ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Myeloid-specific tristetraprolin deficiency in mice results in extreme lipopolysaccharide sensitivity in an otherwise minimal phenotype.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 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
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Who cites it
83 citing papers in PubMed, 107 citations in OpenAlex.
- Lymphatic dysfunction and ZFP36 deficiency contribute to myxomatous valve degeneration in Marfan syndrome mice.The Journal of clinical investigation · 2026Article
- Tristetraprolin protects against ozone-induced acute lung injury and inflammation in mice.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- The ZFP36-FTO axis is a key regulator of macrophage activation and a druggable therapeutic target of sepsis.iScience · 2025Article
- Myeloid-specific tristetraprolin mitigates postsurgical incisional pain by suppressing proinflammatory responses.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Myeloid-specific Tristetraprolin mitigates postsurgical incisional pain by suppressing proinflammatory responses.Research square · 2025Article
- Altered baseline immunological state and impaired immune response to SARS-CoV-2 mRNA vaccination in lung transplant recipients.Cell reports. Medicine · 2025Article
- Senescence-induced p21Cell discovery · 2025Article
- Restraint of inflammasome-driven cytokine responses through the mRNA stability protein TTP.Cell reports · 2025Article
- ZFP36 Regulates Vascular Smooth Muscle Contraction and Maintains Blood Pressure.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Shiga Toxins Produced by EnterohaemorrhagicJournal of microbiology and biotechnology · 2024Article
- Low tristetraprolin expression activates phenotypic plasticity and primes transition to lethal prostate cancer in mice.The Journal of clinical investigation · 2024Article
- Tristetraprolin mediates immune evasion of mycobacterial infection in macrophages.FASEB bioAdvances · 2024Article
- Endothelial Jagged1 levels and distribution are post-transcriptionally controlled by ZFP36 decay proteins.Cell reports · 2024Article
- Synergistic roles of tristetraprolin family members in myeloid cells in the control of inflammation.Life science alliance · 2024Article
- Tristetraprolin regulates the skeletal phenotype and osteoclastogenic potential through monocytic myeloid-derived suppressor cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Post-transcriptional checkpoints in autoimmunity.Nature reviews. Rheumatology · 2023Review
- ZFP36-mediated mRNA decay regulates metabolism.Cell reports · 2023Article
- The Loss of YTHDC1 in Gut Macrophages Exacerbates Inflammatory Bowel Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Tristetraprolin promotes survival of mammary progenitor cells by restraining TNFα levels.Frontiers in cell and developmental biology · 2023Article
- Clinical implications of tristetraprolin (TTP) modulation in the treatment of inflammatory diseases.Pharmacology & therapeutics · 2022Review
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Tristetraprolin (TTP) is a mRNA-destabilizing protein that binds to AU-rich elements in labile transcripts, such as the mRNA encoding TNF, and promotes their deadenylation and degradation. TTP-deficient (knockout [KO]) mice exhibit an early-onset, severe inflammatory phenotype, with cachexia, erosive arthritis, left-sided cardiac valvulitis, myeloid hyperplasia, and autoimmunity, which can be prevented by injections of anti-TNF Abs, or interbreeding with TNF receptor-deficient mice. To determine whether the excess TNF that causes the TTP KO phenotype is produced by myeloid cells, we performed myeloid-specific disruption of Zfp36, the gene encoding TTP. We documented the lack of TTP expression in LPS-stimulated bone marrow-derived macrophages from the mice, whereas fibroblasts expressed TTP mRNA and protein normally in response to serum. The mice exhibited a minimal phenotype, characterized by slight slowing of weight gain late in the first year of life, compared with the early-onset, severe weight loss and inflammation seen in the TTP KO mice. Instead, the myeloid-specific TTP KO mice were highly and abnormally susceptible to a low-dose LPS challenge, with rapid development of typical endotoxemia signs and extensive organ damage, and elevations of serum TNF levels to 110-fold greater than control. We conclude that myeloid-specific TTP deficiency does not phenocopy complete TTP deficiency in C57BL/6 mice under normal laboratory conditions, implying contributions from other cell types to the complete phenotype. However, myeloid cell TTP plays a critical role in protecting mice against LPS-induced septic shock, primarily through its posttranscriptional regulation of TNF mRNA stability.
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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.