ArticleThe Journal of biological chemistry
The methyltransferase PRMT1 regulates γ-globin translation.
Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Protein Arginine Methyltransferases in γ-Globin Regulation and Sickle Cell Disease: Emerging Connections to Oxidative Stress.Antioxidants (Basel, Switzerland) · 2026Review
- MAZ regulates fetal hemoglobin repression by activating MYB transcription.Scientific reports · 2025Article
- Comprehensive regulation of γ-globin expression by epigenetic modifications and protein post-translational modifications.Clinical epigenetics · 2025Review
- The Discovery of Selective Protein Arginine Methyltransferase 5 Inhibitors in the Management of β-Thalassemia through Computational Methods.Molecules (Basel, Switzerland) · 2024Article
- CRISPR/Cas-based gene editing in therapeutic strategies for beta-thalassemia.Human genetics · 2023Review
- PRMT1 methylation of WTAP promotes multiple myeloma tumorigenesis by activating oxidative phosphorylation via m6A modification of NDUFS6.Cell death & disease · 2023Article
- Design and Synthesis of Novel PRMT1 Inhibitors and Investigation of Their Effects on the Migration of Cancer Cell.Frontiers in chemistry · 2022Article
- PRMT1 Confers Resistance to Olaparib via Modulating MYC Signaling in Triple-Negative Breast Cancer.Journal of personalized medicine · 2021Article
- Inhibition of Arginine Methylation Impairs Platelet Function.ACS pharmacology & translational science · 2021Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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 several specific PRMTs may block γ-globin transcription, but also revealed PRMT1 as a unique family member that is able to suppress γ-globin synthesis specifically at the translational level. We further identified that a non-AUG uORF within the 5' untranslated region of γ-globin serves as a barrier for translation, which is bypassed upon PRMT1 deficiency. Finally, we found that this novel mechanism of γ-globin suppression could be pharmacologically targeted by the PRMT1 inhibitor, furamidine dihydrochloride. These data raise new questions regarding methyltransferase function and may offer a new therapeutic direction for β-hemoglobinopathies.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.