ArticleNature communications2017
MafB is a critical regulator of complement component C1q.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 87 citations in OpenAlex.
- MAFB in Pancreatic β-Cell Development and Dysfunction: Implications for Diabetes and Translational Applications.Biomolecules · 2026Review
- Pathogenic myeloid phenotypes drive disease pathology in a novel human neurohistiocytosis model.Blood · 2026Article
- Macrophage efferocytosis promotes inflammation resolution and accelerates wound healing.Communications biology · 2026Review
- Targeting Complement Component 1q Ameliorates Diabetic Endothelial Inflammation Via Orphan Nuclear Receptor 4a1-Dependent Suppression of Nuclear Factor κB Signaling.Journal of the American Heart Association · 2026Article
- Pareto optimality reveals an atlas of cellular archetypes.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- MafB is a conserved transcriptional regulator of macrophage development and functional identity across tissues and species.Immunity · 2026Article
- Viral modulation of synaptic pruning: implications for neuropathology and brain function.Journal of virology · 2026Review
- Targeting C1q signaling in fibro-adipogenic progenitors prevents regenerative fibrosis of aged muscle.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- MAFB regulates hematopoietic stem cell proliferation and maintenance.Scientific reports · 2025Article
- Mycobacterium tuberculosis impairs protective cytokine production via transcription factor MafB manipulation.PLoS pathogens · 2025Article
- RNase T2 deficiency promotes TLR13-dependent replenishment of tissue-protective Kupffer cells.The Journal of experimental medicine · 2025Article
- Article
- Wild-type bone marrow cells repopulate tissue resident macrophages and reverse the impacts of homozygous CSF1R mutation.PLoS genetics · 2025Article
- MAFB in Macrophages Regulates Prostaglandin E2-Mediated Lipid Mediator Class Switch through ALOX15 in Ischemic Acute Kidney Injury.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Transcription Factor Activity Regulating Macrophage Heterogeneity during Skin Wound Healing.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- IRF8 and MAFB drive distinct transcriptional machineries in different resident macrophages of the central nervous system.Communications biology · 2024Article
- Epigenetic regulation of complement C1Q gene expression.Frontiers in immunology · 2024Article
- Monocyte-derived alveolar macrophages are key drivers of smoke-induced lung inflammation and tissue remodeling.Frontiers in immunology · 2024Article
- MafB regulates NLRP3 inflammasome activation by sustaining p62 expression in macrophages.Communications biology · 2023Article
- Gene-regulation modules in nonalcoholic fatty liver disease revealed by single-nucleus ATAC-seq.Life science alliance · 2023Article
Corrections and comments
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Authors and funding
20 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor MafB is expressed by monocytes and macrophages. Efferocytosis (apoptotic cell uptake) by macrophages is important for inhibiting the development of autoimmune diseases, and is greatly reduced in Mafb-deficient macrophages. Here, we show the expression of the first protein in the classical complement pathway C1q is important for mediating efferocytosis and is reduced in Mafb-deficient macrophages. The efferocytosis defect in Mafb-deficient macrophages can be rescued by adding serum from wild-type mice, but not by adding serum from C1q-deficient mice. By hemolysis assay we also show that activation of the classical complement pathway is decreased in Mafb-deficient mice. In addition, MafB overexpression induces C1q-dependent gene expression and signals that induce C1q genes are less effective in the absence of MafB. We also show that Mafb-deficiency can increase glomerular autoimmunity, including anti-nuclear antibody deposition. These results show that MafB is an important regulator of C1q.
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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.