ArticleEBioMedicine2017
Enhanced Mucosal Defense and Reduced Tumor Burden in Mice with the Compromised Negative Regulator IRAK-M.
Article in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 3 of them syntheses that pooled it.
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
19 citing papers in PubMed, 3 syntheses or guidelines pooled it, 23 citations in OpenAlex.
- Pooled it
- Pooled it
- Pooled it
- spaGFM is a scalable graph foundation model for spatial transcriptomics analyses.Research square · 2026Article
- IRAK-M Knockout Exacerbates Inflammation in Mice Infected withMicroorganisms · 2026Article
- Interplay between pathogen-mediated immune evasion and innate immune negative regulation in gastrointestinal tumors.Frontiers in immunology · 2026Review
- IRAK-M Plays A Role in the Pathology of Amyotrophic Lateral Sclerosis Through Suppressing the Activation of Microglia.Molecular neurobiology · 2024Article
- IL-1 receptor-associated kinase 3 (IRAK3) in lung adenocarcinoma predicts prognosis and immunotherapy resistance: involvement of multiple inflammation-related pathways.Translational lung cancer research · 2024Article
- IRAK3-mediated suppression of pro-inflammatory MyD88/IRAK signaling affects disease severity in acute pancreatitis.Scientific reports · 2023Article
- IL-1 receptor-associated kinase-3 acts as an immune checkpoint in myeloid cells to limit cancer immunotherapy.The Journal of clinical investigation · 2023Article
- Chemically Induced Colitis-Associated Cancer Models in Rodents for Pharmacological Modulation: A Systematic Review.Journal of clinical medicine · 2022Review
- Dimeric Structure of the Pseudokinase IRAK3 Suggests an Allosteric Mechanism for Negative Regulation.Structure (London, England : 1993) · 2021Article
- TICAM2-related pathway mediates neutrophil exhaustion.Scientific reports · 2020Article
- Neutrophils Deficient in Innate Suppressor IRAK-M Enhances Anti-tumor Immune Responses.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- Enhanced Neutrophil Immune Homeostasis Due to Deletion of PHLPP.Frontiers in immunology · 2019Article
- Modulating inflammation through the negative regulation of NF-κB signaling.Journal of leukocyte biology · 2018Review
- Noncanonical NF-κB signaling and the essential kinase NIK modulate crucial features associated with eosinophilic esophagitis pathogenesis.Disease models & mechanisms · 2017Article
- Novel insights into microbiome in colitis and colorectal cancer.Current opinion in gastroenterology · 2017Review
- Programming and memory dynamics of innate leukocytes during tissue homeostasis and inflammation.Journal of leukocyte biology · 2017Review
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 2 institutions in 1 country.
Funding
Abstract
Aberrant inflammation is a hallmark of inflammatory bowel disease (IBD) and colorectal cancer. IRAK-M is a critical negative regulator of TLR signaling and overzealous inflammation. Here we utilize data from human studies and Irak-m
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.