ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2024
The G9a histone methyltransferase represses osteoclastogenesis and bone resorption by regulating NFATc1 function.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Epigenetic Regulation of Bone Homeostasis in Osteoporosis: Mechanisms, Evidence Gaps, and Translational Prospects.Cell biochemistry and function · 2026Review
- The histone demethylase KDM5C aggravates titanium particle-induced osteolysis by promoting macrophage inflammation and osteoclastogenesis.Cellular and molecular life sciences : CMLS · 2026Article
- Increasing autophagy activity suppressesAmerican journal of cancer research · 2026Article
- Unveiling the role of melatonin-related gene CSNK1D in osteoclastogenesis and its implications for osteoporosis treatment.Experimental physiology · 2025Article
- Causal inference study of plasma proteins and blood metabolites mediating the effect of obesity-related indicators on osteoporosis.Frontiers in endocrinology · 2025Article
- The histone H3K9 methyltransferase G9a regulates tendon formation during development.Scientific reports · 2024Article
- The G9a histone methyltransferase represses osteoclastogenesis and bone resorption by regulating NFATc1 function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Epigenetic modifications affect cell differentiation via transcriptional regulation. G9a/EHMT2 is an important epigenetic modifier that catalyzes the methylation of histone 3 lysine 9 (H3K9) and interacts with various nuclear proteins. In this study, we investigated the role of G9a in osteoclast differentiation. When we deleted G9a by infection of Cre-expressing adenovirus into bone marrow macrophages (BMMs) from G9a
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Registered trials
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