ArticleNature genetics2017
SMARCD2 subunit of SWI/SNF chromatin-remodeling complexes mediates granulopoiesis through a CEBPɛ dependent mechanism.
Article in Nature genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 79 citations in OpenAlex.
- The Drosophila SWI/SNF complex subunit Bap60 is required for training-induced gene transcription during long-term memory formation.Genetics · 2026Article
- SMARCD1 and Its Functional Relevance in SWI/SNF and Cancer.International journal of molecular sciences · 2026Review
- When Fertilization Is Not Enough: Maternal-Zygotic Transition as a Determinant of Embryo Competence in IVF.International journal of molecular sciences · 2026Review
- A SWI/SNF-specific Ig-like domain, SWIFT, is a transcription factor binding platform.Science (New York, N.Y.) · 2026Article
- Article
- Chromatin Remodeling in VSMC Phenotype Switching During Vascular Remodeling: From Mechanism to Therapeutic Potential.Biomolecules · 2026Review
- Novel Nonsense Mutation inEJHaem · 2025Article
- In-depth functional analysis of BRD9 in fetal hematopoiesis reveals context-dependent roles.iScience · 2025Article
- Genotype-phenotype correlations in specific granule deficiency: loss of DNA-binding ability and impaired nuclear localization cause severe manifestations due to the c.655_665del CEBPE variant.Clinical and experimental immunology · 2025Article
- The long pentraxin 3: the invisible loom weaving the warp and weft of tumor destiny.Frontiers in immunology · 2025Review
- Regulatory Roles of SWI/SNF Chromatin Remodeling Complexes in Immune Response and Inflammatory Diseases.Clinical reviews in allergy & immunology · 2024Review
- Identification of BAF60b as a Chromatin-Remodeling Checkpoint of Diet-Induced Fatty Liver Disease.Diabetes · 2024Article
- Single-Cell RNA Sequencing Reveals Transcriptional Landscape of Neutrophils and Highlights the Role of TREM-1 in EAE.Neurology(R) neuroimmunology & neuroinflammation · 2024Article
- Baf155 controls hematopoietic differentiation and regeneration through chromatin priming.Cell reports · 2024Article
- Pathogenic GATA2 genetic variants utilize an obligate enhancer mechanism to distort a multilineage differentiation program.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Targeting SWI/SNF Complexes in Cancer: Pharmacological Approaches and Implications.Epigenomes · 2024Review
- SWI/SNF Complex in Vascular Smooth Muscle Cells and Its Implications in Cardiovascular Pathologies.Cells · 2024Review
- Intron retention as an excellent marker for diagnosing depression and for discovering new potential pathways for drug intervention.Frontiers in psychiatry · 2024Article
- BRD9 determines the cell fate of hematopoietic stem cells by regulating chromatin state.Nature communications · 2023Article
- Mechanism of action of the SWI/SNF family complexes.Nucleus (Austin, Tex.) · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies suggest that individual subunits of chromatin-remodeling complexes produce biologically specific meaning in different cell types through combinatorial assembly. Here we show that granulocyte development requires SMARCD2, a subunit of ATP-dependent SWI/SNF (BAF) chromatin-remodeling complexes. Smarcd2-deficient mice fail to generate functionally mature neutrophils and eosinophils, a phenotype reminiscent of neutrophil-specific granule deficiency (SGD) in humans, for which loss-of-function mutations in CEBPE (encoding CEBPɛ) have been reported. SMARCD2-containing SWI/SNF complexes are necessary for CEBPɛ transcription factor recruitment to the promoter of neutrophilic secondary granule genes and for granulocyte differentiation. The homologous SMARCD1 protein (63% identical at the amino acid level) cannot replace the role of SMARCD2 in granulocyte development. We find that SMARCD2 functional specificity is conferred by its divergent coiled-coil 1 and SWIB domains. Strikingly, both CEBPE and SMARCD2 loss-of-function mutations identified in patients with SGD abolish the interaction with SWI/SNF and thereby secondary granule gene expression, thus providing a molecular basis for this disease.
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