ArticleThe Journal of clinical investigation1997
Studies on the contribution of c-fos/AP-1 to arthritic joint destruction.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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.
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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.
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Who cites it
26 citing papers in PubMed, 107 citations in OpenAlex.
- Targeting FOSL1-KCa3.1 inhibits ferroptosis and cartilage destruction by suppressing mitochondrial hyperfusion.Acta pharmacologica Sinica · 2026Article
- TAK1 inhibition restores p53 expression and suppresses inflammation and hyperplasia in JIA synovial fibroblasts.Rheumatology (Oxford, England) · 2026Article
- The universal role of adaptive transcription in health and disease.The FEBS journal · 2025Review
- Integration of ATAC-seq and RNA-seq identifies MX1-mediated AP-1 transcriptional regulation as a therapeutic target for Down syndrome.Biological research · 2023Article
- Drivers of heterogeneity in synovial fibroblasts in rheumatoid arthritis.Nature immunology · 2023Article
- Astragalin Suppresses Inflammatory Responses and Bone Destruction in Mice With Collagen-Induced Arthritis and in Human Fibroblast-Like Synoviocytes.Frontiers in pharmacology · 2019Article
- A wogonin-rich-fraction of Scutellaria baicalensis root extract exerts chondroprotective effects by suppressing IL-1β-induced activation of AP-1 in human OA chondrocytes.Scientific reports · 2017Article
- Harpagoside suppresses IL-6 expression in primary human osteoarthritis chondrocytes.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2017Article
- Small molecule inhibitors targeting activator protein 1 (AP-1).Journal of medicinal chemistry · 2014Article
- N-(2-hydroxy phenyl) acetamide produces profound inhibition of c-Fos protein and mRNA expression in the brain of adjuvant-induced arthritic rats.Molecular and cellular biochemistry · 2014Article
- Soft coral-derived lemnalol alleviates monosodium urate-induced gouty arthritis in rats by inhibiting leukocyte infiltration and iNOS, COX-2 and c-Fos protein expression.Marine drugs · 2013Article
- c-Jun N-Terminal Kinase in Inflammation and Rheumatic Diseases.The open rheumatology journal · 2012Article
- A systems approach to rheumatoid arthritis.PloS one · 2012Article
- Fibroblast-like synoviocytes: key effector cells in rheumatoid arthritis.Immunological reviews · 2010Review
- A triple altered collagen II peptide with consecutive substitutions of TCR contacting residues inhibits collagen-induced arthritis.Annals of the rheumatic diseases · 2007Article
- Inhibitory effect of ribbon-type NF-kappaB decoy oligodeoxynucleotides on osteoclast induction and activity in vitro and in vivo.Arthritis research & therapy · 2006Article
- Punica granatum L. extract inhibits IL-1beta-induced expression of matrix metalloproteinases by inhibiting the activation of MAP kinases and NF-kappaB in human chondrocytes in vitro.The Journal of nutrition · 2005Article
- Regulation of matrix metalloproteinases: an overview.Molecular and cellular biochemistry · 2003Review
- Article
- c-Fos/activator protein-1 transactivates wee1 kinase at G(1)/S to inhibit premature mitosis in antigen-specific Th1 cells.The EMBO journal · 2001Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Features characteristic to rheumatoid joint destruction, including synovial overgrowth and bone resorption, are experimentally produced by augmenting c-fos gene expression. We tested here if arthritic joint destruction was inhibited upon inactivation of the c-fos/AP-1 signal by administering short double-stranded AP-1 DNA oligonucleotides into mice with collagen-induced arthritis to compete for the binding of AP-1 in vivo at the promoter binding site. Arthritic joint destruction was inhibited in a sequence-specific and dose-dependent manner by oligonucleotides containing the AP-1 sequence. The oligonucleotides inhibited gene expression at the transcriptional level. Nucleotide sequences besides AP-1 also appeared to be important structurally for binding of AP-1 onto DNA and for the stability of oligonucleotides against nucleases. Immunohistochemical chase experiment administering biotinylated oligonucleotides into arthritic mice showed that AP-1 oligonucleotides reached the inflamed joint. Thus, activation of c-fos/AP-1 appears essentially important in arthritic joint destruction.
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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.