Genetic complexity in sickle cell disease
- 19 August 2008
- journal article
- editorial
- Published by Proceedings of the National Academy of Sciences in Proceedings of the National Academy of Sciences
- Vol. 105 (33) , 11595-11596
- https://doi.org/10.1073/pnas.0806633105
Abstract
No abstract availableThis publication has 21 references indexed in Scilit:
- DNA polymorphisms at the BCL11A , HBS1L-MYB , and β- globin loci associate with fetal hemoglobin levels and pain crises in sickle cell diseaseProceedings of the National Academy of Sciences, 2008
- Common and rare variants in multifactorial susceptibility to common diseasesNature Genetics, 2008
- Genome-wide association study shows BCL11A associated with persistent fetal hemoglobin and amelioration of the phenotype of β-thalassemiaProceedings of the National Academy of Sciences, 2008
- A QTL influencing F cell production maps to a gene encoding a zinc-finger protein on chromosome 2p15Nature Genetics, 2007
- Intergenic variants of HBS1L-MYB are responsible for a major quantitative trait locus on chromosome 6q23 influencing fetal hemoglobin levels in adultsProceedings of the National Academy of Sciences, 2007
- Fetal gene reactivationCurrent Opinion in Genetics & Development, 1998
- Pain in Sickle Cell DiseaseNew England Journal of Medicine, 1991
- The Interaction of Alpha-Thalassemia and Homozygous Sickle-Cell DiseaseNew England Journal of Medicine, 1982
- Fetal Hemoglobin Restriction to a Few Erythrocytes (F Cells) in Normal Human AdultsScience, 1975
- Sickle Cell Anemia, a Molecular DiseaseScience, 1949