ArticleScience signaling2010
Purinergic signaling: a fundamental mechanism in neutrophil activation.
Article in Science signaling, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 1 of them a synthesis 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
133 citing papers in PubMed, 1 synthesis or guideline pooled it, 197 citations in OpenAlex.
- Knowledge domain and evolutionary trends of P2Y receptors in cardiovascular diseases: a bibliometric and altmetric analysis.Frontiers in pharmacology · 2025Pooled it
- Mitochondria regulate neutrophil activation by generating ATP for autocrine purinergic signaling.The Journal of biological chemistry · 2014Trial
- CR1-mediated ATP release by human red blood cells promotes CR1 clustering and modulates the immune transfer process.The Journal of biological chemistry · 2013Trial
- From danger to resolution: targeting purinergic signaling in CNS diseases.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Review
- Nucleotide signaling in neutrophils: a key player in cancer dynamics.Purinergic signalling · 2026Review
- Purinergic signaling in the gut neuro-glial-immune axis: mechanisms of homeostasis, inflammation, and gastrointestinal dysfunction.Frontiers in gastroenterology (Lausanne, Switzerland) · 2026Review
- Review
- Adenosine accumulation in the blood of newborn mice weakens antimicrobial host defenses.Journal of leukocyte biology · 2025Article
- Anti-β2GPI/β2GPI complex promotes thrombosis by activating the P2Y2/MAPKs pathway to increase human neutrophil peptides.PloS one · 2025Article
- Challenges for the human immune system after leaving Earth.NPJ microgravity · 2024Review
- Not just sugar: metabolic control of neutrophil development and effector functions.Journal of leukocyte biology · 2024Review
- Release of ATP in the lung evoked by inhalation of irritant gases in rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2024Article
- Adenosine Triphosphate Release From Influenza-Infected Lungs Enhances Neutrophil Activation and Promotes Disease Progression.The Journal of infectious diseases · 2024Article
- Impaired ATP hydrolysis in blood plasma contributes to age-related neutrophil dysfunction.Immunity & ageing : I & A · 2024Article
- "Find Me" and "Eat Me" signals: tools to drive phagocytic processes for modulating antitumor immunity.Cancer communications (London, England) · 2024Review
- Article
- Distribution of P2Y and P2X purinergic receptor expression within the intestine.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Stimulation of platelet P2YBritish journal of pharmacology · 2024Article
- Exploring bias in platelet P2YBritish journal of pharmacology · 2024Review
- The emerging role for neutrophil mitochondrial metabolism in lung inflammation.Immunometabolism (Cobham, Surrey) · 2024Review
73 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
11 authors at 2 institutions in 1 country.
Funding
Abstract
Efficient activation of neutrophils is a key requirement for effective immune responses. We found that neutrophils released cellular adenosine triphosphate (ATP) in response to exogenous stimuli such as formylated bacterial peptides and inflammatory mediators that activated Fcgamma, interleukin-8, C5a complement, and leukotriene B(4) receptors. Stimulation of the formyl peptide receptor (FPR) led to ATP release through pannexin-1 (panx1) hemichannels, and FPRs colocalized with P2Y2 nucleotide receptors on the cell surface to form a purinergic signaling system that facilitated neutrophil activation. Disruption of this purinergic signaling system by inhibiting or silencing panx1 hemichannels or P2Y2 receptors blocked neutrophil activation and impaired innate host responses to bacterial infection. Thus, purinergic signaling is a fundamental mechanism required for neutrophil activation and immune defense.
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.