A link between hypoxia and fetal hemoglobin provides hope for sickle cell disease

Scientists at St. Jude Children’s Research Hospital have shown how a protein responsible for adapting to low oxygen conditions (hypoxia), causes increased expression of fetal hemoglobin (HbF) in adults. The finding has implications for treating sickle cell disease and beta-thalassemia, serious blood disorders that affect millions of individuals. The research was published today in Nature, with associated code published on GitHub.

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