ArticleCell reports2016
Non-canonical PI3K-Cdc42-Pak-Mek-Erk Signaling Promotes Immune-Complex-Induced Apoptosis in Human Neutrophils.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 79 citations in OpenAlex.
- Redundant γc cytokines license IL-1-driven neutrophil inflammation through MEK/ERK convergence.bioRxiv : the preprint server for biology · 2026Article
- CDC42 Regulates the ERK Pathway to Improve Oxygen‒Glucose Deprivation/Reoxygenation-Induced Neural Oxidative Stress and Apoptosis.Molecular neurobiology · 2025Article
- A Natural Small Molecule Mitigates Kidney Fibrosis by Targeting Cdc42-mediated GSK-3β/β-catenin Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- PI3K Functions Downstream of Cdc42 to Drive Cancer phenotypes in a Melanoma Cell Line.Small GTPases · 2023 · on this mapArticle
- Anti-Inflammatory Neutrophil Functions in the Resolution of Inflammation and Tissue Repair.Cells · 2022Review
- Comprehensive analysis of the prognostic implications and functional exploration of PAK gene family in human cancer.Cancer cell international · 2022Article
- Class I PI3K Biology.Current topics in microbiology and immunology · 2022Article
- Notch-1 signaling promotes reattachment of suspended cancer cells by cdc42-dependent microtentacles formation.Cancer science · 2021Article
- Crosstalk between B cells and neutrophils in rheumatoid arthritis.Immunology · 2021Review
- Article
- Immune complex-induced apoptosis and concurrent immune complex clearance are anti-inflammatory neutrophil functions.Cell death & disease · 2021Article
- Siglec-8 Signals Through a Non-Canonical Pathway to Cause Human Eosinophil DeathFrontiers in immunology · 2021Article
- Inhibition of leucine-rich repeats and calponin homology domain containing 1 accelerates microglia-mediated neuroinflammation in a rat traumatic spinal cord injury model.Journal of neuroinflammation · 2020Article
- Cross-talk between Rho GTPases and PI3K in the neutrophil.Small GTPases · 2019Review
- HoxB8 neutrophils replicate Fcγ receptor and integrin-induced neutrophil signaling and functions.Journal of leukocyte biology · 2019Article
- Expanding Neutrophil Horizons: New Concepts in Inflammation.Journal of innate immunity · 2018Review
- A Small GTPase, RhoA, Inhibits Bacterial Infection Through Integrin Mediated Phagocytosis in Invertebrates.Frontiers in immunology · 2018Article
- Therapeutic Effect of a Novel Phosphatidylinositol-3-Kinase δ Inhibitor in Experimental Epidermolysis Bullosa Acquisita.Frontiers in immunology · 2018Article
- Differential Impacts of Alternative Splicing Networks on Apoptosis.International journal of molecular sciences · 2016Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Neutrophils are peripheral blood leukocytes that represent the first line of immune cell defense against bacterial and fungal infections but are also crucial players in the generation of the inflammatory response. Many neutrophil cell surface receptors regulate important cellular processes via activation of agonist-activated PI3Ks. We show here that activation of human neutrophils with insoluble immune complexes drives a previously uncharacterized, PI3K-dependent, non-canonical, pro-apoptotic signaling pathway, FcγR-PI3Kβ/δ-Cdc42-Pak-Mek-Erk. This is a rare demonstration of Ras/Raf-independent activation of Erk and of PI3K-mediated activation of Cdc42. In addition, comparative analysis of immune-complex- and fMLF-induced signaling uncovers key differences in pathways used by human and murine neutrophils. The non-canonical pathway we identify in this study may be important for the resolution of inflammation in chronic inflammatory diseases that rely on immune-complex-driven neutrophil activation.
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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.