Linkage Analysis of Nondeletion Hereditary Persistence of Fetal Hemoglobin
- 19 February 1982
- journal article
- research article
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 215 (4535) , 981-982
- https://doi.org/10.1126/science.6186021
Abstract
Nondeletion forms of hereditary persistence of fetal hemoglobin may result from regulatory disorders of globin gene expression. The defects in two such conditions were localized by demonstrating a tight genetic linkage between the disorders and polymorphic restriction endonuclease sites within the beta-like globin gene complex. In one instance, the defect probably occurred outside the region of DNA between the epsilon- and beta-globin genes.This publication has 14 references indexed in Scilit:
- Major rearrangement in the human β-globin gene clusterNature, 1981
- F-Cell Production in Sickle Cell Anemia: Regulation by Genes Linked to β-Hemoglobin LocusScience, 1981
- Heterogeneity in the molecular basis of hereditary persistence of fetal haemoglobinNature, 1980
- Molecular cloning and characterization of the human β-like globin gene clusterCell, 1980
- Polymorphism of DNA Sequence in the β-Globin Gene RegionNew England Journal of Medicine, 1980
- DNA sequence variants in the Gγ-, Aγ-, δ- and β-globin genes of manCell, 1979
- Characterisation of deletions which affect the expression of fetal globin genes in manNature, 1979
- Heterocellular Hereditary Persistence of Fetal Haemoglobin (Heterocellular HPFH) and its Interaction with β ThalassaemiaBritish Journal of Haematology, 1977
- Interaction of heterocellular hereditary persistence of foetal haemoglobin with β thalassaemia and sickle cell anaemiaNature, 1976
- A Form of Hereditary Persistence of Fetal Haemoglobin Characterized by Uneven Cellular Distribution of Haemoglobin F and the Production of Haemoglobins A and A2 in HomozygotesBritish Journal of Haematology, 1975