Virginia Commonwealth University researchers studying hemoglobin genes, mutations of which play a role in genetic blood disorders like sickle cell anemia and beta-thalassemia, have shown in studies with mice that the KLF2 protein is crucial for making young red blood cells.
The findings may point researchers to future gene therapies for patients with sickle cell anemia and beta-thalassemia.
In the October issue of Blood, the journal of the American Association for Hematology, researchers demonstrated that a protein called KLF2 regulates the production of embryonic globin genes and the maturation and stability of embryonic red blood cells in a mouse model. Researchers observed that KLF2 is responsible for controlling and “turning on” the embryonic globin gene.
Sathya Achia-Abraham | EurekAlert!
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