Back to Search
Start Over
Fetal globin expression is regulated by Friend of Prmt1
- Source :
- Blood, 116(20), 4349-4352. American Society of Hematology
- Publication Year :
- 2010
-
Abstract
- An estimated 6% to 7% of the earth's population carries a mutation affecting red blood cell function. The beta-thalassemias and sickle cell disease are the most common monogenic disorders caused by these mutations. Increased levels of gamma-globin ameliorate the severity of these diseases because fetal hemoglobin (HbF; alpha 2 gamma 2) can effectively re-place adult hemoglobin (HbA; alpha 2 beta 2) and counteract polymerization of sickle hemoglobin (HbS; alpha 2 beta(S)2). Therefore, understanding the molecular mechanism of globin switching is of biologic and clinical importance. Here, we show that the recently identified chromatin factor Friend of Prmt1 (FOP) is a critical modulator of gamma-globin gene expression. Knockdown of FOP in adult erythroid progenitors strongly induces HbF. Importantly, gamma-globin expression can be elevated in cells from beta-thalassemic patients by reducing FOP levels. These observations identify FOP as a novel therapeutic target in beta-hemoglobinopathies. (Blood. 2010;116(20):4349-4352)
- Subjects :
- medicine.medical_specialty
Immunology
Population
Biology
medicine.disease_cause
Biochemistry
Mice
Red Cells, Iron, and Erythropoiesis
Erythroid Cells
Internal medicine
hemic and lymphatic diseases
Fetal hemoglobin
medicine
Animals
Humans
Globin
education
Cells, Cultured
Fetal Hemoglobin
education.field_of_study
Gene knockdown
Mutation
Hematology
Gene Expression Regulation, Developmental
Nuclear Proteins
Cell Biology
Embryo, Mammalian
Red blood cell
medicine.anatomical_structure
Cancer research
Hemoglobin
Transcription Factors
Subjects
Details
- ISSN :
- 00064971
- Database :
- OpenAIRE
- Journal :
- Blood, 116(20), 4349-4352. American Society of Hematology
- Accession number :
- edsair.doi.dedup.....942336120db2ed25d3608e43c99a9942