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This study investigates the role of Aurora B Kinase (AURKB) phosphorylation on the erythroid transcription factor KLF1 during erythropoiesis. The findings reveal that mutation of a specific phosphorylation site on KLF1 results in increased fetal hemoglobin levels and delays in differentiation, suggesting a mechanism that could be targeted for therapies in beta hemoglobinopathies. Overall, the research highlights the regulatory relationship between AURKB and KLF1, with implications for understanding red bloo

Author

libupt

Language

EN