ArticleScience advances2024
Folate depletion induces erythroid differentiation through perturbation of de novo purine synthesis.
Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- The FOLR2-IRF2BP2 axis mediates erythropoiesis impairment by excess folic acid in myelodysplastic neoplasms.Leukemia · 2026Article
- Dynamic control of nucleotide metabolism in physiology and disease.Nature cell biology · 2026Review
- Article
- Roles of RRM2 and RRM2B in pyrimidine stress responses and differentiation of acute myeloid leukemia cells.Cell death discovery · 2026Article
- The oncogenic control of nucleotide synthesis.Oncogenesis · 2026Review
- RAGER: A user-friendly computational platform for integrated analysis of RNA-Seq and ATAC-seq data.PloS one · 2026Article
- Influence of age and sex on platelet count: Implications for optimizing growth factor-rich plasma preparation.Journal of clinical and experimental dentistry · 2025Review
- Folic acid supplementation ameliorates alcohol-induced hepatic steatosis by inhibiting SREBP-1c-mediated lipogenesis.Frontiers in nutrition · 2025Article
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
Abstract
Folate, an essential vitamin, is a one-carbon acceptor and donor in key metabolic reactions. Erythroid cells harbor a unique sensitivity to folate deprivation, as revealed by the primary pathological manifestation of nutritional folate deprivation: megaloblastic anemia. To study this metabolic sensitivity, we applied mild folate depletion to human and mouse erythroid cell lines and primary murine erythroid progenitors. We show that folate depletion induces early blockade of purine synthesis and accumulation of the purine synthesis intermediate and signaling molecule, 5'-phosphoribosyl-5-aminoimidazole-4-carboxamide (AICAR), followed by enhanced heme metabolism, hemoglobin synthesis, and erythroid differentiation. This is phenocopied by inhibition of folate metabolism using the inhibitor SHIN1, and by AICAR supplementation. Mechanistically, the metabolically driven differentiation is independent of mechanistic target of rapamycin complex 1 (mTORC1) and adenosine 5'-monophosphate-activated protein kinase (AMPK) and is instead mediated by protein kinase C. Our findings suggest that folate deprivation-induced premature differentiation of erythroid progenitor cells is a molecular etiology to folate deficiency-induced anemia.
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Registered trials
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.