ArticlePloS one2012
The adaptor molecule Nck localizes the WAVE complex to promote actin polymerization during CEACAM3-mediated phagocytosis of bacteria.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Microglial phagocytosis in Alzheimer disease.Nature reviews. Neurology · 2026Review
- Neutrophil CEACAMs and the Inflammatory Response toJournal of innate immunity · 2026Review
- Regulation of the Scar/WAVE complex in migrating cells: A summary of our understanding.Journal of biosciences · 2023Review
- PINCH1 Promotes Fibroblast Migration in Extracellular Matrices and Influences Their Mechanophenotype.Frontiers in cell and developmental biology · 2022Article
- Nck adaptors at a glance.Journal of cell science · 2021Article
- WASP Restricts Active Rac to Maintain Cells' Front-Rear Polarization.Current biology : CB · 2019Article
- CEACAM3-A Prim(at)e Invention for Opsonin-Independent Phagocytosis of Bacteria.Frontiers in immunology · 2019Review
- Myosin XVI Regulates Actin Cytoskeleton Dynamics in Dendritic Spines of Purkinje Cells and Affects Presynaptic Organization.Frontiers in cellular neuroscience · 2019Article
- Selective Regulation of Cytoskeletal Dynamics and Filopodia Formation by Teleost Leukocyte Immune-Type Receptors Differentially Contributes to Target Capture During the Phagocytic Process.Frontiers in immunology · 2018Article
- GWAS analysis of QTL for enteric septicemia of catfish and their involved genes suggest evolutionary conservation of a molecular mechanism of disease resistance.Molecular genetics and genomics : MGG · 2017Article
- Moraxella catarrhalis induces CEACAM3-Syk-CARD9-dependent activation of human granulocytes.Cellular microbiology · 2016Article
- Inhibition of WAVE Regulatory Complex Activation by a Bacterial Virulence Effector Counteracts Pathogen Phagocytosis.Cell reports · 2016Article
- The WASF3-NCKAP1-CYFIP1 Complex Is Essential for Breast Cancer Metastasis.Cancer research · 2016Article
- Review
- The granulocyte orphan receptor CEACAM4 is able to trigger phagocytosis of bacteria.Journal of leukocyte biology · 2015Article
- MiR-146a activates WAVE2 expression and enhances phagocytosis in lipopolysaccharide-stimulated RAW264.7 macrophages.American journal of translational research · 2015Article
- Rho GTPases as pathogen targets: Focus on curable sexually transmitted infections.Small GTPases · 2015Review
- Signaling by epithelial members of the CEACAM family - mucosal docking sites for pathogenic bacteria.Cell communication and signaling : CCS · 2014Review
- Innate recognition by neutrophil granulocytes differs between Neisseria gonorrhoeae strains causing local or disseminating infections.Infection and immunity · 2013Article
- Grb14 is a negative regulator of CEACAM3-mediated phagocytosis of pathogenic bacteria.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCEACAM3 is a granulocyte receptor mediating the opsonin-independent recognition and phagocytosis of human-restricted CEACAM-binding bacteria. CEACAM3 function depends on an intracellular immunoreceptor tyrosine-based activation motif (ITAM)-like sequence that is tyrosine phosphorylated by Src family kinases upon receptor engagement. The phosphorylated ITAM-like sequence triggers GTP-loading of Rac by directly associating with the guanine nucleotide exchange factor (GEF) Vav. Rac stimulation in turn is critical for actin cytoskeleton rearrangements that generate lamellipodial protrusions and lead to bacterial uptake. PRINCIPAL
findingsIn our present study we provide biochemical and microscopic evidence that the adaptor proteins Nck1 and Nck2, but not CrkL, Grb2 or SLP-76, bind to tyrosine phosphorylated CEACAM3. The association is phosphorylation-dependent and requires the Nck SH2 domain. Overexpression of the isolated Nck1 SH2 domain, RNAi-mediated knock-down of Nck1, or genetic deletion of Nck1 and Nck2 interfere with CEACAM3-mediated bacterial internalization and with the formation of lamellipodial protrusions. Nck is constitutively associated with WAVE2 and directs the actin nucleation promoting WAVE complex to tyrosine phosphorylated CEACAM3. In turn, dominant-negative WAVE2 as well as shRNA-mediated knock-down of WAVE2 or the WAVE-complex component Nap1 reduce internalization of bacteria.
conclusionsOur results provide novel mechanistic insight into CEACAM3-initiated phagocytosis. We suggest that the CEACAM3 ITAM-like sequence is optimized to co-ordinate a minimal set of cellular factors needed to efficiently trigger actin-based lamellipodial protrusions and rapid pathogen engulfment.
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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.