Maximal γ-globin expression in the compound heterozygous state for -175 Gγ HPFH and β°39 nonsense thalassaemia: a case study
Author:
Publisher
Wiley
Subject
Hematology,General Medicine
Link
http://onlinelibrary.wiley.com/wol1/doi/10.1111/j.1600-0609.1997.tb01678.x/fullpdf
Reference27 articles.
1. The effects of HPFH mutations in the human γ-globin promoter on binding of ubiquitous and erythroid specific nuclear factors;Mantovani;Nucleic Acids Res,1988
2. Increased γ-globin expression in a nondeletion HPFH mediated by an erythroid-specific DNA-binding factor;Martin;Nature,1989
3. Altered binding to the γ-globin promoter of two erythroid specific nuclear proteins in different HPFH syndromes;Ottolenghi;Prog Clin Biol,1989
4. Increased erythroid-specific expression of a mutated HPFH γ-globin promoter requires the erythroid factor NFE-1;Nicolis;Nucleic Acids Res,1989
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1. Disorders of the synthesis of human fetal hemoglobin;IUBMB Life;2008
2. Differential Segregation of β+IVS‐I‐110 (G→A),Aγ − 117 (G→A), andGγ − 158 (C→T) Mutations in Members of an Albanian Family;Hemoglobin;2003-01
3. THALASSEMIA INTERMEDIA AND EXTRAMEDULLARY HEMATOPOIESIS ASSOCIATED WITH COMPOUND HETEROZYGOSITY FOR THE 532 BP DELETION OF THE β-GLOBIN GENE AND GENE DELETION HEREDITARY PERSISTENCE OF FETAL HEMOGLOBIN;Hemoglobin;2001-01
4. Fetal hemoglobin expression in the compound heterozygous state for ?117 (G?A)A? HPFH and IVSII-745 (C?G) ?+ thalassemia: A case study;American Journal of Hematology;1999-06
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