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Article

Transcriptional silencing of fetal hemoglobin by BCL11A

1 Aug 2010

Abstract excerpt

The beta-thalassemia syndromes are a major global health problem. Increased levels of fetal hemoglobin (HbF) ameliorate the clinical symptoms seen in this disease. By taking advantage of the natural variation in the level of HbF in various populations, we and others identified several common genetic variants in three major loci that regulate HbF levels. One of these variants resides in the gene BCL11A. We have...

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PMID: 20712774
DOI: 10.1111/j.1749-6632.2010.05574.x

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Transcriptional silencing of fetal hemoglobin by BCL11APMID 20712774Read ↗

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Human Fetal Hemoglobin Expression Is Regulated by the Developmental Stage-Specific Repressor BCL11ASemantic proximity Read ↗

Corepressor-dependent silencing of fetal hemoglobin expression by BCL11ASemantic proximity Read ↗

Genome-wide association study shows BCL11A associated with persistent fetal hemoglobin and amelioration of the phenotype of beta-thalassemia.Semantic proximity Read ↗

Pathogenic BCL11A variants provide insights into the mechanisms of human fetal hemoglobin silencing.Semantic proximity Read ↗

Molecular analysis of the erythroid phenotype of a patient with BCL11A haploinsufficiency.Semantic proximity Read ↗

Hemoglobin switching's surprise: the versatile transcription factor BCL11A is a master repressor of fetal hemoglobinSemantic proximity Read ↗

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Transcription factors LRF and BCL11A independently repress expression of fetal hemoglobinSemantic proximity Read ↗

The Fetal-to-Adult Hemoglobin Switch — Mechanism and TherapySemantic proximity Read ↗

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