ArticleMolecular and cellular biology2007
Eos, MITF, and PU.1 recruit corepressors to osteoclast-specific genes in committed myeloid progenitors.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 85 citations in OpenAlex.
- Cell signaling and transcriptional regulation of osteoclast lineage commitment, differentiation, bone resorption and diseases.Cell discovery · 2026Review
- p38 MAPK-dependent phosphorylation of TFEB promotes monocyte-to-macrophage differentiation.EMBO reports · 2023Article
- Biology of melanocytes in mammals.Frontiers in cell and developmental biology · 2023Review
- Human Peripheral Blood Mononucleocyte Derived Myeloid Committed Progenitor Cells Mitigate H-ARS by Exosomal Paracrine Signal.International journal of molecular sciences · 2022Article
- Article
- The underestimated role of the microphthalmia-associated transcription factor (MiTF) in normal and pathological haematopoiesis.Cell & bioscience · 2021Review
- Article
- Molecular mechanisms and clinical management of cancer bone metastasis.Bone research · 2020Review
- Intrinsic Restriction of TNF-Mediated Inflammatory Osteoclastogenesis and Bone Resorption.Frontiers in endocrinology · 2020Review
- EZH2 Supports Osteoclast Differentiation and Bone Resorption Via Epigenetic and Cytoplasmic Targets.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020Article
- Bone Remodeling: Histone Modifications as Fate Determinants of Bone Cell Differentiation.International journal of molecular sciences · 2019Review
- Regulation of Osteoclast Differentiation and Skeletal Maintenance by Histone Deacetylases.Molecules (Basel, Switzerland) · 2019Review
- Eomes partners with PU.1 and MITF to Regulate Transcription Factors Critical for osteoclast differentiation.iScience · 2019Article
- Overexpressed ACP5 has prognostic value in colorectal cancer and promotes cell proliferation and tumorigenesis via FAK/PI3K/AKT signaling pathway.American journal of cancer research · 2019Article
- Enhancer variants reveal a conserved transcription factor network governed by PU.1 during osteoclast differentiation.Bone research · 2018Article
- The master role of microphthalmia-associated transcription factor in melanocyte and melanoma biology.Laboratory investigation; a journal of technical methods and pathology · 2017Review
- The Ikaros family of zinc-finger proteins.Acta pharmaceutica Sinica. B · 2016Review
- Sirt6 cooperates with Blimp1 to positively regulate osteoclast differentiation.Scientific reports · 2016Article
- Failure to Target RANKL Signaling Through p38-MAPK Results in Defective Osteoclastogenesis in the Microphthalmia Cloudy-Eyed Mutant.Journal of cellular physiology · 2016Article
- Investigation of proteome changes in osteoclastogenesis in low serum culture system using quantitative proteomics.Proteome science · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Transcription factors MITF and PU.1 collaborate to increase expression of target genes like cathepsin K (Ctsk) and acid phosphatase 5 (Acp5) during osteoclast differentiation. We show that these factors can also repress transcription of target genes in committed myeloid precursors capable of forming either macrophages or osteoclasts. The direct interaction of MITF and PU.1 with the zinc finger protein Eos, an Ikaros family member, was necessary for repression of Ctsk and Acp5. Eos formed a complex with MITF and PU.1 at target gene promoters and suppressed transcription through recruitment of corepressors CtBP (C-terminal binding protein) and Sin3A, but during osteoclast differentiation, Eos association with Ctsk and Acp5 promoters was significantly decreased. Subsequently, MITF and PU.1 recruited coactivators to these target genes, resulting in robust expression of target genes. Overexpression of Eos in bone marrow-derived precursors disrupted osteoclast differentiation and selectively repressed transcription of MITF/PU.1 targets, while small interfering RNA knockdown of Eos resulted in increased basal expression of Ctsk and Acp5. This work provides a mechanism to account for the modulation of MITF and PU.1 activity in committed myeloid progenitors prior to the initiation of osteoclast differentiation in response to the appropriate extracellular signals.
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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.