ArticleCell reports2016
Bcl11a Deficiency Leads to Hematopoietic Stem Cell Defects with an Aging-like Phenotype.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
What it found
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The trial behind it
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Who cites it
75 citing papers in PubMed, 117 citations in OpenAlex.
- Systemic delivery of phagocytosis-shielded retroviral vectors enables in vivo HSC gene therapy for sickle cell disease.Cell stem cell · 2026Article
- Molecular and phenotypic blueprint of human hematopoiesis links proliferation stress to stem cell aging.The Journal of experimental medicine · 2026Article
- Cross-tissue molecular responses in the liver and blood after toxicant exposures.Research square · 2025Article
- Leukemia mutated proteins PHF6 and PHIP form a chromatin complex that represses acute myeloid leukemia stemness.Genes & development · 2025Article
- Association Between KLF1, BCL11A and HBS1L-MYB Polymorphisms and Phenotypes With β-Thalassemia Patients in Hainan.Molecular genetics & genomic medicine · 2025Article
- The hidden risks of CRISPR/Cas: structural variations and genome integrity.Nature communications · 2025Review
- The transcription factor Bcl11a is essential for B-1a cell maintenance during aging.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- BCL11A-deficient human erythropoiesis is impaired in vitro and after xenotransplantation into mice.Blood advances · 2025Article
- Large-scale discovery of potent, compact and erythroid specific enhancers for gene therapy vectors.Nature communications · 2025Article
- Commonalities and differences in gene expression patterns in major depressive disorder and chronic spontaneous urticaria: implications for comorbidity.Frontiers in genetics · 2025Article
- A multiomic atlas identifies a treatment-resistant, bone marrow progenitor-like cell population in T cell acute lymphoblastic leukemia.Nature cancer · 2025Article
- Redirecting E3 ubiquitin ligases for targeted protein degradation with heterologous recognition domains.The Journal of biological chemistry · 2025Article
- Review
- A mutant BCL11B-N440K protein interferes with BCL11A function during T lymphocyte and neuronal development.Nature immunology · 2024Article
- Exploring the contribution of Zfp521/ZNF521 on primary hematopoietic stem/progenitor cells and leukemia progression.Cell and tissue research · 2024Review
- The glucocorticoid receptor elicited proliferative response in human erythropoiesis is BCL11A-dependent.Stem cells (Dayton, Ohio) · 2024Article
- Machine Learning-Directed Conversion of Glioblastoma Cells to Dendritic Cell-Like Antigen-Presenting Cells as Cancer Immunotherapy.Cancer immunology research · 2024Article
- Repression of developmental transcription factor networks triggers aging-associated gene expression in human glial progenitor cells.Nature communications · 2024Article
- Base editing of key residues in the BCL11A-XL-specific zinc finger domains derepresses fetal globin expression.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Transcriptional Repressor BCL11A in Erythroid Cells.Advances in experimental medicine and biology · 2024Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
B cell CLL/lymphoma 11A (BCL11A) is a transcription factor and regulator of hemoglobin switching that has emerged as a promising therapeutic target for sickle cell disease and thalassemia. In the hematopoietic system, BCL11A is required for B lymphopoiesis, yet its role in other hematopoietic cells, especially hematopoietic stem cells (HSCs) remains elusive. The extensive expression of BCL11A in hematopoiesis implicates context-dependent roles, highlighting the importance of fully characterizing its function as part of ongoing efforts for stem cell therapy and regenerative medicine. Here, we demonstrate that BCL11A is indispensable for normal HSC function. Bcl11a deficiency results in HSC defects, typically observed in the aging hematopoietic system. We find that downregulation of cyclin-dependent kinase 6 (Cdk6), and the ensuing cell-cycle delay, correlate with HSC dysfunction. Our studies define a mechanism for BCL11A in regulation of HSC function and have important implications for the design of therapeutic approaches to targeting BCL11A.
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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.