ArticleMolecular and cellular biology2011
Human globin knock-in mice complete fetal-to-adult hemoglobin switching in postnatal development.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 18 citations in OpenAlex.
- LDB1 represses fetal hemoglobin expression by enhancing BCL11A transcription.Redox biology · 2026Article
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- Evaluating sheep hemoglobins with MD simulations as an animal model for sickle cell disease.Scientific reports · 2024Article
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- Neonatal mice resist Plasmodium yoelii infection until exposed to para-aminobenzoic acid containing diet after weaning.Scientific reports · 2021Article
- In Utero Gene Therapy (IUGT) Using GLOBE Lentiviral Vector Phenotypically Corrects the Heterozygous Humanised Mouse Model and Its Progress Can Be Monitored Using MRI Techniques.Scientific reports · 2019Article
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- Allogeneic bone marrow transplant in the absence of cytoreductive conditioning rescues mice with β-thalassemia major.Blood advances · 2017Article
- Non-invasive MRI biomarkers for the early assessment of iron overload in a humanized mouse model of β-thalassemia.Scientific reports · 2017Article
- Animal models of β-hemoglobinopathies: utility and limitations.Journal of blood medicine · 2016Review
- The expression of embryonic globin mRNA in a severely anemic mouse model induced by treatment with nitrogen-containing bisphosphonate.BMC hematology · 2016Article
- Exploiting genomics and natural genetic variation to decode macrophage enhancers.Trends in immunology · 2015Review
- PGC-1 coactivator activity is required for murine erythropoiesis.Molecular and cellular biology · 2014Article
- Mithramycin encapsulated in polymeric micelles by microfluidic technology as novel therapeutic protocol for beta-thalassemia.International journal of nanomedicine · 2012Article
- Neurodevelopmental consequences of sub-clinical carbon monoxide exposure in newborn mice.PloS one · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Elevated levels of fetal γ-globin can cure disorders caused by mutations in the adult β-globin gene. This clinical finding has motivated studies to improve our understanding of hemoglobin switching. Unlike humans, mice do not express a distinct fetal globin. Transgenic mice that contain the human β-globin locus complete their fetal-to-adult hemoglobin switch prior to birth, with human γ-globin predominantly restricted to primitive erythroid cells. We established humanized (100% human hemoglobin) knock-in mice that demonstrate a distinct fetal hemoglobin (HbF) stage, where γ-globin is the dominant globin chain produced during mid- to late gestation. Human γ- and β-globin gene competition is evident around the time of birth, and γ-globin chain production diminishes in postnatal life, with transient production of HbF reticulocytes. Following completion of the γ- to-β-globin switch, adult erythroid cells synthesize low levels of HbF. We conclude that the knock-in globin genes are expressed in a pattern strikingly similar to that in human development, most notably with postnatal resolution of the fetal-to-adult hemoglobin switch. Our findings are consistent with the importance of BCL11A in hemoglobin switching, since removal of intergenic binding sites for BCL11A results in human γ-globin expression in mouse definitive erythroid cells.
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Registered trials
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