RNAi profiling by array of human CD34-derived erythroid progenitors treated with BCL11A siRNAs

ABSTRACT: Differences in the amount of fetal hemoglobin (HbF) that persists into adulthood affect the severity of sickle cell disease and the beta-thalassemia syndromes. Genetic association studies have identified sequence variants in the gene BCL11A that influence HbF levels. Here we examine BCL11A as a potential regulator of HbF expression. The high HbF BCL11A genotype is associated with reduced BCL11A expression. Moreover, abundant expression of full-length forms of BCL11A is developmentally restricted to adult erythroid cells. Down-regulation of BCL11A expression in primary adult erythroid cells leads to robust HbF expression. Consistent with a direct role of BCL11A in globin gene regulation, we find that BCL11A occupies several discrete sites in the beta-globin gene cluster. BCL11A emerges as a

ORGANISM(S): Homo sapiens

SUBMITTER: Vijay Sankaran 

PROVIDER: E-GEOD-13284 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress