ArticleEpigenetics & chromatin2018
H3K27me1 is essential for MMP-9-dependent H3N-terminal tail proteolysis during osteoclastogenesis.
Article in Epigenetics & chromatin, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
- B1486 is a highly potent VprBP inhibitor capable of blocking osteoclast differentiation and bone resorption.The Journal of biological chemistry · 2026Article
- VprBP drives prostate tumorigenesis by its kinase activity targeting histone H2A.Cell communication and signaling : CCS · 2026Article
- Cell-penetrating H3 tail peptides suppress osteoclast differentiation via inhibition of MMP-9-mediated histone H3 clipping.BMB reports · 2026Article
- Down-regulation of EHMT2 through irisin-mediated epigenetic modification promotes osteogenesis via promoting DLX3 transcription.Cell communication and signaling : CCS · 2026Article
- Dynamic Balance of Histone H3 Methylation: Regulatory Mechanisms and Therapeutic Prospects in RA Immune Dysregulation and Bone Metabolism Imbalance.Journal of immunology research · 2026Review
- Escape of Kdm6a from X Chromosome Is Detrimental to Ischemic Brains via IRF5 Signaling.Translational stroke research · 2025Article
- Beyond Bone Loss: A Biology Perspective on Osteoporosis Pathogenesis, Multi-Omics Approaches, and Interconnected Mechanisms.Biomedicines · 2025Review
- Causal inference study of plasma proteins and blood metabolites mediating the effect of obesity-related indicators on osteoporosis.Frontiers in endocrinology · 2025Article
- VprBP regulates osteoclast differentiation via an epigenetic mechanism involving histone H2A phosphorylation.Epigenetics & chromatin · 2024Article
- Histone Tail Cleavage as a Mechanism for Epigenetic Regulation.International journal of molecular sciences · 2024Review
- Escape of Kdm6a from X chromosome is detrimental to ischemic brains via IRF5 signaling.Research square · 2024Article
- MMP-9-dependent proteolysis of the histone H3 N-terminal tail: a critical epigenetic step in driving oncogenic transcription and colon tumorigenesis.Molecular oncology · 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
- Epigenetic Regulation of Autophagy in Bone Metabolism.Function (Oxford, England) · 2024Review
- Innate immune memory in inflammatory arthritis.Nature reviews. Rheumatology · 2023Review
- The MMP-2 histone H3 N-terminal tail protease is selectively targeted to the transcription start sites of active genes.Epigenetics & chromatin · 2023Article
- Comprehensive analysis of epigenetics mechanisms in osteoporosis.Frontiers in genetics · 2023Review
- The micronuclear histone H3 clipping in the unicellular eukaryoteMarine life science & technology · 2022Review
- Article
- MMP-9 drives the melanomagenic transcription program through histone H3 tail proteolysis.Oncogene · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundMMP-9 plays a direct role in the activation of pro-osteoclastogenic genes by cleaving histone H3N-terminal tail (H3NT) and altering chromatin architecture. Although H3 acetylation at K18 has been shown to stimulate MMP-9 enzymatic activity toward H3NT, nothing is known about the influence of other H3NT modifications on this epigenetic reaction.
resultsWe show that H3 monomethylation at lysine 27 (H3K27me1) is essential for MMP-9-dependent H3NT proteolysis during RANKL-induced osteoclast differentiation. Through the recognition of H3K27me1 mark, MMP-9 localizes and generates H3NT proteolysis at the genes encoding osteoclast differentiation factors. By using RNAi and small molecule inhibitor approaches, we also confirmed that G9a is the major methyltransferase to catalyze H3K27me1 for MMP-9-dependent H3NT proteolysis and trigger the expression of osteoclast-specific genes.
conclusionsOur data establish new functions for G9a-mediated H3K27me1 in MMP-9-dependent H3NT proteolysis and demonstrate how histone modification can be exploited to regulate osteoclastogenic gene expression at the molecular level. Further studies are warranted to investigate the detailed mechanism by which G9a overexpression with concomitant dysregulation of osteoclastogenesis contributes to the pathogenesis of bone disorders.
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Registered trials
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.