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The circRNA expression profiles of reticulocytes for β-thalssemia carriers with high fetal hemoglobin

ABSTRACT: The circRNA expression profiles of reticulocytes for β-thalssemia carriers with high fetal hemoglobin

PROVIDER: PRJNA806844 | ENA |

REPOSITORIES: ENA

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The circRNA expression profiles of reticulocytes for β-thalssemia carriers with high fetal hemoglobin

Project description:To explore the involvement of circRNAs in β-thalassemia and their actions on fetal hemoglobin (HbF), we surveyed circRNA expression profiles using circulating reticulocytes isolated from individuals with β-thalassaemia carriers with high HbF.

2022-05-27 | GSE196682 | GEO

microRNA expression profiles of reticulocytes for hereditary persistence of fetal hemoglobin and β-thalssemia minor with high fetal hemoglobin.

Project description:We used microarrays to investigate differential microRNA (miRNA) expression in reticulocytes comparing reticulocytes from control individuals with normal fetal hemoglobin (HbF) level to hereditary persistence of fetal hemoglobin (HPFH) and β-thalssemia minor with high HbF, and try to find out some miRNAs associated with the mechanisms of HbF induction.

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The long noncoding RNA expression profiles of reticulocytes for hereditary persistence of fetal hemoglobin and β-thalssemia minor with high fetal hemoglobin.

Project description:To explore long noncoding RNA (lncRNA) expression and the biological functions of lncRNAs in fetal hemoglobin (HbF) induction, we surveyed lncRNA and mRNA expression profiles using circulating reticulocytes isolated from individuals with hereditary persistence of fetal hemoglobin (HPFH) and β-thalassaemia minor with high HbF.

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Critical Vulnerabilities of the NuRD Complex for Fetal Hemoglobin Control

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EHMT1 and EHMT2 inhibition induce fetal hemoglobin expression [RNA-seq]

Project description:Using UNC0638 and genetic assays to inhibit EHMT1/2 and derepress fetal hemoglobin in adult hematopoietic cells.

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EHMT1 and EHMT2 inhibition induce fetal hemoglobin expression [RNA-seq]

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2015-11-02 | E-GEOD-71421 | biostudies-arrayexpress

EHMT1 and EHMT2 inhibition induce fetal hemoglobin expression [ChIP-seq]

Project description:Using UNC0638 and genetic assays to inhibit EHMT1/2 and derepress fetal hemoglobin in adult hematopoietic cells. ChIP-seq for 2 histone modifications and total H3 (for quantitative normalization) in biological triplicates of cord blood, adult bone marrow, and UNC0638-treated adult bone marrow.

2015-11-02 | E-GEOD-69516 | biostudies-arrayexpress

Genome-wide DNA methylation differences between ex vivo differentiated cells that recapitulate the fetal-to-adult hemoglobin switch

Project description:The aim of this study is to characterize de genome-wide DNA methylation changes that occur during the fetal-to-adult hemoglobin switch in erythroblasts. We differentiated CD34+ hematopoietic progenitor cells collected for either fetal liver or bone marrow into erythroblasts. After differentiation, cells produce respectively fetal hemoglobin and adult hemoglobin in majority. We compared genome-wide DNA methylation states of fetal-stage erythroblasts to those of adult-stage erythroblasts.

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Direct Promoter Repression by BCL11A Controls the Fetal to Adult Hemoglobin Switch

Project description:Fetal hemoglobin (HbF) level is genetically controlled and modifies severity of adult hemoglobin (HbA) disorders. Common genetic variation affects expression of BCL11A, a critical regulator of HbF silencing. Current models suggest that BCL11A acts at a distance from the gamma-globin genes via long-distance chromosomal interactions. Here we use a functional cellular assay and protein-binding microarray to establish a requirement for a zinc-finger cluster of BCL11A for globin repression, and identify a preferred DNA recognition sequence (TGACCA). The motif is present in embryonic and fetal-expressed globin promoters, and duplicated in gamma-globin promoters, yet only the distal motif is mutated in alleles of individuals with hereditary persistence of hemoglobin. Using CUT&RUN to map protein binding sites, we detected BCL11A occupancy preferentially at the distal motif, and validated its absence in HbF-expressing, promoter-edited erythroid cells. Taken together, our findings reveal that direct gamma-globin gene promoter repression by BCL11A underlies hemoglobin switching.

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