ReviewNature reviews. Immunology2013
Mitogen-activated protein kinases in innate immunity.
Review in Nature reviews. Immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,001 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
1,001 citing papers in PubMed, 1,792 citations in OpenAlex.
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- Regulation of G Protein Signaling 14 protects against cerebral ischemic reperfusion injury by inhibiting the TAK1-JNK/p38 signaling pathway.Histology and histopathology · 2026Article
- Anti-Inflammatory Activity of Capparis cartilaginea Decne. Essential Oil and Its Main Constituents via Modulation of the NLRP3 Inflammasome.Chemistry & biodiversity · 2026Article
- From Claims to Evidence: Re-Evaluating the Molecular Pharmacology ofInternational journal of molecular sciences · 2026Review
- Dehydrocorydaline Accelerates Palatal Wound Healing in Mice Through Suppression of the p38 MAPK/CCL2 Axis and Macrophage Chemotaxis: A Preliminary Study.Biomedicines · 2026Article
- Toll-Like Receptors in the Mechanism of Hexabromocyclododecane-Induced Production of Pro-Inflammatory Cytokines.Journal of applied toxicology : JAT · 2026Article
- The integrated stress response kinase GCN2 prevents ZAKα-Dependent inflammatory hyperactivation in macrophages.The Journal of biological chemistry · 2026Article
941 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
Following pathogen infection or tissue damage, the stimulation of pattern recognition receptors on the cell surface and in the cytoplasm of innate immune cells activates members of each of the major mitogen-activated protein kinase (MAPK) subfamilies--the extracellular signal-regulated kinase (ERK), p38 and Jun N-terminal kinase (JNK) subfamilies. In conjunction with the activation of nuclear factor-κB and interferon-regulatory factor transcription factors, MAPK activation induces the expression of multiple genes that together regulate the inflammatory response. In this Review, we discuss our current knowledge about the regulation and the function of MAPKs in innate immunity, as well as the importance of negative feedback loops in limiting MAPK activity to prevent host tissue damage. We also examine how pathogens have evolved complex mechanisms to manipulate MAPK activation to increase their virulence. Finally, we consider the potential of the pharmacological targeting of MAPK pathways to treat autoimmune and inflammatory diseases.
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.