The methyltransferase PRMT1 regulates γ-globin translation.

ABSTRACT: Induction of fetal hemoglobin to overcome adult β-globin gene deficiency is an effective therapeutic strategy to ameliorate human β-hemoglobinopathies. Previous work has revealed that fetal γ-globin can be translationally induced via integrated stress signaling, but other studies have indicated that activating stress may eventually suppress γ-globin expression transcriptionally. The mechanism by which γ-globin expression is regulated at the translational level remains largely unknown, limiting our ability to determine whether activating stress is a realistic therapeutic option for these disorders. In this study, we performed a functional CRISPR screen targeting protein arginine methyltransferases (PRMTs) to look for changes in γ-globin expression in K562 cells. We not only discovered that

SUBMITTER: Wang Y 

PROVIDER: S-EPMC7966866 | biostudies-literature | 2021 Jan-Jun

REPOSITORIES: biostudies-literature