ArticleProceedings of the National Academy of Sciences of the United States of America2015
Spontaneous retrotransposon insertion into TNF 3'UTR causes heart valve disease and chronic polyarthritis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
18 citing papers in PubMed, 35 citations in OpenAlex.
- Crosstalk between Regnase-1 and -3 shapes mast cell survival and cytokine expression.Life science alliance · 2024Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Deletion of Gpatch2 does not alter Tnf expression in mice.Cell death & disease · 2023Article
- Genome-wide analysis of RNA-binding proteins co-expression with alternative splicing events in mitral valve prolapse.Frontiers in immunology · 2023Article
- ZC3H12C expression in dendritic cells is necessary to prevent lymphadenopathy of skin-draining lymph nodes.Immunology and cell biology · 2022Article
- Oligomerization-driven MLKL ubiquitylation antagonizes necroptosis.The EMBO journal · 2021Article
- Natural variation of the cardiac transcriptome in humans.RNA biology · 2021Article
- Analysis of SINE Families B2, Dip, and Ves with Special Reference to Polyadenylation Signals and Transcription Terminators.International journal of molecular sciences · 2021Article
- Artificial Intelligence Models Reveal Sex-Specific Gene Expression in Aortic Valve Calcification.JACC. Basic to translational science · 2021Article
- Premature Onset Aortic Stenosis in Systemic Sclerosis: A Report of a Series of Cases.Internal medicine (Tokyo, Japan) · 2020Article
- The Balance of TNF Mediated Pathways Regulates Inflammatory Cell Death Signaling in Healthy and Diseased Tissues.Frontiers in cell and developmental biology · 2020Review
- Cardiac phenotype in mouse models of systemic autoimmunity.Disease models & mechanisms · 2019Review
- Constitutive overexpression of TNF in BPSM1 mice causes iBALT and bone marrow nodular lymphocytic hyperplasia.Immunology and cell biology · 2019Article
- Mouse germ line mutations due to retrotransposon insertions.Mobile DNA · 2019Review
- Mesenchymal TNFR2 promotes the development of polyarthritis and comorbid heart valve stenosis.JCI insight · 2018Article
- miR-27a protects human mitral valve interstitial cell from TNF-α-induced inflammatory injury via up-regulation of NELL-1.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018Article
- The RNA-binding protein Tristetraprolin (TTP) is a critical negative regulator of the NLRP3 inflammasome.The Journal of biological chemistry · 2017Article
- TNF-induced chronic inflammation does not affect tumorigenesis driven by p53 loss.Cell death & disease · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) are chronic inflammatory diseases that together affect 2-3% of the population. RA and AS predominantly involve joints, but heart disease is also a common feature in RA and AS patients. Here we have studied a new spontaneous mutation that causes severe polyarthritis in bone phenotype spontaneous mutation 1 (BPSM1) mice. In addition to joint destruction, mutant mice also develop aortic root aneurism and aorto-mitral valve disease that can be fatal depending on the genetic background. The cause of the disease is the spontaneous insertion of a retrotransposon into the 3' untranslated region (3'UTR) of the tumor necrosis factor (TNF), which triggers its strong overexpression in myeloid cells. We found that several members of a family of RNA-binding, CCCH-containing zinc-finger proteins control TNF expression through its 3'UTR, and we identified a previously unidentified regulatory element in the UTR. The disease in BPSM1 mice is independent of the adaptive immune system and does not appear to involve inflammatory cytokines other than TNF. To our knowledge, this is the first animal model showing both polyarthritis and heart disease as a direct result of TNF deregulation. These results emphasize the therapeutic potential of anti-TNF drugs for the treatment of heart valve disease and identify potential therapeutic targets to control TNF expression and inflammation.
Indexed as
Identifiers
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.