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Syk Is Required for Integrin Signaling in Neutrophils
Open accessAbstract
The Syk tyrosine kinase plays a critical role in the signaling machinery of various receptors of the adaptive immune system. Here we show that Syk is also an essential component of integrin signaling in neutrophils. syk(-/-) neutrophils failed to undergo respiratory burst, degranulation, or spreading in response to proinflammatory stimuli while adherent to immobilized integrin ligands or when stimulated by direct crosslinking of integrins. Signaling from the beta(1), beta(2), or beta(3) integrins was defective in syk(-/-) cells. Syk colocalized with CD18 during cell spreading and initiated downstream signaling events leading to actin polymerization. Surprisingly, these defects in integrin-mediated activation did not impair the integrin-dependent in vitro or in vivo migration of syk(-/-) neutrophils or of cells deficient in Src-family kinases. Thus, integrins use different signaling mechanisms to support migration and adherent activation.
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SYK tyrosine kinase is a critical component of integrin signaling in neutrophils, mediating NOx activation.
“SYK tyrosine kinase is a critical component of integrin signaling in neutrophils, mediating NOx activation [95].”
From The Role of Reactive Species on Innate Immunity (2022) · cites this paper as [95]
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Metadata
- Authors
- Mócsai, A., Zhou, M., Meng, F., Tybulewicz, V. L., & Lowell, C. A.
- Affiliations
- University of California, San Francisco (US)
- National Institute for Medical Research (GB)
- Corresponding author
- Lowell, Clifford A.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2002-04
- Volume
- 16
- Issue
- 4
- Pages
- 547-558
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2050069950
- Cited by
- 421
- References
- 43
- Citations by year
- 2026: 8 · 2025: 10 · 2024: 15 · 2023: 15 · 2022: 12 · 2021: 15 · 2020: 12 · 2019: 13 · 2018: 13 · 2017: 17 · 2016: 17 · 2015: 8 · 2014: 24 · 2013: 15 · 2012: 25
- FWCI
- 9.81
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 4125 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (DK-58066, HL-54476)
- Topics
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- Syk, integrin signaling, neutrophils, beta1 integrin, beta2 integrins, CD61, CD18, respiratory burst, degranulation, cell spreading, actin polymerization, neutrophil migration, Src family kinases
- MeSH terms
- Syk Kinase, Animals, Bone Marrow Cells, Cell Adhesion, Cell Movement, Cross-Linking Reagents, Enzyme Activation, Enzyme Precursors, Female, Hematopoietic Stem Cells, Male, Mice, Inbred C57BL, Neutrophils, Platelet Membrane Glycoproteins, Protein-Tyrosine Kinases, Signal Transduction, Antigens, CD, Mice, Knockout, CD18 Antigens, Integrin beta1, Integrin beta3, Intracellular Signaling Peptides and Proteins, Mice
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