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• W2062735863 abstract "Abstract An estimated 6% to 7% of the earth's population carries a mutation affecting red blood cell function. The β-thalassemias and sickle cell disease are the most common monogenic disorders caused by these mutations. Increased levels of γ-globin ameliorate the severity of these diseases because fetal hemoglobin (HbF; α2γ2) can effectively replace adult hemoglobin (HbA; α2β2) and counteract polymerization of sickle hemoglobin (HbS; α2βS2). 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 γ-globin gene expression. Knockdown of FOP in adult erythroid progenitors strongly induces HbF. Importantly, γ-globin expression can be elevated in cells from β-thalassemic patients by reducing FOP levels. These observations identify FOP as a novel therapeutic target in β-hemoglobinopathies." @default.
• W2062735863 created "2016-06-24" @default.
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• W2062735863 date "2010-11-18" @default.
• W2062735863 modified "2023-10-13" @default.
• W2062735863 title "Fetal globin expression is regulated by Friend of Prmt1" @default.
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• W2062735863 doi "https://doi.org/10.1182/blood-2010-03-274399" @default.
• W2062735863 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2993632" @default.
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