Dataset Information


Expression data from BCL11A-null and wild-type bone marrow erythroid pregenitors

ABSTRACT: BCL11A is a critical mediator of hemoglobin switching and gamma-globin silencing. In this study, we showed the BCL11A is required in vivo for developmental silencing of gamma-globin genes in adult animals. We used microarray to determine the changes in gene expression profile after loss of BCL11A in adult erythroid cells CD71+Ter119+ erythroid progenitor cells were FACS-sorted from bone marrows of 6-week old control (Bcl11a +/+) and BCL11A knockout (Bcl11a fl/fl EpoR-Cre+) mice.

ORGANISM(S): Mus musculus  

SUBMITTER: Jian Xu   Stuart H Orkin 

PROVIDER: E-GEOD-28333 | ArrayExpress | 2012-03-22



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Correction of sickle cell disease in adult mice by interference with fetal hemoglobin silencing.

Xu Jian J   Peng Cong C   Sankaran Vijay G VG   Shao Zhen Z   Esrick Erica B EB   Chong Bryan G BG   Ippolito Gregory C GC   Fujiwara Yuko Y   Ebert Benjamin L BL   Tucker Philip W PW   Orkin Stuart H SH  

Science (New York, N.Y.) 20111013 6058

Persistence of human fetal hemoglobin (HbF, α(2)γ(2)) in adults lessens the severity of sickle cell disease (SCD) and the β-thalassemias. Here, we show that the repressor BCL11A is required in vivo for silencing of γ-globin expression in adult animals, yet dispensable for red cell production. BCL11A serves as a barrier to HbF reactivation by known HbF inducing agents. In a proof-of-principle test of BCL11A as a potential therapeutic target, we demonstrate that inactivation of BCL11A in SCD trans  ...[more]

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