ArticleThe Journal of cell biology2015
mTOR and differential activation of mitochondria orchestrate neutrophil chemotaxis.
Article in The Journal of cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
What it found
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Who cites it
92 citing papers in PubMed, 136 citations in OpenAlex.
- KArchiv der Pharmazie · 2026Article
- Neutrophil-based immunotherapy: A metabolic lens on mechanisms and therapeutic implications.Clinical and translational medicine · 2026Review
- Single-cell transcriptomic unveils tumor-mediated reprogramming of neutrophils and their unique vulnerability that inhibits metastasis.Science advances · 2026Article
- Decoding mitochondrial signaling: neutrophil-tumor cell crosstalk in orchestrating cancer progression.Journal of translational medicine · 2026Review
- Evaluation of neutrophil activation in autoimmune kidney diseases using blood heparin-binding protein: a pilot study.Frontiers in medicine · 2026Article
- Glucose metabolic reprogramming in systemic lupus erythematosus and lupus nephritis: theoretical foundations and therapeutic implications.Frontiers in immunology · 2026Review
- Multi‑omics reveal neutrophil heterogeneity in sepsis (Review).International journal of molecular medicine · 2025Review
- The first proteomics analysis of tonsils in patients with periodic fever, aphthous stomatitis, pharyngitis, and adenitis syndrome (PFAPA).Pediatric research · 2025Article
- Adenosine accumulation in the blood of newborn mice weakens antimicrobial host defenses.Journal of leukocyte biology · 2025Article
- Metabolic phenotype of bovine blood-derived neutrophils is altered in milk.Scientific reports · 2025Article
- Remifentanil Ameliorates Lipopolysaccharide-Induced Neuroinflammation by Regulating the Phosphatidylinositol 3-Kinase/Serine-Threonine Protein Kinase/Hypoxia-Inducible Factor 1 Alpha Pathway.Pharmacology research & perspectives · 2025Article
- Effects of the pan-caspase inhibitor Q-VD-OPh on human neutrophil lifespan and function.PloS one · 2025Article
- A high-throughput chemotaxis assay for assessing immunotoxicity using multiple human immune cell types.NAM journal · 2025Article
- Carbohydrate metabolism in supporting and regulating neutrophil effector functions.Current opinion in immunology · 2024Review
- Ribosome Quality Control mitigates the cytotoxicity of ribosome collisions induced by 5-Fluorouracil.Nucleic acids research · 2024Article
- GPCRs: emerging targets for novel T cell immune checkpoint therapy.Cancer immunology, immunotherapy : CII · 2024Review
- The P2YPurinergic signalling · 2024Article
- Impaired ATP hydrolysis in blood plasma contributes to age-related neutrophil dysfunction.Immunity & ageing : I & A · 2024Article
- Neutrophil glucose flux as a therapeutic target in antiphospholipid syndrome.The Journal of clinical investigation · 2024Article
- Editorial overview: "Purinergic immune cell regulation reveals novel pharmacological targets".Current opinion in pharmacology · 2024Article
32 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
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Neutrophils use chemotaxis to locate invading bacteria. Adenosine triphosphate (ATP) release and autocrine purinergic signaling via P2Y2 receptors at the front and A2a receptors at the back of cells regulate chemotaxis. Here, we examined the intracellular mechanisms that control these opposing signaling mechanisms. We found that mitochondria deliver ATP that stimulates P2Y2 receptors in response to chemotactic cues, and that P2Y2 receptors promote mTOR signaling, which augments mitochondrial activity near the front of cells. Blocking mTOR signaling with rapamycin or PP242 or mitochondrial ATP production (e.g., with CCCP) reduced mitochondrial Ca(2+) uptake and membrane potential, and impaired cellular ATP release and neutrophil chemotaxis. Autocrine stimulation of A2a receptors causes cyclic adenosine monophosphate accumulation at the back of cells, which inhibits mTOR signaling and mitochondrial activity, resulting in uropod retraction. We conclude that mitochondrial, purinergic, and mTOR signaling regulates neutrophil chemotaxis and may be a pharmacological target in inflammatory diseases.
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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.