ArticleScientific reports2025
MAZ regulates fetal hemoglobin repression by activating MYB transcription.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
β-hemoglobinopathies, such as sickle cell disease and β-thalassemia, are common genetic disorders remaining significant global health challenges due to their associated morbidity and mortality. Increasing fetal hemoglobin (HbF) levels has emerged as a promising therapeutic strategy for these disorders. In this study, we report Myc-associated zinc finger (MAZ) as an indirect repressor of γ-globin (HBG) expression in human erythroid cells. Depletion of MAZ in HUDEP-2 and patient-derived β-thalassemia cells leads to significant inductions of both HBG mRNA and protein levels, resulting in increased HbF percentages and HbF + erythroid cells. We demonstrate that MAZ occupies at the promoter of MYB, a well-known HBG repressor. MAZ depletion reduced MYB levels. Restoration of MYB re-silenced the HBG levels in MAZ depleted cells. Our findings uncover the MAZ-MYB axis in HBG regulation, highlighting MAZ as a potential target to enhance HbF levels in patients with hemoglobin disorders.
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