ArticlePloS one2013
MicroRNA-486-3p regulates γ-globin expression in human erythroid cells by directly modulating BCL11A.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 119 citations in OpenAlex.
- Recent Advances in Thalassemia Research: A Comprehensive Assessment From Diagnostic Technologies to Clinical Treatment.Journal of clinical laboratory analysis · 2026Review
- miRNA-Mediated Regulation of γ-Globin to β-Globin Switching: Therapeutic Potential in β-Hemoglobinopathies.International journal of molecular sciences · 2026Review
- Comprehensive Review of Genetic and Epigenetic Regulation of Fetal Hemoglobin in β-Hemoglobinopathies: From Molecular Mechanisms to Clinical Applications.Mediterranean journal of hematology and infectious diseases · 2026Review
- The Molecular Pathology of Non-Malignant Haematological Disease.British journal of biomedical science · 2026Review
- Comprehensive regulation of γ-globin expression by epigenetic modifications and protein post-translational modifications.Clinical epigenetics · 2025Review
- Dysregulated Expression of miR-222 and miR-15a in Transfusion-Dependent Thalassemia: Associations with Torque Teno Virus and Cytomegalovirus Infections.International journal of hematology-oncology and stem cell research · 2025Article
- Upregulation of miR-17-3p is associated with HbF in patients with β-thalassemia and induces γ-globin expression by targeting BCL11A.Orphanet journal of rare diseases · 2025Article
- Decoding HbF reactivation by hydroxyurea in hemoglobinopathy patients through microRNA signatures.Annals of hematology · 2025Article
- Systematic identification and validation of ceRNA-driven regulatory mechanisms in pediatric β-Thalassemia major.Annals of hematology · 2025Article
- Research Progress of Bioactive Peptides in Improving Type II Diabetes.Foods (Basel, Switzerland) · 2025Review
- Article
- Pharmacogenomics of Drugs Used in β-Thalassemia and Sickle-Cell Disease: From Basic Research to Clinical Applications.International journal of molecular sciences · 2024Review
- The role of CEMIP in cancers and its transcriptional and post-transcriptional regulation.PeerJ · 2024Review
- Transcriptional Repressor BCL11A in Erythroid Cells.Advances in experimental medicine and biology · 2024Review
- miR-365-3p mediates BCL11A and SOX6 erythroid-specific coregulation: A new player in HbF activation.Molecular therapy. Nucleic acids · 2023Article
- COVID-19 Vaccination in Pregnancy: Pilot Study for Maternal and Neonatal MicroRNA Profiles.Vaccines · 2023Article
- Transcriptional repression of lncRNA and miRNA subsets mediated by LRF during erythropoiesis.Journal of molecular medicine (Berlin, Germany) · 2023Article
- BCL11A Expression in Non-Small Cell Lung Cancers.International journal of molecular sciences · 2023Article
- Mutual Regulation of ncRNAs and Chromatin Remodeling Complexes in Normal and Pathological Conditions.International journal of molecular sciences · 2023Review
- BCL11A Expression in Breast Cancer.Current issues in molecular biology · 2023Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) play key roles in modulating a variety of cellular processes through repression of mRNAs target. The functional relevance of microRNAs has been proven in normal and malignant hematopoiesis. While analyzing miRNAs expression profile in unilineage serum-free liquid suspension unilineage cultures of peripheral blood CD34(+) hematopoietic progenitor cells (HPCs) through the erythroid, megakaryocytic, granulocytic and monocytic pathways, we identified miR-486-3p as mainly expressed within the erythroid lineage. We showed that miR-486-3p regulates BCL11A expression by binding to the extra-long isoform of BCL11A 3'UTR. Overexpression of miR-486-3p in erythroid cells resulted in reduced BCL11A protein levels, associated to increased expression of γ-globin gene, whereas inhibition of physiological miR-486-3p levels increased BCL11A and, consequently, reduced γ-globin expression. Thus, miR-486-3p regulating BCL11A expression might contributes to fetal hemoglobin (HbF) modulation and arise the question as to what extent this miRNA might contribute to different HbF levels observed among β-thalassemia patients. Erythroid cells, differentiated from PB CD34(+) cells of a small cohort of patients affected by major or intermedia β-thalassemia, showed miR-486-3p levels significantly higher than those observed in normal counterpart. Importantly, in these patients, miR-486-3p expression correlates with increased HbF synthesis. Thus, our data indicate that miR-486-3p might contribute to different HbF levels observed among thalassemic patients and, possibly, to the clinical severity of the disease.
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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.