ArticleJournal of proteome research2007
Tumor Necrosis Factor-alpha- and interleukin-1-induced cellular responses: coupling proteomic and genomic information.
Article in Journal of proteome research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 87 citations in OpenAlex.
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- Novel Targets and Nanotechnology Approaches in Treating Vulvovaginal Candidiasis: Insights into Host-Microbe Interactions and Immunotherapy.Current pharmaceutical design · 2026Review
- S100A12 drives inflammatory and metabolic reprogramming in sepsis-associated acute kidney injury.Frontiers in molecular biosciences · 2026Review
- Cardiovascular risk factors associated with BMI and metabolic health phenotypes based on measures of coagulation factors.International journal of obesity (2005) · 2025Article
- Histopathological and Molecular Insights into Chronic Nasopharyngeal and Otic Disorders in Children: Structural and Immune Mechanisms Underlying Disease Chronicity.Life (Basel, Switzerland) · 2025Review
- Novel insights into bexarotene's role in preventing cholestasis: mechanisms and implications.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Profiling of Environmental Mixtures Containing Metals for Their Toxicity Pathways and Mechanism of Action.Environmental science & technology · 2025Article
- Extracellular mitochondria contribute to acute lung injury via disrupting macrophages after traumatic brain injury.Journal of neuroinflammation · 2025Article
- Rational engineering of minimally immunogenic nucleases for gene therapy.Nature communications · 2025Article
- Single-cell multi-omics reveals the TNF-α activation threshold for Classical Monocytes by studying healthy donors and rheumatoid arthritis patients.Frontiers in immunology · 2025Article
- Omega-3 attenuates the severity of medication-related osteonecrosis of the jaws in rats treated with zoledronate.PloS one · 2025Article
- Review
- A Review on Risk Factors, Traditional Diagnostic Techniques, and Biomarkers for Pneumonia Prognostication and Management in Diabetic Patients.Diseases (Basel, Switzerland) · 2024Review
- Connexin 43 Modulation in Human Chondrocytes, Osteoblasts and Cartilage Explants: Implications for Inflammatory Joint Disorders.International journal of molecular sciences · 2024Article
- Article
- Causal effect of interleukin (IL)-6 on blood pressure and hypertension: A mendelian randomization study.Immunogenetics · 2024Article
- Influencing Endothelial Cells' Roles in Inflammation and Wound Healing Through Nucleic Acid Delivery.Tissue engineering. Part A · 2024Review
- Deletion ofInternational journal of molecular sciences · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
The pro-inflammatory cytokines, Tumor Necrosis Factor-alpha (TNFalpha) and Interleukin-1 (IL-1) mediate the innate immune response. Dysregulation of the innate immune response contributes to the pathogenesis of cancer, arthritis, and congestive heart failure. TNFalpha- and IL-1-induced changes in gene expression are mediated by similar transcription factors; however, TNFalpha and IL-1 receptor knock-out mice differ in their sensitivities to a known initiator (lipopolysaccharide, LPS) of the innate immune response. The contrasting responses to LPS indicate that TNFalpha and IL-1 regulate different processes. A large-scale proteomic analysis of TNFalpha- and IL-1-induced responses was undertaken to identify processes uniquely regulated by TNFalpha and IL-1. When combined with genomic studies, our results indicate that TNFalpha, but not IL-1, mediates cell cycle arrest.
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.