia is a deficiency in the beta globin component. [7] The severity of alpha and beta thalassemia depends on how many of the four genes for alpha globin or two genes for beta globin are faulty. [ 2 ]
Hemoglobin S/ beta thalassemia: common in African and Mediterranean populations, it is clinically similar to sickle-cell anemia. [35] Delta-beta thalassemia is a rare form of thalassemia in which there is a reduced production of both the delta and beta globins. It is generally asymptomatic. [36] There are two clinically significant combinations ...
Hemoglobin subunit beta (beta globin, β-globin, haemoglobin beta, hemoglobin beta) is a globin protein, coded for by the HBB gene, which along with alpha globin , makes up the most common form of haemoglobin in adult humans, hemoglobin A (HbA). [5] It is 147 amino acids long and has a molecular weight of 15,867 Da.
Beta-thalassemia (β-thalassemia) is an inherited mutation of the β-globulin gene which causes the reduced synthesis of the β-globin chain of hemoglobin. [14] The majority of the mutations are point mutations that affect translation, transcriptional control, and splicing of the hemoglobin β gene and gene product. [15]
While Hemoglobin D can be detected without a DNA test, one is needed to ascertain that a person who carries Hemoglobin D carries hemoglobin D-Punjab. [citation needed] There is no clinical disease detected, however children of affected individuals have increased risk of having Hemoglobin D Disease, Hemoglobin SD disease or Beta-thalassemia Disease.
Hemoglobin E/β-thalassemia is a severe disease, and it still has no universal cure. However, the mutation is amenable to genome editing at high efficiency in preclinical studies. [ 6 ] It affects more than a million people in the world. [ 7 ]
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