Mi2β-mediated silencing of the fetal γ-globin gene in adult erythroid cells
Open accessAbstract
Key Points: Mi2β exerts a major part of its silencing effect on embryonic and fetal globin genes by positively regulating the BCL11A and KLF1 genes. Partial depletion of Mi2β induces increased γ-globin gene expression in primary human erythroid cells without impairing differentiation.
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Knockdown or KO of Mi-2β reactivates γ-globin genes in the β-YAC transgenic mice.
“Consistent with a role in HbF silencing, knockdown or KO of Mi-2 β reactivates γ -globin genes in the β -YAC transgenic mice (23, 24).”
From Corepressor-dependent silencing of fetal hemoglobin expression by BCL11A (2013) · cites this paper as [24]
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- Authors
- Amaya, M., Desai, M., Gnanapragasam, M. N., Wang, S. Z., Zu Zhu, S., Williams, D. C., & Ginder, G. D.
- Affiliations
- VCU Massey Comprehensive Cancer Center (US)
- Massey Cancer Center,
- Virginia Commonwealth University (US)
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2013-04-25
- Volume
- 121
- Issue
- 17
- Pages
- 3493-3501
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- PMC
- PMC3637018
- OpenAlex
- W2019982035
- Cited by
- 102
- References
- 9
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 13 · 2023: 6 · 2022: 6 · 2021: 9 · 2020: 9 · 2019: 5 · 2018: 4 · 2017: 12 · 2016: 12 · 2015: 6 · 2014: 5 · 2013: 3
- FWCI
- 4.26
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Blood (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (P30CA16059, P30CA016059)
- National Institute of General Medical Sciences (R01GM098264)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK029902, R01 DK 29902, F31DK094650)
- Topics
- Health Sciences › Medicine › Genetics › Hemoglobinopathies and Related Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hemoglobin structure and function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Kruppel-like factors research
- Keywords
- CHD4, fetal to adult hemoglobin switch, NuRD complex, KLF1, BCL11A, erythroid cells, CD34+ progenitors, sickle cell disease, beta-thalassemia, fetal hemoglobin induction, chromatin-modifying complexes
- MeSH terms
- Adult, Animals, Autoantigens, Carrier Proteins, Cell Differentiation, Cells, Cultured, Fetal Hemoglobin, Gene Expression Regulation, Hematopoietic Stem Cells, Humans, Mice, Transgenic, Nuclear Proteins, Repressor Proteins, Gene Silencing, RNA, Small Interfering, Erythroid Cells, Chromatin Immunoprecipitation, Mice, Kruppel-Like Transcription Factors, gamma-Globins, Mi-2 Nucleosome Remodeling and Deacetylase Complex
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