ArticleBMC molecular biology2006
The transcription factor ATF3 is upregulated during chondrocyte differentiation and represses cyclin D1 and A gene transcription.
Article in BMC molecular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 87 citations in OpenAlex.
- HDAC7-Induced Epigenetic Repression Modulates ATF3 Functional Plasticity in Colorectal Cancer Pathogenesis.International journal of biological sciences · 2026Article
- Human brain cell types shape host-rabies virus transcriptional interactions revealing a preexisting pro-viral astrocyte subpopulation.Cell reports · 2025Article
- Atf3 + senescent chondrocytes mediate meniscus degeneration in aging.Arthritis research & therapy · 2025Article
- Effects of weaning on intestinal longitudinal muscle-myenteric plexus function in piglets.Science China. Life sciences · 2024Article
- Key role for Rac in the early transcriptional response to extracellular matrix stiffness and stiffness-dependent repression of ATF3.Journal of cell science · 2023Article
- Characterization of Chromatin Accessibility in Fetal Bovine Chondrocytes.Animals : an open access journal from MDPI · 2023Article
- Transcription Factor ATF3 Participates in DeltaNp63-Mediated Proliferation of Corneal Epithelial Cells.Journal of personalized medicine · 2023Article
- Identification and validation of hub genes and potential drugs involved in osteoarthritis through bioinformatics analysis.Frontiers in genetics · 2023Article
- Comparison of Gene Expression Patterns in Articular Cartilage and Xiphoid Cartilage.Biochemical genetics · 2022Article
- Stem Cell-Laden Hydrogel-Based 3D Bioprinting for Bone and Cartilage Tissue Engineering.Frontiers in bioengineering and biotechnology · 2022Review
- Impact of perlecan, a core component of basement membrane, on regeneration of cartilaginous tissues.Acta biomaterialia · 2021Review
- Altered microRNA profile during fracture healing in rats with diabetes.Journal of orthopaedic surgery and research · 2020Article
- Respiratory chain inactivation links cartilage-mediated growth retardation to mitochondrial diseases.The Journal of cell biology · 2019Article
- Overexpression of activating transcription factor 3 exerts suppressive effects in HepG2 cells.Molecular medicine reports · 2019Article
- Article
- Cytokine-induced MMP13 Expression in Human Chondrocytes Is Dependent on Activating Transcription Factor 3 (ATF3) Regulation.The Journal of biological chemistry · 2017Article
- ATF3 controls proliferation of osteoclast precursor and bone remodeling.Scientific reports · 2016Article
- Runx2, a target gene for activating transcription factor-3 in human breast cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Choline kinase beta is required for normal endochondral bone formation.Biochimica et biophysica acta · 2014Article
- A gene expression study of normal and damaged cartilage in anteromedial gonarthrosis, a phenotype of osteoarthritis.Osteoarthritis and cartilage · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCoordinated chondrocyte proliferation and differentiation are required for normal endochondral bone growth. Transcription factors binding to the cyclicAMP response element (CRE) are known to regulate these processes. One member of this family, Activating Transcription Factor 3 (ATF3), is expressed during skeletogenesis and acts as a transcriptional repressor, but the function of this protein in chondrogenesis is unknown.
resultsHere we demonstrate that Atf3 mRNA levels increase during mouse chondrocyte differentiation in vitro and in vivo. In addition, Atf3 mRNA levels are increased in response to cytochalasin D treatment, an inducer of chondrocyte maturation. This is accompanied by increased Atf3 promoter activity in cytochalasin D-treated chondrocytes. We had shown earlier that transcription of the cell cycle genes cyclin D1 and cyclin A in chondrocytes is dependent on CREs. Here we demonstrate that overexpression of ATF3 in primary mouse chondrocytes results in reduced transcription of both genes, as well as decreased activity of a CRE reporter plasmid. Repression of cyclin A transcription by ATF3 required the CRE in the cyclin A promoter. In parallel, ATF3 overexpression reduces the activity of a SOX9-dependent promoter and increases the activity of a RUNX2-dependent promoter.
conclusionOur data suggest that transcriptional induction of the Atf3 gene in maturing chondrocytes results in down-regulation of cyclin D1 and cyclin A expression as well as activation of RUNX2-dependent transcription. Therefore, ATF3 induction appears to facilitate cell cycle exit and terminal differentiation of chondrocytes.
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