ArticleThe Journal of biological chemistry2014
Defective entry into mitosis 1 (Dim1) negatively regulates osteoclastogenesis by inhibiting the expression of nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 1 (NFATc1).
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 22 citations in OpenAlex.
- Denatonium inhibits RANKL-induced osteoclast differentiation and rescues the osteoporotic phenotype by blocking p65 signaling pathway.Molecular medicine (Cambridge, Mass.) · 2024Article
- TMBIM6 deficiency leads to bone loss by accelerating osteoclastogenesis.Redox biology · 2023Article
- Predicting the targets of IRF8 and NFATc1 during osteoclast differentiation using the machine learning method framework cTAP.BMC genomics · 2022Article
- The KDM4B-CCAR1-MED1 axis is a critical regulator of osteoclast differentiation and bone homeostasis.Bone research · 2021Article
- Myeloperoxidase Controls Bone Turnover by Suppressing Osteoclast Differentiation Through Modulating Reactive Oxygen Species Level.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- Transcriptome Analysis Reveals ThatBiology · 2020Article
- Ethyl Acetate Fraction of Aqueous Extract of Lentinula edodes Inhibits Osteoclastogenesis by Suppressing NFATc1 Expression.International journal of molecular sciences · 2020Article
- Loss of Stromal Galectin-1 Enhances Multiple Myeloma Development: Emphasis on a Role in Osteoclasts.Cancers · 2019Article
- NHA2 promotes cyst development in an in vitro model of polycystic kidney disease.The Journal of physiology · 2019Article
- Angiotensin II Triggers Peripheral Macrophage-to-Sensory Neuron Redox Crosstalk to Elicit Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Spliceosomal components protect embryonic neurons from R-loop-mediated DNA damage and apoptosis.Disease models & mechanisms · 2018Article
- Replication and discovery of musculoskeletal QTLs in LG/J and SM/J advanced intercross lines.Physiological reports · 2018Article
- Review and Meta-Analyses of TAAR1 Expression in the Immune System and Cancers.Frontiers in pharmacology · 2018Article
- SRC kinase inhibition with saracatinib limits the development of osteolytic bone disease in multiple myeloma.Oncotarget · 2016Article
- MMP-9 facilitates selective proteolysis of the histone H3 tail at genes necessary for proficient osteoclastogenesis.Genes & development · 2016Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone remodeling is a continuous process of osteoblastic bone formation and osteoclastic bone resorption to maintain normal bone mass. NFATc1 is the master regulator of osteoclastogensis and transcriptionally activated by c-Fos and NF-κB in response to receptor activator of NF-κB ligand (RANKL) treatment. Defective entry into mitosis 1 (Dim1) is a nuclear protein that is implicated in pre-mRNA splicing and cell cycle progression, but the possible role of Dim1 in regulating other cellular processes remains unknown. Here, we demonstrate that Dim1 attenuates RANKL-induced osteoclastogenesis by targeting NFATc1 signaling pathway. Expression levels of Dim1 and NFATc1 are significantly increased during the formation of multinucleated osteoclasts. RNAi-mediated knockdown of Dim1 markedly enhances the expression of NFATc1 and its target genes, leading to the increase of RANKL-induced osteoclastogenesis in bone marrow-derived macrophages. Conversely, ectopic expression of Dim1 decreases RANKL-induced osteoclast differentiation by silencing NFATc1 and its target genes, further linking Dim1 to the dynamic regulation of osteoclastogenesis. Consistent with this notion, ChIP and interaction studies show that Dim1 directly associates with c-Fos and prevents c-Fos from binding to the NFATc1 promoter, resulting in targeted inactivation of the NFATc1 gene. Therefore, our studies reveal an unrecognized role for Dim1 as a master modulator of osteoclast differentiation, as well as the molecular mechanism underlying its repressive action toward osteoclastogensis.
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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.