ArticleCell death and differentiation2024
The histone methyltransferase ASH1L protects against bone loss by inhibiting osteoclastogenesis.
Article in Cell death and differentiation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 7 citations in OpenAlex.
- The histone demethylase KDM5C aggravates titanium particle-induced osteolysis by promoting macrophage inflammation and osteoclastogenesis.Cellular and molecular life sciences : CMLS · 2026Article
- Histone arginine demethylase JMJD7 promotes bone formation through regulating α-Ketoglutarate metabolism.Cell death and differentiation · 2026Article
- Epigenetic suppression of synovial inflammation and osteoclast differentiation in rheumatoid arthritis by I-BET762.Scientific reports · 2026Article
- Targeting Ash1L-STING Axis Restores NK Cell Function and Ameliorates Immune-Mediated Bone Marrow Failure Diseases.International journal of biological sciences · 2026Article
- Comparative transcriptomic and machine learning analysis identifies key genes and immune dysregulation in goats exposed to peste des petits ruminants virus.Virus genes · 2025Article
- Antler stem cell-derived exosomes restore periodontal homeostasis in a rat model with diabetic periodontitis through enhancing ROS scavenging and osteogenesis.Cell death discovery · 2025Article
- Novel heterozygousFrontiers in neurology · 2025Article
- ASH1L in Hepatoma Cells and Hepatic Stellate Cells Promotes Fibrosis-Associated Hepatocellular Carcinoma by Modulating Tumor-Associated Macrophages.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Low frequency sinusoidal electromagnetic fields promote the osteogenic differentiation of rat bone marrow mesenchymal stem cells by modulating miR-34b-5p/STAC2.Communications biology · 2024Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Absent, small, or homeotic1-like (ASH1L) is a histone lysine methyltransferase that generally functions as a transcriptional activator in controlling cell fate. So far, its physiological relevance in bone homeostasis and osteoclast differentiation remains elusive. Here, by conditional deleting Ash1l in osteoclast progenitors of mice, we found ASH1L deficiency resulted in osteoporosis and potentiation of osteoclastogenesis in vivo and in vitro. Mechanistically, ASH1L binds the promoter of the Src homology 3 and cysteine-rich domain 2 (Stac2) and increases the gene's transcription via histone 3 lysine 4 (H3K4) trimethylation modification, thus augmenting the STAC2's protection against receptor activator of nuclear factor kB ligand (RANKL)-initiated inflammation during osteoclast formation. Collectively, we demonstrate the first piece of evidence to prove ASH1L as a critical checkpoint during osteoclastogenesis. The work sheds new light on our understanding about the biological function of ASH1L in bone homeostasis, therefore providing a valuable therapeutic target for the treatment of osteoporosis or inflammatory bone diseases.
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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.