ArticleDevelopment (Cambridge, England)2016
AP-1 family members act with Sox9 to promote chondrocyte hypertrophy.
Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 62 citations in OpenAlex.
- IRF2BP2-FOSL2 interaction regulates SOX9-mediated cartilage regeneration in osteoarthritis models.The Journal of clinical investigation · 2026Article
- Integrated Toxicogenomic Analysis Reveals Potential Molecular Signatures Associated with Cadmium-Related Osteoarthritis.Biological trace element research · 2026Article
- SOX9 represses the human galectin-3 promoter in SW1353 cells: potential implications for osteoarthritis.Scientific reports · 2026Article
- APEX1, a transcriptional hub for endochondral ossification and fracture repair.Bone research · 2026Article
- The craniofacial shape of modern humans embodies genomic signatures of evolution, diversity, and clinical conditions.bioRxiv : the preprint server for biology · 2026Article
- Article
- The universal role of adaptive transcription in health and disease.The FEBS journal · 2025Review
- Transfer learning reveals sequence determinants of the quantitative response to transcription factor dosage.Cell genomics · 2025Article
- The Expression Level of SOX Family Transcription Factors' mRNA as a Diagnostic Marker for Osteoarthritis.Journal of clinical medicine · 2025Article
- Superstable lipid vacuoles endow cartilage with its shape and biomechanics.Science (New York, N.Y.) · 2025Article
- Brca1 haploinsufficiency promotes early tumor onset and epigenetic alterations in a mouse model of hereditary breast cancer.Nature genetics · 2024Article
- Review
- Transfer learning reveals sequence determinants of the quantitative response to transcription factor dosage.bioRxiv : the preprint server for biology · 2024Article
- Cooperation of MLL1 and Jun in controlling H3K4me3 on enhancers in colorectal cancer.Genome biology · 2023Article
- Article
- Runt-related Transcription Factors and Gene Regulatory Mechanisms in Skeletal Development and Diseases.Current osteoporosis reports · 2023Review
- Metabolic rewiring controlled by c-Fos governs cartilage integrity in osteoarthritis.Annals of the rheumatic diseases · 2023Article
- Lineage-specific differences and regulatory networks governing human chondrocyte development.eLife · 2023Article
- Emerging RUNX2-Mediated Gene Regulatory Mechanisms Consisting of Multi-Layered Regulatory Networks in Skeletal Development.International journal of molecular sciences · 2023Review
- Hypomorphic and dominant-negative impact of truncated SOX9 dysregulates Hedgehog-Wnt signaling, causing campomelia.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
An analysis of Sox9 binding profiles in developing chondrocytes identified marked enrichment of an AP-1-like motif. Here, we have explored the functional interplay between Sox9 and AP-1 in mammalian chondrocyte development. Among AP-1 family members, Jun and Fosl2 were highly expressed within prehypertrophic and early hypertrophic chondrocytes. Chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq) showed a striking overlap in Jun- and Sox9-bound regions throughout the chondrocyte genome, reflecting direct binding of each factor to the same enhancers and a potential for protein-protein interactions within AP-1- and Sox9-containing complexes. In vitro reporter analysis indicated that direct co-binding of Sox9 and AP-1 at target motifs promoted gene activity. By contrast, where only one factor can engage its DNA target, the presence of the other factor suppresses target activation consistent with protein-protein interactions attenuating transcription. Analysis of prehypertrophic chondrocyte removal of Sox9 confirmed the requirement of Sox9 for hypertrophic chondrocyte development, and in vitro and ex vivo analyses showed that AP-1 promotes chondrocyte hypertrophy. Sox9 and Jun co-bound and co-activated a Col10a1 enhancer in Sox9 and AP-1 motif-dependent manners consistent with their combined action promoting hypertrophic gene expression. Together, the data support a model in which AP-1 family members contribute to Sox9 action in the transition of chondrocytes to the hypertrophic program.
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What OpenQuestion holds
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.