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Cited by 33Phagocytosis and Immune RegulationCell death mechanisms and regulationBlood Coagulation and Thrombosis Mechanisms

Regulation of phagocytosis by TAM receptors and their ligands

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Lu, Qingxian, Li, Qiutang, Lu, Qingjun·2010·Frontiers in Biology
DOI 10.1007/s11515-010-0034-5PMC PMC2971555
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Abstract

The TAM family of receptors is preferentially expressed by professional and non-professional phagocytes, including macrophages, dendritic cells and natural killer cells in the immune system, osteoclasts in bone, Sertoli cells in testis, and retinal pigmental epithelium cells in the retina. Mutations in the Mertk single gene or in different combinations of the double or triple gene mutations in the same cell cause complete or partial impairment in phagocytosis of their preys; and as a result, either the normal apoptotic cells cannot be efficiently removed or the tissue neighbor cells die by apoptosis. This scenario of TAM regulation represents a widely adapted model system used by phagocytes in all different tissues. The present review will summarize current known functional roles of TAM receptors and their ligands, Gas 6 and protein S, in the regulation of phagocytosis.

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  • Activation of the tyrosine kinase of TAM receptors upon ligand binding recruits the p85 subunit of PI3K and activates PI3K/Akt signaling.

    “Activation of the tyrosine kinase of TAM receptors upon ligand binding recruits the p85 subunit of PI3K and activates PI3K/Akt signaling [147–150].”

    From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [150]

    Sections 2 and 11 describe ligand-linked TAM receptor phosphorylation, and Section 4 reports association of the p85 subunit of PI3K with Mertk and identifies PI3K as a signaling pathway. The body text does not state that this recruitment activates Akt; Akt appears only in the title of a cited work in the References. The supported mechanism is also described specifically for Mertk, rather than demonstrated here for every TAM receptor. (LLM, conf=0.86)

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Cited by

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Authors
Lu, Q., Li, Q., & Lu, Q.
Affiliations
  • Beijing Tongren Hospital (CN)
  • University of Louisville (US)
Corresponding author
Lu, Qingxian
Venue
Frontiers in Biology
Publisher
Springer Science and Business Media LLC
Published
2010-06
Volume
5
Issue
3
Pages
227-237
ISSN
  • 1673-3509 (ISSN-L)
  • 1674-7984
  • 1674-7992
DOI
10.1007/s11515-010-0034-5
PMC
PMC2971555
OpenAlex
W1601842221
Cited by
33
References
14
Citations by year
2026: 1 · 2025: 1 · 2024: 4 · 2023: 3 · 2022: 1 · 2021: 2 · 2020: 3 · 2019: 3 · 2018: 1 · 2017: 2 · 2016: 1 · 2015: 1 · 2014: 5 · 2013: 2 · 2012: 2
FWCI
0.55
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Frontiers in Biology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Research to Prevent Blindness
  • National Natural Science Foundation of China
  • National Institutes of Health
  • National Eye Institute (R01EY018830)
  • National Center for Research Resources (P20RR018733, P20RR017702)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
Keywords
TAM receptors, phagocytosis, Gas6, protein S, MERTK, receptor tyrosine kinase, efferocytosis, macrophages, dendritic cells, natural killer cells, osteoclasts, Sertoli cells, retinal pigment epithelium

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