Affinage

FCER1G

High affinity immunoglobulin epsilon receptor subunit gamma · UniProt P30273

Length
86 aa
Mass
9.7 kDa
Annotated
2026-04-28
39 papers in source corpus 20 papers cited in narrative 20 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FCER1G encodes FcεRIγ, an ITAM-containing transmembrane adaptor that is essential for surface expression, maturation, and signal transduction of diverse activating immune receptors including FcεRI, NKp46, NKp30, PIR-A3, Mincle/MCL, DCAR1, and activating KIRs. FcεRIγ associates with partner receptor chains via a transmembrane arginine; in its absence, receptors such as FcεRIα accumulate in the ER as immature, core-glycosylated forms unable to traffic to the cell surface (PMID:12671054, PMID:31220194, PMID:29895693). Upon receptor cross-linking, dual phosphorylation of the FcεRIγ ITAM tyrosines creates a high-affinity (Kd ~1.4 nM) docking site for the tandem SH2 domains of Syk, initiating downstream Syk/AKT/NF-κB signaling that drives effector functions including degranulation, phagocytosis, ADCC, and cytokine production (PMID:8810294, PMID:31216232, PMID:41481135). FcεRIγ protein levels are regulated post-translationally by a USP5/Cbl-b ubiquitylation axis that controls K48-linked polyubiquitin-mediated degradation, and transcriptionally by DNA methylation of the FCER1G promoter, whose demethylation drives de novo expression in monocytes, CD8+ T cells, and NK cells (PMID:40729432, PMID:22150093, PMID:29895693, PMID:36066491).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1996 High

    Establishing how ITAM phosphorylation couples FcεRIγ to downstream kinase recruitment resolved the molecular basis of signal initiation: the dual-phosphorylated γ ITAM binds Syk tandem SH2 domains with nanomolar affinity in a crossed orientation requiring both phosphotyrosines.

    Evidence Scintillation proximity assay with radiolabeled phosphopeptides and SH2 domain knockout constructs in vitro

    PMID:8810294

    Open questions at the time
    • No structural data for the full-length γ–Syk complex
    • Binding measured with peptides rather than intact receptor
    • Kinetic parameters of association/dissociation not reported
  2. 1998 High

    Determining whether FcεRIγ functions beyond FcεRI, triple-knockout mice revealed that FcεRIγ can partially substitute for ζ/η chains in TCR complexes, establishing it as a shared ITAM adaptor across receptor families.

    Evidence Compound ζ/η/FcεRIγ knockout mice with flow cytometric analysis of T cell development

    PMID:9529325

    Open questions at the time
    • Quantitative contribution of FcεRIγ versus ζ/η to TCR signaling strength not resolved
    • Tissue-specific expression patterns not fully mapped
  3. 1999 High

    Identifying how activating receptors beyond FcεRI engage FcεRIγ, the demonstration that PIR-A3 associates via a transmembrane arginine (Arg632) established the charged-residue pairing mechanism now recognized as a general rule for FcεRIγ-dependent receptor assembly.

    Evidence Co-IP from transfected 293T cells with Arg632 point mutants and nitric oxide functional assay in macrophages

    PMID:10477705

    Open questions at the time
    • Structural basis of transmembrane arginine–aspartate pairing not resolved at atomic level
    • Other PIR-A family members' dependence on FcεRIγ not systematically tested
  4. 2003 High

    Revealing FcεRIγ as the rate-limiting chaperone for FcεRI surface expression showed that without γ, the α chain accumulates as a core-glycosylated ER-retained form, thus coupling γ expression level directly to receptor density and allergic responsiveness.

    Evidence Co-IP, glycosylation-state Western blot, ER/Golgi colocalization in atopic vs. non-atopic dendritic cells

    PMID:12671054

    Open questions at the time
    • Identity of ER quality-control machinery retaining unassembled α chain unknown
    • Stoichiometry of αβγ2 assembly intermediates not defined
  5. 2004 Medium

    Extension to NK cell biology: NKp46 was shown to associate with both FcεRIγ and CD3ζ, linking γ-chain signaling to NK cytotoxicity pathways.

    Evidence IP and Western blot from IL-2-activated primary rat NK cells with redirected lysis assay

    PMID:15356098

    Open questions at the time
    • Relative contribution of FcεRIγ vs. CD3ζ to NKp46 signaling not dissected
    • Not confirmed with knockout cells at this stage
  6. 2011 High

    Identification of DNA methylation as the transcriptional switch for FCER1G expression explained how monocytes acquire FcεRI: promoter hypomethylation directly increases γ transcription and receptor surface density.

    Evidence Bisulfite sequencing, patch-methylation luciferase reporter, 5-azacytidine treatment in healthy monocytes

    PMID:22150093

    Open questions at the time
    • Upstream signals initiating demethylation in vivo not identified
    • Transcription factors binding the demethylated promoter not characterized
  7. 2013 High

    Discovery of the Mincle/MCL/FcεRIγ trimeric complex revealed that FcεRIγ can be recruited indirectly through a bridging receptor (Mincle), expanding the modes of γ-dependent receptor assembly beyond direct transmembrane pairing.

    Evidence Reciprocal co-IP from rat primary cells and phagocytosis assay

    PMID:23921530

    Open questions at the time
    • Stoichiometry of the trimeric complex not determined
    • Whether MCL contributes signaling or only scaffolding is unclear
  8. 2018 High

    Demonstrating that IL-15-driven promoter demethylation induces de novo FcεRIγ in CD8+ T cells, and that γ is required for NKp30 surface expression, revealed a cytokine–epigenetic axis that arms T cells with innate-like receptor function.

    Evidence siRNA knockdown with NKp30 surface expression readout, promoter methylation analysis, xenograft model

    PMID:29895693

    Open questions at the time
    • Whether IL-15-induced demethylation is mediated by TET enzymes not tested
    • In vivo relevance in human disease settings not established
  9. 2019 High

    Multivalent binding studies and Fcer1g-knockout NK cells clarified that Syk engages γ ITAM dimers in cis and trans configurations modulated by Y130 autophosphorylation, and that γ loss selectively destabilizes NKp46 to impair antiviral NK responses.

    Evidence MD simulation with reconstitution in γ-KO cells expressing disulfide-linked γ variants; Fcer1g−/− mice infected with LCMV

    PMID:31216232 PMID:31220194

    Open questions at the time
    • Relative physiological importance of cis vs. trans Syk engagement in intact cells unknown
    • Whether NKp46 instability reflects misfolding or accelerated degradation not resolved
  10. 2022 Medium

    Linking FcεRIγ protein levels to mTOR-dependent proliferation and cytokine milieu explained how adaptive-like (FcεRIγ-low) NK cells arise: TGFβ and IFNα suppress proliferation and thereby limit γ upregulation.

    Evidence Rapamycin treatment in vivo/in vitro, cytokine stimulation/blocking, flow cytometry for FcεRIγ protein

    PMID:36066491

    Open questions at the time
    • Whether mTOR acts at translational or epigenetic level on FCER1G not distinguished
    • Relationship between proliferation-dependent γ expression and promoter methylation not clarified
  11. 2024 Medium

    Biochemical confirmation that covalent small molecules targeting the Syk tandem SH2 domains can disrupt the phospho-γ ITAM–Syk interaction validated this interface as a druggable node.

    Evidence TR-FRET binding assay and high-throughput covalent inhibitor screening

    PMID:38359047

    Open questions at the time
    • Selectivity of covalent inhibitors over other SH2-domain proteins not fully profiled
    • No cellular efficacy data reported
    • In vivo pharmacology unknown
  12. 2025 High

    Identification of USP5 as the deubiquitylase that removes K48-linked polyubiquitin from FcεRIγ, opposing Cbl-b-mediated degradation, established the first post-translational stability mechanism for γ and linked it to mast cell degranulation and allergic inflammation in vivo.

    Evidence Co-IP, K48-linkage-specific ubiquitylation assay, USP5 knockdown, Cbl-b competition, USP5 inhibitor WP1130 in mouse allergy model

    PMID:40729432

    Open questions at the time
    • Whether other E3 ligases besides Cbl-b ubiquitylate FcεRIγ not tested
    • Structural basis of USP5–FcεRIγ recognition unknown
    • Relevance of this axis in non-mast cell lineages not examined
  13. 2026 Medium

    Demonstration that FcεRIγ mediates ADCC in double-negative T cells through a Syk/AKT/NF-κB cascade extended the effector role of γ-chain signaling beyond classical NK and mast cells to unconventional T cell subsets.

    Evidence Fcer1g-deficient DNT cells, Syk inhibition, cytotoxicity assay, subcutaneous tumor model, Western blot for AKT/NF-κB phosphorylation

    PMID:41481135

    Open questions at the time
    • Mechanism of IgG1 Fc receptor expression on DNT cells not identified
    • Whether γ-chain signaling in DNT cells utilizes DAP12 as alternative not excluded
    • Single-lab finding

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the atomic structure of intact FcεRIγ in complex with partner receptors and Syk, the identity of transcription factors that bind the demethylated FCER1G promoter to drive lineage-specific expression, and the interplay between mTOR-dependent translational control and epigenetic regulation of FCER1G.
  • No high-resolution structure of full-length γ in any receptor complex
  • Transcription factor(s) driving FCER1G expression after demethylation not identified
  • Relative contributions of transcriptional vs. post-translational regulation in different immune lineages not systematically compared

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 6 GO:0060089 molecular transducer activity 4
Localization
GO:0005886 plasma membrane 5 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-168256 Immune System 10 R-HSA-162582 Signal Transduction 6 R-HSA-392499 Metabolism of proteins 1
Partners
CBLBCLEC4DCLEC4EFCER1ANCR1NCR3SYKUSP5
Complex memberships
FcεRI (αβγ2)Mincle/MCL/FcεRIγTCR/CD3 complex (γ-containing variant)

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1996 The dual phosphorylated FcεRIγ ITAM binds to the tandem SH2 domains of p72Syk with high affinity (Kd ~1.4 nM), requiring both tyrosine residues to be phosphorylated; both N-terminal and C-terminal SH2 domains contribute cooperatively, with the preferred binding orientation having the N-terminal phosphotyrosine occupying the C-terminal SH2 domain and vice versa. Scintillation proximity assay with 125I-labeled phosphopeptides, competition binding, SH2 domain knockout constructs The Journal of biological chemistry High 8810294
1998 FcεRIγ (Fcgamma) functions as a signal-transducing subunit in TCR complexes; in the absence of zeta/eta chains, FcεRIγ can partially substitute, but T cells lacking all three zeta-family members (zeta, eta, FcεRIγ) still develop some αβ-T cells via zeta-family-independent surface complexes. FcεRIγ and zeta/eta have distinct expression patterns that impart distinctive signaling properties to TCR complexes on specific T cell populations. Triple knockout mouse generation (zeta/eta/FcεRIγ-deficient), flow cytometry, phenotypic comparison of single and compound knockouts The Journal of experimental medicine High 9529325
1999 PIR-A3 physically interacts with FcεRIγ through its transmembrane domain arginine residue (Arg632); this interaction is required for PIR-A3-mediated macrophage activation (synergy with IFN-γ for nitric oxide production). Chimeric receptor cotransfection in 293T cells and ANA-1 macrophages, co-immunoprecipitation, nitric oxide functional assay with point mutants Blood High 10477705
2003 FcεRIγ is mandatory for surface expression of FcεRI on dendritic cells; without FcεRIγ, the FcεRIα chain accumulates in the ER in an immature, core-glycosylated form. When FcεRIγ is present (as in atopic DCs), it co-precipitates with FcεRIα, allowing maturation and complex glycosylation of FcεRIα and its transport through the Golgi to the cell surface. Co-immunoprecipitation, subcellular fractionation/colocalization (ER vs. Golgi), Western blot for glycosylation state, flow cytometry The Journal of clinical investigation High 12671054
2004 Rat NKp46 associates with both FcεRIγ and CD3ζ (ITAM-bearing adaptor proteins) in NK cells, enabling NK cell cytotoxic activation by similar pathways as CD16. Immunoprecipitation and Western blot from IL-2-activated NK cell lysates, redirected lysis assay with antibody F(ab')2 fragments Journal of leukocyte biology Medium 15356098
2007 IgE-mediated phosphorylation of FcεRIγ ITAM tyrosines is inhibited by the antiallergic drug azelastine in RBL-2H3 cells, without affecting FcεRI subunit mRNA or protein levels or assembly; this identifies ITAM phosphorylation as the drug's target in blocking FcεRI signaling cascade initiation. Immunoprecipitation of IgE-bound FcεRI, Western blot with anti-phosphotyrosine, northern blot for mRNA levels International immunopharmacology Medium 17499202
2011 Hypomethylation of the FCER1G promoter directly drives increased FcεRIγ transcription and surface FcεRI expression on monocytes; patch methylation of the promoter reduced luciferase reporter activity ~2.8-fold, and treatment with 5-azacytidine caused promoter demethylation and induced FcεRIγ transcription and FcεRI surface expression in healthy monocytes. Bisulfite sequencing, patch-methylation luciferase reporter assay, 5-azacytidine treatment, real-time RT-PCR, flow cytometry Allergy High 22150093
2013 Mincle and MCL form heteromers on the cell surface; MCL associates with FcεRIγ via Mincle (not directly), forming a Mincle/MCL/FcεRIγ trimeric complex. Association with MCL and FcεRIγ increased Mincle surface expression and enhanced phagocytosis of antibody-coated beads. Flow cytometry, co-immunoprecipitation from rat primary cells and cell lines, phagocytosis assay European journal of immunology High 23921530
2014 Type II phosphatidylinositol 4-kinases (PtdIns 4-kinases) associate with the FcεRIγ subunit via the ITAM tyrosine residues (Y65 and Y76); FcεRI ligation increases this association threefold, and mutation of both ITAM tyrosines abolishes the interaction. Anti-FcεRIγ immunoprecipitation with kinase activity assay, ITAM tyrosine mutants in RBL-2H3 cells Molecular and cellular biochemistry Medium 24481753
2017 FcεRIγ (Fcer1g) on myeloid APCs plays a regulatory role in limiting B cell extrafollicular plasmablast responses; mice lacking Fcer1g (in non-B cells) showed markedly enhanced and prolonged anti-self autoantibody responses, an effect dependent on CD40L, indicating FcRγ on myeloid cells downregulates T cell help. Adoptive transfer of autoreactive B cells into Fcer1g-/- recipient mice, flow cytometry, CD40L-blocking antibody epistasis Journal of immunology Medium 28659358
2018 IL-15 induces de novo FcεRIγ expression in a CD8+ T cell subset, and FcεRIγ is required for NKp30 surface expression and function in these cells; FcεRIγ expression required promoter demethylation and was accompanied by acquisition of Syk and PLZF. Flow cytometry, intracellular staining, promoter methylation analysis, siRNA knockdown of FcεRIγ with functional NKp30 surface expression readout, xenograft mouse model Proceedings of the National Academy of Sciences of the United States of America High 29895693
2019 Syk binds FcεRIγ ITAM via multivalent cis and trans configurations of its tandem SH2 domains; multivalent interactions improve cis-oriented binding by ~three orders of magnitude. Syk autophosphorylation on Y130 in interdomain A modulates the cis/trans binding bias. Short distances between γ ITAM pairs are required for trans docking. Molecular dynamics simulation, hybrid MD/worm-like chain polymer modeling, live cell imaging in γ-KO reconstituted cells expressing disulfide-linked γ subunits or monomeric ITAM/hemITAM chimeras, Y130E phosphomimetic mutant analysis Molecular biology of the cell High 31216232
2019 FcεRIγ stabilizes NKp46 expression on NK cells; Fcer1g-/- NK cells have reduced NKp46 but normal levels of other activating receptors, and this specifically limits their ability to regulate virus-specific CD8+ T cell responses during chronic LCMV infection. Fcer1g-/- mice, flow cytometry for NK receptor expression, LCMV infection model, adoptive transfer experiments PLoS pathogens High 31220194
2019 DCAR1 associates with FcεRIγ adaptor protein; this association enables efficient phagocytosis of antibody-coated beads and cross-linking of DCAR1 leads to reactive oxygen species production in eosinophils. Co-immunoprecipitation, phagocytosis assay with antibody-coated beads, ROS production assay Frontiers in immunology Medium 31134097
2021 Rhesus macaque activating KIRs associate with FcεRIγ (not DAP12) through a positively charged arginine in their transmembrane region; this association results in increased and stabilized surface expression of KIR3DS05 and enables signal transduction upon ligand binding. Co-immunoprecipitation from transfected and primary cells, flow cytometry for surface expression, functional signaling assays Frontiers in immunology Medium 33968088
2022 FcεRIγ upregulation in NK cells is dependent on cell proliferation mediated by IL-2, IL-15, or IL-12, is sensitive to mTOR suppression, and is inhibited by TGFβ or IFNα; diminished proliferation drives the adaptive-like FcεRIγ-low NK cell phenotype. Pharmacological mTOR inhibition (rapamycin) in vivo and in vitro, cytokine stimulation/blocking, flow cytometry for FcεRIγ protein, proliferation assays The Journal of experimental medicine Medium 36066491
2023 Inhibition of FCER1G in CD4+ T cells (via DNA hypermethylation of its promoter) mediates resistance to cyclosporin A plus corticosteroid treatment; CLB reverses this resistance by inducing FCER1G expression through DNA demethylation. RNA sequencing, TMT proteomics, gain- and loss-of-function assays, rescue assays, methylation analysis of FCER1G promoter in patient CD4+ T cells Clinical immunology Medium 37821074
2024 The doubly phosphorylated FCER1G ITAM peptide binds the tandem SH2 domains of SYK (SYK-tSH2), enabling SYK activation via phosphorylation; covalent small molecules targeting SYK-tSH2 can disrupt this interaction, inhibiting SYK activation. Biochemical binding assay (TR-FRET), biophysical orthogonal assays, high-throughput screening, covalent inhibitor characterization PloS one Medium 38359047
2025 USP5 deubiquitylase interacts with FcεRIγ in mast cells, removing K48-linked polyubiquitin chains to stabilize FcεRIγ protein; USP5 knockdown increased binding of the E3 ligase Cbl-b to FcεRIγ, leading to increased polyubiquitylation and degradation of FcεRIγ, and attenuated IgE-induced mast cell activation and allergic inflammation. Co-immunoprecipitation, USP5 knockdown, Cbl-b interaction assay, ubiquitylation assay (K48-linkage specific), USP5 inhibitor (WP1130) in mouse allergy model, β-hexosaminidase/histamine release assay Science signaling High 40729432
2026 FcεRIγ mediates antibody-dependent cellular cytotoxicity (ADCC) in double-negative T (DNT) cells by activating the FcεRIγ/Syk/AKT/NF-κB signaling pathway upon IgG1 binding; Fcer1g-deficient DNT cells fail to respond to IgG1 stimulation and show no enhancement of tumor cell killing. Fcer1g-deficient DNT cells, Syk inhibition, flow cytometry for IgG Fc receptor/cytotoxic molecule expression, in vitro cytotoxicity assay, subcutaneous tumor model, Western blot for AKT and NF-κB phosphorylation Journal of molecular cell biology Medium 41481135

Source papers

Stage 0 corpus · 39 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2003 Evidence for a differential expression of the FcepsilonRIgamma chain in dendritic cells of atopic and nonatopic donors. The Journal of clinical investigation 95 12671054
2013 Mincle, the receptor for mycobacterial cord factor, forms a functional receptor complex with MCL and FcεRI-γ. European journal of immunology 90 23921530
2011 Demethylation of the FCER1G promoter leads to FcεRI overexpression on monocytes of patients with atopic dermatitis. Allergy 64 22150093
2018 Distinct human circulating NKp30+FcεRIγ+CD8+ T cell population exhibiting high natural killer-like antitumor potential. Proceedings of the National Academy of Sciences of the United States of America 61 29895693
2004 Rat NKp46 activates natural killer cell cytotoxicity and is associated with FcepsilonRIgamma and CD3zeta. Journal of leukocyte biology 59 15356098
1996 Interaction of phosphorylated FcepsilonRIgamma immunoglobulin receptor tyrosine activation motif-based peptides with dual and single SH2 domains of p72syk. Assessment of binding parameters and real time binding kinetics. The Journal of biological chemistry 54 8810294
1998 T cell development in mice lacking all T cell receptor zeta family members (Zeta, eta, and FcepsilonRIgamma). The Journal of experimental medicine 42 9529325
2019 NK cell-intrinsic FcεRIγ limits CD8+ T-cell expansion and thereby turns an acute into a chronic viral infection. PLoS pathogens 41 31220194
2022 Diminished cell proliferation promotes natural killer cell adaptive-like phenotype by limiting FcεRIγ expression. The Journal of experimental medicine 36 36066491
2021 FcεRIγ-negative NK cells persist in vivo and enhance efficacy of therapeutic monoclonal antibodies in multiple myeloma. Blood advances 30 34357379
1999 Functional association of FcepsilonRIgamma with arginine(632) of paired immunoglobulin-like receptor (PIR)-A3 in murine macrophages. Blood 27 10477705
2017 B Cell-Extrinsic Myd88 and Fcer1g Negatively Regulate Autoreactive and Normal B Cell Immune Responses. Journal of immunology (Baltimore, Md. : 1950) 26 28659358
2012 Altered expression of the TCR signaling related genes CD3 and FcεRIγ in patients with aplastic anemia. Journal of hematology & oncology 22 22401598
2019 Phenotypic and Functional Analysis of Human NK Cell Subpopulations According to the Expression of FcεRIγ and NKG2C. Frontiers in immunology 21 31867015
2021 FCER1G and PTGS2 Serve as Potential Diagnostic Biomarkers of Acute Myocardial Infarction Based on Integrated Bioinformatics Analyses. DNA and cell biology 19 34115526
2016 NK cells lacking FcεRIγ are associated with reduced liver damage in chronic hepatitis C virus infection. European journal of immunology 18 26712042
2019 Combinatorial diversity of Syk recruitment driven by its multivalent engagement with FcεRIγ. Molecular biology of the cell 17 31216232
2012 Expression feature of CD3, FcεRIγ, and Zap-70 in patients with chronic lymphocytic leukemia. Hematology (Amsterdam, Netherlands) 15 22664044
2024 Characterization of covalent inhibitors that disrupt the interaction between the tandem SH2 domains of SYK and FCER1G phospho-ITAM. PloS one 8 38359047
2022 FCER1G Gene Hypomethylation in Patients with Rheumatoid Arthritis. Journal of clinical medicine 8 36012903
2021 Rhesus Macaque Activating Killer Immunoglobulin-Like Receptors Associate With Fc Receptor Gamma (FCER1G) and Not With DAP12 Adaptor Proteins Resulting in Stabilized Expression and Enabling Signal Transduction. Frontiers in immunology 6 33968088
2019 Dendritic Cell Activating Receptor 1 (DCAR1) Associates With FcεRIγ and Is Expressed by Myeloid Cell Subsets in the Rat. Frontiers in immunology 6 31134097
2023 Characterization of covalent inhibitors that disrupt the interaction between the tandem SH2 domains of SYK and FCER1G phospho-ITAM. bioRxiv : the preprint server for biology 4 37547005
2013 [Construction of special reporter to detect DNA methylation regulatory activity in FCER1G gene promoter through patch-methylation]. Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences 4 23456064
2024 FCER1G as a novel immune-associated blood biomarker in cardiogenic stroke. Heliyon 3 39071704
2022 Identification of FCER1G related to Activated Memory CD4+ T Cells Infiltration by Gene Co-expression Network and Construction of a Risk Prediction Module in Diffuse Large B-Cell Lymphoma. Frontiers in genetics 3 35711924
2014 Type II phosphatidylinositol 4-kinases interact with FcεRIγ subunit in RBL-2H3 cells. Molecular and cellular biochemistry 3 24481753
2007 Inhibition of IgE-mediated phosphorylation of FcepsilonRIgamma protein by antiallergic drugs in rat basophilic leukemia (RBL-2H3) cells: a novel action of antiallergic drugs. International immunopharmacology 3 17499203
2024 Development of a time-resolved fluorescence resonance energy transfer ultra-high throughput screening assay targeting SYK and FCER1G interaction. SLAS discovery : advancing life sciences R & D 2 39154664
2023 Phenotypic and functional analysis in HER2+ targeted therapy of human NK cell subpopulation according to the expression of FcεRIγ and NKG2C in breast cancer patients. Cancer immunology, immunotherapy : CII 2 37081323
2023 Skipping of FCER1G Exon 2 Is Common in Human Brain But Not Associated with the Alzheimer's Disease Genetic Risk Factor rs2070902. Journal of Alzheimer's disease reports 2 38143775
2025 USP5 deubiquitylates and stabilizes FcεRIγ to enhance IgE-induced mast cell activation and allergic inflammation. Science signaling 1 40729432
2023 Identification of FCER1G as a cyclosporin A plus corticosteroid sensitization gene in female patients with Vogt-Koyanagi-Harada disease. Clinical immunology (Orlando, Fla.) 1 37821074
2026 FcεRIγ Reinforces Double-Negative T cell-mediated Antibody-dependent Cellular Cytotoxicity Against Tumor Cells. Journal of molecular cell biology 0 41481135
2026 A macrophage-induced subpopulation of mesenchymal cells expressing Fcer1g contributes to wound-induced fibrosis. Nature communications 0 41680182
2026 Fcer1g and St3gal1: Macrophage-associated angiogenesis biomarkers and therapeutic targets in sepsis-induced acute lung injury. PloS one 0 41758834
2026 FCER1G: A multifunctional regulator in the immune microenvironment (Review). Experimental and therapeutic medicine 0 41994604
2025 Comprehensive analysis reveals the tumor suppressor role of macrophage signature gene FCER1G in hepatocellular carcinoma. Scientific reports 0 39893200
2024 Development of a Time-Resolved Fluorescence Resonance Energy Transfer ultra-high throughput screening assay for targeting SYK and FCER1G interaction. bioRxiv : the preprint server for biology 0 38915662