ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Focal adhesion kinase regulates pathogen-killing capability and life span of neutrophils via mediating both adhesion-dependent and -independent cellular signals.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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
28 citing papers in PubMed, 46 citations in OpenAlex.
- Dual inhibition of neutrophil superoxide generation and elastase releaseRSC advances · 2026Article
- Neutrophil death-more than meets the eye.Experimental hematology · 2025Review
- Focal adhesion kinase plays an essential role in Th17 cell differentiation by stimulating NF-κB signaling.Frontiers in immunology · 2025Article
- HNature communications · 2024Article
- Myeloid Poldip2 Contributes to the Development of Pulmonary Inflammation by Regulating Neutrophil Adhesion in a Murine Model of Acute Respiratory Distress Syndrome.Journal of the American Heart Association · 2022Article
- Review
- Article
- Mirage or long-awaited oasis: reinvigorating T-cell responses in pancreatic cancer.Journal for immunotherapy of cancer · 2020Review
- Review
- Gasdermin D Exerts Anti-inflammatory Effects by Promoting Neutrophil Death.Cell reports · 2018Article
- Neutrophil microparticle production and inflammasome activation by hyperglycemia due to cytoskeletal instability.The Journal of biological chemistry · 2017Article
- Multiple Phenotypic Changes Define Neutrophil Priming.Frontiers in cellular and infection microbiology · 2017Review
- Molecular Pathways: Endothelial Cell FAK-A Target for Cancer Treatment.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Review
- Alleviation of skin inflammation after Lin(-) cell transplantation correlates with their differentiation into myeloid-derived suppressor cells.Scientific reports · 2015Article
- Focal adhesion kinase is required for synovial fibroblast invasion, but not murine inflammatory arthritis.Arthritis research & therapy · 2014Article
- FAK in cancer: mechanistic findings and clinical applications.Nature reviews. Cancer · 2014Review
- Neutrophils generate microparticles during exposure to inert gases due to cytoskeletal oxidative stress.The Journal of biological chemistry · 2014Article
- Focal adhesion kinase negatively regulates Lck function downstream of the T cell antigen receptor.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Focal adhesion kinase regulates the localization and retention of pro-B cells in bone marrow microenvironments.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Reactive oxygen species-induced actin glutathionylation controls actin dynamics in neutrophils.Immunity · 2012Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Various neutrophil functions such as phagocytosis, superoxide production, and survival are regulated by integrin signaling. Despite the essential role of focal adhesion kinase (FAK) in mediating this signaling pathway, its exact function in neutrophils is ill defined. In this study, we investigated the role of FAK in neutrophils using a myeloid-specific conditional FAK knockout mouse. As reported in many other cell types, FAK is required for regulation of focal adhesion dynamics when neutrophils adhere to fibronectin or ICAM-1. Adhesion on VCAM-1-coated surfaces and chemotaxis after adhesion were not altered in FAK null neutrophils. In addition, we observed significant reduction in NADPH oxidase-mediated superoxide production and complement-mediated phagocytosis in FAK null neutrophils. As a result, these neutrophils displayed decreased pathogen killing capability both in vitro and in vivo in a mouse peritonitis model. In adherent cells, the defects associated with FAK deficiency are likely due to suppression of phosphatidylinositol (3,4,5)-trisphosphate (PtdIns(3,4,5)P3) signaling and chemoattractant-elicited calcium signaling. Disruption of FAK also reduced chemoattractant-elicited superoxide production in suspended neutrophils in the absence of cell adhesion. This may be solely caused by suppression of PtdIns(3,4,5)P3 signaling in these cells, because the fMLP-elicited calcium signal was not altered. Consistent with decreased PtdIns(3,4,5)P3/Akt signaling in FAK null neutrophils, we also observed accelerated spontaneous death in these cells. Taken together, our results revealed previously unrecognized roles of FAK in neutrophil function and provided a potential therapeutic target for treatment of a variety of infectious and 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.