A role for PKC-epsilon in Fc gamma R-mediated phagocytosis by RAW 264.7 cells

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Bibtex

@article{94c2c8ffa21443ac804d8433b42776bd,
title = "A role for PKC-epsilon in Fc gamma R-mediated phagocytosis by RAW 264.7 cells",
abstract = "Protein kinase C (PKC) plays a prominent role in immune signaling, and the paradigms for isoform selective signaling are beginning to be elucidated. Real-time microscopy was combined with molecular and biochemical approaches to demonstrate a role for PKC-epsilon in Fcgamma receptor (FcgammaR)-dependent phagocytosis. RAW 264.7 macrophages were transfected with GFP-conjugated PKC isoforms, and GFP movement was followed during phagocytosis of fluorescent IgG-opsonized beads. PKC-epsilon, but not PKC-delta, concentrated around the beads. PKC-epsilon accumulation was transient; apparent as a {"}flash{"} on target ingestion. Similarly, endogenous PKC-epsilon was specifically recruited to the nascent phagosomes in a time-dependent manner. Overexpression of PKC-epsilon, but not PKC-alpha, PKC-delta, or PKC-gamma enhanced bead uptake 1.8-fold. Additionally, the rate of phagocytosis in GFP PKC-epsilon expressors was twice that of cells expressing GFP PKC-delta. Expression of the regulatory domain (ERD) and the first variable region (epsilonV1) of PKC-epsilon inhibited uptake, whereas the corresponding PKC-delta region had no effect. Actin polymerization was enhanced on expression of GFP PKC-epsilon and ERD, but decreased in cells expressing epsilonV1, suggesting that the epsilonRD and epsilonV1 inhibition of phagocytosis is not due to effects on actin polymerization. These results demonstrate a role for PKC-epsilon in FcgammaR-mediated phagocytosis that is independent of its effects on actin assembly.",
keywords = "immunoglobulin, protein kinase C-epsilon, signal transduction, macrophage, confocal",
author = "EC Larsen and T Ueyama and PM Brannock and Y Shirai and N Saito and Christer Larsson and D Loegering and PB Weber and MR Lennartz",
note = "The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Tumour Cell Biology (013017530)",
year = "2002",
doi = "10.1083/jcb.200205140",
language = "English",
volume = "159",
pages = "939--944",
journal = "Journal of Cell Biology",
issn = "0021-9525",
publisher = "Rockefeller University Press",
number = "6",

}