ArticleStem cell reports2016
Loss of Asxl1 Alters Self-Renewal and Cell Fate of Bone Marrow Stromal Cell, Leading to Bohring-Opitz-like Syndrome in Mice.
Article in Stem cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Targeted disruption of PRC1.1 complex enhances bone remodeling.Nature communications · 2025Article
- Generation and Characterization of Induced Pluripotent Stem Cells Carrying An ASXL1 Mutation.Stem cell reviews and reports · 2024Article
- Rapid progression of myelofibrosis in polycythemia vera patient carrying SRSF2 c.284C>A p.(Pro95His) and unique ASXL1 splice site c.1720-2A>G variant.Journal of clinical laboratory analysis · 2022Article
- RNF213 gene silencing upregulates transforming growth factor β1 expression in bone marrow-derived mesenchymal stem cells and is involved in the onset of Moyamoya disease.Experimental and therapeutic medicine · 2021Article
- AFrontiers in pediatrics · 2021Article
- IGF-1 enhances BMSC viability, migration, and anti-apoptosis in myocardial infarction via secreted frizzled-related protein 2 pathway.Stem cell research & therapy · 2020Article
- AJournal of genetics · 2019Article
- H₂O₂ Damages the Stemness of Rat Bone Marrow-Derived Mesenchymal Stem Cells: Developing a "Stemness Loss" Model.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- TET2 Loss Dysregulates the Behavior of Bone Marrow Mesenchymal Stromal Cells and Accelerates Tet2Stem cell reports · 2018Article
- Loss of ASXL1 in the bone marrow niche dysregulates hematopoietic stem and progenitor cell fates.Cell discovery · 2018Article
- Loss of Asxl2 leads to myeloid malignancies in mice.Nature communications · 2017Article
- ASXL1 interacts with the cohesin complex to maintain chromatid separation and gene expression for normal hematopoiesis.Science advances · 2017Article
Corrections and comments
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Authors and funding
17 authors at 8 institutions in 2 countries.
Funding
Abstract
De novo ASXL1 mutations are found in patients with Bohring-Opitz syndrome, a disease with severe developmental defects and early childhood mortality. The underlying pathologic mechanisms remain largely unknown. Using Asxl1-targeted murine models, we found that Asxl1 global loss as well as conditional deletion in osteoblasts and their progenitors led to significant bone loss and a markedly decreased number of bone marrow stromal cells (BMSCs) compared with wild-type littermates. Asxl1(-/-) BMSCs displayed impaired self-renewal and skewed differentiation, away from osteoblasts and favoring adipocytes. RNA-sequencing analysis revealed altered expression of genes involved in cell proliferation, skeletal development, and morphogenesis. Furthermore, gene set enrichment analysis showed decreased expression of stem cell self-renewal gene signature, suggesting a role of Asxl1 in regulating the stemness of BMSCs. Importantly, re-introduction of Asxl1 normalized NANOG and OCT4 expression and restored the self-renewal capacity of Asxl1(-/-) BMSCs. Our study unveils a pivotal role of ASXL1 in the maintenance of BMSC functions and skeletal development.
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