ArticleeLife2021
The mitochondrial iron transporter ABCB7 is required for B cell development, proliferation, and class switch recombination in mice.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- Ferroptosis: Newly Emerged Regulator for Human Disease.MedComm · 2026Review
- Review
- Cryo-EM structures of human ABCB7 reveal the molecular basis of mitochondrial matrix heme export.Communications biology · 2026Article
- Targeting ferroptosis: a novel pathway in oral, oropharyngeal, hypopharyngeal, and laryngeal cancers.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Multifaceted roles of mitochondria in asthma.Cell biology and toxicology · 2024Review
- ATP-Binding Cassette Transporter of Clinical Significance: Sideroblastic Anemia.Journal of personalized medicine · 2024Review
- Ferroptosis in cancer: From molecular mechanisms to therapeutic strategies.Signal transduction and targeted therapy · 2024Review
- HCells · 2024Article
- Structural bioinformatics studies of six human ABC transporters and their AlphaFold2-predicted water-soluble QTY variants.QRB discovery · 2024Article
- Mechanistic elucidation of ferroptosis and ferritinophagy: implications for advancing our understanding of arthritis.Frontiers in physiology · 2024Review
- Cross-species comparison illuminates the importance of iron homeostasis for splenic anti-immunosenescence.Aging cell · 2023Article
- Dietary iron regulates intestinal goblet cell function and alleviates Salmonella typhimurium invasion in mice.Science China. Life sciences · 2023Article
- Emerging roles of ferroptosis-related miRNAs in tumor metastasis.Cell death discovery · 2023Review
- ATP-dependent transporters: emerging players at the crossroads of immunity and metabolism.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Iron-sulfur (Fe-S) clusters are cofactors essential for the activity of numerous enzymes including DNA polymerases, helicases, and glycosylases. They are synthesized in the mitochondria as Fe-S intermediates and are exported to the cytoplasm for maturation by the mitochondrial transporter ABCB7. Here, we demonstrate that ABCB7 is required for bone marrow B cell development, proliferation, and class switch recombination, but is dispensable for peripheral B cell homeostasis in mice. Conditional deletion of ABCB7 using Mb1-cre resulted in a severe block in bone marrow B cell development at the pro-B cell stage. The loss of ABCB7 did not alter expression of transcription factors required for B cell specification or commitment. While increased intracellular iron was observed in ABCB7-deficient pro-B cells, this did not lead to increased cellular or mitochondrial reactive oxygen species, ferroptosis, or apoptosis. Interestingly, loss of ABCB7 led to replication-induced DNA damage in pro-B cells, independent of VDJ recombination, and these cells had evidence of slowed DNA replication. Stimulated ABCB7-deficient splenic B cells from CD23-cre mice also had a striking loss of proliferation and a defect in class switching. Thus, ABCB7 is essential for early B cell development, proliferation, and class switch recombination.
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Registered trials
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