ArticleInternational journal of hematology2006
Molecular mechanism of high hemoglobin F production in Southeast Asian-type hereditary persistence of fetal hemoglobin.
Article in International journal of hematology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Molecular basis of non-deletional HPFH in Thailand and identification of two novel mutations at the binding sites of CCAAT and GATA-1 transcription factors.Scientific reports · 2023Article
- Editing the core region in HPFH deletions alters fetal and adult globin expression for treatment of β-hemoglobinopathies.Molecular therapy. Nucleic acids · 2023Article
- Molecular and hematological studies in a cohort of beta zero South East Asia deletion (β°-thal SEA) from Malaysian perspective.Frontiers in pediatrics · 2022Article
- Manipulation of Developmental Gamma-Globin Gene Expression: an Approach for Healing Hemoglobinopathies.Molecular and cellular biology · 2020Review
- Genetic research and clinical analysis of deletional ChineseAnnals of hematology · 2020Article
- β‑thalassemia caused by compound heterozygous mutations and cured by bone marrow transplantation: A case report.Molecular medicine reports · 2017Article
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5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hereditary persistence of fetal hemoglobin (HPFH) is associated with a high level of hemoglobin F (HbF) synthesis in adult heterozygotes. In this study, 2 of 6 unrelated HPFH Thai families were found to be Southeast Asian-type HPFH (SEA-HPFH) by analyses of the hematologic data and Southern blot hybridization with polymerase chain reaction-amplified DNA probes. DNA mapping with a probe for a delta-globin fragment showed a 27-kb deletion of DNA that included the beta-globin gene and the 3' deoxyribonuclease I hypersensitive site 1 (3'HS1) sequence downstream. Deletion of the insulator, 3'HS1, and the juxta-position of the HPFH-3 core enhancer downstream to the 3' breakpoint have been postulated to be the cause of high HbF production in these individuals. To test this hypothesis, we transfected K562 cells with 4 different bacterial artificial chromosome constructs containing the enhanced green fluorescent protein (EGFP) gene at the position of the Agamma-globin gene (pEBAC/148beta:EGFP). Flow cytometry was used to compare EGFP expression from the pEBAC/148beta:EGFP construct with the HPFH-3 core enhancer immediately 5' to the SEA-HPFH breakpoint (pEnH), from the pEBAC/148beta:EGFP construct with 8 kb of the breakpoint sequence and the HPFH-3 core enhancer (pSEA-HPFH), and from the construct with 3'HS1 followed by the pSEA-HPFH sequence (pSEA-HPFH_3pHS1). The results show that high HbF production in SEA-HPFH occurs from a deletion of the 3'HS1 sequence and the juxtaposition of the HPFH-3 enhancer downstream to the delta-globin gene.
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