Cited by 114Autophagy in Disease and TherapyPhagocytosis and Immune RegulationCellular transport and secretion

Membrane proteomics of phagosomes suggests a connection to autophagy

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Shui, Wenqing, Sheu, Leslie, Liu, Jun, Smart, Brian, Petzold, Christopher J., Hsieh, Tsung-yen, Pitcher, Austin, Keasling, Jay D. +1 more·2008·Proceedings of the National Academy of Sciences

Abstract

Phagocytosis is the central process by which macrophage cells internalize and eliminate infectious microbes as well as apoptotic cells. During maturation, phagosomes containing engulfed particles fuse with various endosomal compartments through the action of regulatory molecules on the phagosomal membrane. In this study, we performed a proteomic analysis of the membrane fraction from latex bead-containing (LBC) phagosomes isolated from macrophages. The profile, which comprised 546 proteins, suggests diverse functions of the phagosome and potential connections to secretory processes, toll-like receptor signaling, and autophagy. Many identified proteins were not previously known to reside in the phagosome. We characterized several proteins in LBC phagosomes that change in abundance on induction of autophagy, a process that has been previously implicated in the host defense against microbial pathogens. These observations suggest crosstalk between autophagy and phagocytosis that may be relevant to the innate immune response of macrophages.

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  • Proteomics analysis of purified phagosome membranes in cells that have taken up differing cargoes by phagocytosis revealed that absence of TLR signaling leads to failure of LC3 recruitment to phagosome membranes.

    “Proteomics analysis of purified phagosome membranes in cells that have taken up differing cargoes by phagocytosis has revealed that the absence of TLR signaling leads to failure of LC3 recruitment to phagosome membranes [18,39].”

    From LC3-Associated Phagocytosis (LAP): Connections with Host Autophagy (2012) · cites this paper as [39]

    The Results and Discussion sections on validation and autophagy induction report proteomic identification of LC3-II on latex-bead phagosome membranes and show that 3-MA treatment abolished GFP-LC3 recruitment. They do not report a comparison of differing phagocytic cargoes or show that absence of TLR signaling caused recruitment to fail; the reported inhibition was attributed to PI3K inhibition. (LLM, conf=0.88)

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Cited by

Sorted by citations

Authors
Shui, W., Sheu, L., Liu, J., Smart, B., Petzold, C. J., Hsieh, T.-Y., Pitcher, A., Keasling, J. D., & Bertozzi, C. R.
Affiliations
  • Howard Hughes Medical Institute (US)
  • Molecular and Cell Biology, and
  • Biological Products Division, Bayer HealthCare LLC, Berkeley, CA 94701;
  • Departments of Chemistry,
  • Physical Bioscience Division, and
  • Joint BioEnergy Institute (US)
Venue
Proceedings of the National Academy of Sciences
Published
2008-11-04
Volume
105
Issue
44
Pages
16952-16957
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2089438839
Cited by
114
References
3
Citations by year
2026: 2 · 2025: 4 · 2024: 8 · 2023: 5 · 2022: 2 · 2021: 10 · 2020: 4 · 2019: 4 · 2018: 5 · 2017: 4 · 2016: 5 · 2015: 2 · 2014: 7 · 2013: 6 · 2012: 15
FWCI
7.69
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • University of North Texas Digital Library (University of North Texas) (submittedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
  • OSTI OAI (U.S. Department of Energy Office of Scientific and Technical Information) (submittedVersion)
Funders
  • Howard Hughes Medical Institute
  • National Institute of Allergy and Infectious Diseases (R01AI051622, AI 51622)
Topics
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
Keywords
phagocytosis, autophagy, macrophages, phagosome maturation, endosomal membrane fusion, Toll-like receptor signaling, innate immunity, host defense against infection
MeSH terms
Animals, Autophagy, Cell Membrane, Macrophages, Membrane Proteins, Phagocytosis, Phagosomes, Proteome, Proteomics, Mice

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