Affinage

FCER1G

High affinity immunoglobulin epsilon receptor subunit gamma · UniProt P30273

Length
86 aa
Mass
9.7 kDa
Annotated
2026-06-09
40 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

FCER1G (FcεRIγ) is a transmembrane ITAM-bearing adaptor subunit that couples a broad array of immune-activating receptors to intracellular tyrosine-kinase signaling (PMID:8810294, PMID:15356098). Its central biochemical activity is presentation of a dual-phosphorylated ITAM to the tandem SH2 domains of Syk, which it binds with high affinity (Kd ~1.4 nM) in a cooperative, orientation-specific manner, whereas monophosphorylated ITAM binds far more weakly (PMID:8810294); multivalent cis and trans docking configurations on γ homodimers, tuned by Syk Y130 autophosphorylation and by the spacing between paired ITAMs, further govern Syk recruitment (PMID:31216232). ITAM tyrosine phosphorylation is a discrete, druggable initiation step in receptor signaling (PMID:17499203, PMID:38359047), and the assembled FcεRIγ/Syk module drives downstream activation through the Syk/AKT/NF-κB axis to mediate effector functions such as antibody-dependent cytotoxicity (PMID:41481135). FcεRIγ acts as an obligate assembly and trafficking partner for partner receptors: it is rate-limiting for surface expression of FcεRIα, allowing it to mature past the ER and traffic to the cell surface (PMID:12671054), and it stabilizes the surface expression of NK-cell activating receptors NKp46 and NKp30 (PMID:31220194, PMID:29895693). Through transmembrane charge-pair interactions it serves as the activating adaptor for diverse receptors including PIR-A, NKp46, Mincle/MCL, DCAR1, and activating KIR, enabling phagocytosis, ROS production, nitric oxide release, and cytotoxicity (PMID:10477705, PMID:15356098, PMID:23921530, PMID:31134097, PMID:33968088). FcεRIγ abundance is controlled at multiple levels: its transcription is repressed by FCER1G promoter DNA methylation and induced upon demethylation (PMID:22150093, PMID:23456064), its surface availability is coupled to proliferation/mTOR signaling (PMID:36066491), and its protein stability is set by a K48-ubiquitylation switch in which Cbl-b targets it for degradation and the deubiquitylase USP5 reverses this to stabilize it (PMID:40729432). Beyond its canonical activating role, FcεRIγ on myeloid antigen-presenting cells negatively regulates extrafollicular B-cell responses in a CD40L-dependent manner (PMID:28659358), and it can substitute for ζ/η chains in the TCR complex during T-cell development (PMID:9529325).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 1996 High

    Established the core biochemical logic of FcεRIγ signaling: how the phosphorylated ITAM is read by Syk, defining affinity, cooperativity, and orientation requirements.

    Evidence In vitro scintillation proximity and competition binding with 125I-ITAM peptides and SH2-domain knockout mutants

    PMID:8810294

    Open questions at the time
    • Performed with isolated peptides and domains, not intact receptor complexes
    • Did not address kinase activation downstream of docking
  2. 1998 High

    Showed FcεRIγ is functionally interchangeable with ζ/η chains as a TCR signal-transducing subunit, revealing a shared ITAM-adaptor role across receptor families.

    Evidence Single and triple ζ-family knockout mice analyzed for αβ-T cell development by flow cytometry

    PMID:9529325

    Open questions at the time
    • Did not define the molecular signaling differences between γ and ζ in the TCR
    • Low residual T cell numbers leave quantitative contribution unclear
  3. 1999 High

    Defined the transmembrane charge-pair mechanism by which a partner receptor (PIR-A3) physically engages FcεRIγ to deliver activation signals.

    Evidence Chimeric receptor cotransfection, co-IP with endogenous FcεRIγ, Arg632 point mutant, and nitric oxide functional assay

    PMID:10477705

    Open questions at the time
    • Single receptor pairing; generality across receptors not yet shown
    • Downstream signaling steps not dissected
  4. 2003 High

    Revealed FcεRIγ as an obligate assembly/trafficking chaperone, rate-limiting for surface delivery of FcεRIα.

    Evidence Reciprocal co-IP, glycosylation maturation analysis, and confocal colocalization in monocyte-derived dendritic cells

    PMID:12671054

    Open questions at the time
    • Mechanism of ER-to-Golgi escort not resolved at structural level
    • Did not address whether γ chaperones other partner receptors similarly
  5. 2004 Medium

    Extended the adaptor role to NK cytotoxicity by showing NKp46 uses FcεRIγ (and CD3ζ) for signal transduction.

    Evidence Co-IP from activated NK cells with redirected lysis and F(ab')2 blocking

    PMID:15356098

    Open questions at the time
    • Rat system; single lab
    • Relative contribution of γ vs ζ not quantified
  6. 2007 Medium

    Isolated ITAM tyrosine phosphorylation as a discrete, separable step in signaling, distinct from receptor expression and assembly.

    Evidence Pharmacological inhibition (azelastine) with phospho-γ Western blot and mRNA/protein controls in RBL-2H3 cells

    PMID:17499203

    Open questions at the time
    • Single cell line and single drug
    • Did not identify the kinase responsible for the phosphorylation step
  7. 2011 High

    Identified FCER1G promoter DNA methylation as a causal transcriptional control point governing FcεRIγ and surface FcεRI levels.

    Evidence Bisulfite sequencing, patch-methylation luciferase reporter, and 5-azacytidine demethylation in monocytes

    PMID:22150093

    Open questions at the time
    • Methyltransferases/demethylases acting at the locus not identified
    • Physiological signals controlling methylation state unknown
  8. 2013 Medium

    Confirmed and extended the methylation-dependent repression of the FCER1G promoter and showed γ assembly into a Mincle/MCL trimeric complex enhances phagocytosis.

    Evidence Patch-methylation luciferase reporter; co-IP, flow cytometry, and phagocytosis assays in rat cells

    PMID:23456064 PMID:23921530

    Open questions at the time
    • Reporter assays are in vitro reconstitutions
    • Stoichiometry and surface organization of the trimeric complex not resolved
  9. 2014 Medium

    Showed that ITAM tyrosines recruit effectors beyond Syk, coupling FcεRIγ to type II PtdIns 4-kinase upon receptor ligation.

    Evidence Anti-FcεRIγ IP with PtdIns 4-kinase activity assay and Y65F/Y76F ITAM mutants in RBL-2H3 cells

    PMID:24481753

    Open questions at the time
    • Direct vs indirect (Syk-bridged) association not distinguished
    • Functional consequence of lipid kinase coupling not defined
  10. 2017 Medium

    Uncovered a negative-regulatory role for FcεRIγ on myeloid APCs in restraining B-cell responses, broadening its biology beyond direct activation.

    Evidence Adoptive transfer into Fcer1g-/- and Myd88-/- mice with CD40L blockade epistasis

    PMID:28659358

    Open questions at the time
    • Receptor delivering the suppressive signal not identified
    • Molecular mechanism of CD40L-dependent downregulation unresolved
  11. 2018 Medium

    Linked FcεRIγ induction (via demethylation) to functional acquisition of NKp30 and NK-like cytotoxicity in CD8+ T cells.

    Evidence IL-15 stimulation, promoter demethylation analysis, cytotoxicity assays, and xenograft model

    PMID:29895693

    Open questions at the time
    • Correlative coupling of γ, Syk, and PLZF; causal ordering not established
    • Single lab
  12. 2019 High

    Defined the biophysics of Syk recruitment (cis/trans multivalent docking, ITAM spacing, Y130 autophosphorylation bias) and showed FcεRIγ stabilizes NKp46 surface protein independent of transcription, with in vivo immunological consequences.

    Evidence MD/polymer modeling with γ-KO reconstitution and engineered constructs; Fcer1g-/- mice in LCMV infection; co-IP/functional assays for DCAR1

    PMID:31134097 PMID:31216232 PMID:31220194

    Open questions at the time
    • Structural model of the multivalent docking states not experimentally resolved
    • Mechanism by which γ stabilizes partner surface protein not molecularly defined
  13. 2021 Medium

    Demonstrated adaptor specificity, showing activating KIR3DS05 selectively pairs with FcεRIγ rather than DAP12 for ligand-triggered signaling.

    Evidence Co-IP in transfected and primary cells with MHC-I ligand signaling assays

    PMID:33968088

    Open questions at the time
    • Structural basis of adaptor selectivity not defined
    • Rhesus system; single lab
  14. 2022 Medium

    Identified proliferation/mTOR signaling as a post-transcriptional determinant of FcεRIγ protein abundance in NK cells.

    Evidence Cytokine and mTOR-inhibitor treatments of NK cells with in vivo rapamycin clinical correlation

    PMID:36066491

    Open questions at the time
    • Molecular link between mTOR/proliferation and γ protein levels not defined
    • Correlative in vivo data
  15. 2024 Medium

    Validated the FcεRIγ ITAM–Syk-tSH2 interface as a tractable drug target via covalent small-molecule disruptors.

    Evidence HTS with TR-FRET and orthogonal PPI assays plus biophysical characterization of covalent SYK-tSH2 modification

    PMID:38359047

    Open questions at the time
    • Cellular and in vivo efficacy not established
    • Selectivity against other tSH2 proteins not characterized
  16. 2025 High

    Established a ubiquitin-based control of FcεRIγ stability, defining the Cbl-b/USP5 K48-ubiquitylation switch that tunes mast cell activation.

    Evidence Co-IP, K48-linkage-specific ubiquitylation assays, USP5 siRNA/inhibitor, and in vivo mouse allergy models

    PMID:40729432

    Open questions at the time
    • Signals that regulate Cbl-b/USP5 activity toward γ unknown
    • Whether this axis operates in non-mast-cell lineages not tested
  17. 2026 Medium

    Mapped the full effector signaling axis (FcεRIγ/Syk/AKT/NF-κB) underlying antibody-dependent cytotoxicity in double-negative T cells.

    Evidence Fcer1g-KO DNT cells, Syk inhibitor epistasis, phospho-AKT/NF-κB Western blots, and subcutaneous tumor model

    PMID:41481135

    Open questions at the time
    • Intermediate steps between Syk and AKT/NF-κB not delineated
    • Single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the diverse upstream regulatory inputs (DNA methylation, mTOR/proliferation, and Cbl-b/USP5 ubiquitylation) are integrated to set FcεRIγ levels in a given cell, and the structural basis of its selective pairing with distinct partner receptors, remain unresolved.
  • No unified model linking transcriptional, translational, and degradative control
  • No high-resolution structure of γ–partner-receptor transmembrane assemblies

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 6
Localization
GO:0005886 plasma membrane 3 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-168256 Immune System 4 R-HSA-162582 Signal Transduction 3
Partners
CBLBCLEC4D (MCL)FCER1ANCR1 (NKP46)NCR3 (NKP30)PIRASYKUSP5
Complex memberships
FcεRI (high-affinity IgE receptor)Mincle/MCL/FcεRIγ trimeric complexTCR-CD3 complex

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); both SH2 domains contribute cooperatively, with the preferred orientation placing the N-terminal phosphotyrosine at the C-terminal SH2 domain and the C-terminal phosphotyrosine at the N-terminal SH2 domain. Monophosphorylated peptides bind with substantially lower affinity. Scintillation proximity assay with 125I-labeled ITAM peptides, competition binding with C-terminal and N-terminal SH2 domain knockouts, saturation binding isotherms The Journal of biological chemistry High 8810294
1998 FcεRIγ can substitute for ζ/η chains as a signal-transducing subunit in TCR complexes during T cell development; mice lacking all three ζ-family members (ζ, η, FcεRIγ) still generate low numbers of αβ-T cells, demonstrating that TCR surface complexes lacking any ζ-family dimer can transduce developmental signals. ζ/η and FcεRIγ have distinct expression patterns correlated with thymus dependency. Genetic knockout mice lacking ζ/η, FcεRIγ, or all three; T cell development phenotyping by flow cytometry The Journal of experimental medicine High 9529325
1999 PIR-A3 physically interacts with FcεRIγ via an arginine residue (Arg632) in the PIR-A3 transmembrane domain; this interaction is required for PIR-A3 to deliver activation signals (nitric oxide production synergizing with IFN-γ) in macrophages. Cotransfection of CD4-PIR-A3 chimeric receptors in 293T cells, co-immunoprecipitation with endogenous FcεRIγ in ANA-1 macrophages, Arg632 point mutant, nitric oxide assay Blood High 10477705
2003 FcεRIγ expression is rate-limiting for surface expression of the high-affinity IgE receptor (FcεRI) on dendritic cells. Without FcεRIγ, FcεRIα accumulates as an immature, core-glycosylated form in the ER; co-expression of FcεRIγ allows FcεRIα to acquire complex glycosylation and traffic through the Golgi to the cell surface. FcεRIγ co-precipitates with FcεRIα. Co-immunoprecipitation, Western blot (glycosylation analysis), confocal microscopy/colocalization, monocyte-derived DC differentiation from atopic vs. normal donors The Journal of clinical investigation High 12671054
2004 Rat NKp46 associates with both FcεRIγ and CD3ζ as signal-transducing adaptor proteins, enabling NK cell cytotoxicity; this was demonstrated by co-immunoprecipitation from IL-2-activated NK cell lysates and confirmed by redirected lysis and F(ab')2 blocking assays. Immunoprecipitation/Western blot, redirected lysis assay, F(ab')2 blocking Journal of leukocyte biology Medium 15356098
2007 Antiallergic drug azelastine inhibits IgE-induced phosphorylation of FcεRIγ ITAM tyrosines in RBL-2H3 cells without affecting FcεRIγ mRNA or protein levels or the amount of γ chain assembled into IgE-bound FcεRI, indicating that ITAM tyrosine phosphorylation is a discrete step required for FcεRI signaling cascade initiation. Immunoprecipitation, Western blot for phospho-γ chain, Northern blot for mRNA levels, pharmacological inhibition in RBL-2H3 cells International immunopharmacology Medium 17499203
2011 Hypomethylation of the FCER1G promoter drives FcεRIγ transcription and surface FcεRI expression on monocytes; patch methylation luciferase reporter assay confirmed direct methylation-dependent repression of the FCER1G promoter, and treatment of healthy monocytes with 5-azacytidine reduced methylation and induced FcεRIγ transcription and surface FcεRI. Bisulfite sequencing, patch methylation luciferase reporter assay, 5-azacytidine demethylation, real-time RT-PCR, Western blot, flow cytometry Allergy High 22150093
2013 Mincle and MCL form heteromers on the cell surface; MCL associates with FcεRIγ via Mincle, forming a Mincle/MCL/FcεRIγ trimeric complex. Association with MCL and FcεRIγ increases Mincle surface expression and enhances phagocytosis of antibody-coated beads. Co-immunoprecipitation, flow cytometry, phagocytosis assay in rat primary cells and cell lines European journal of immunology Medium 23921530
2013 FCER1G promoter activity is methylation-sensitive: full methylation of the promoter regulatory element reduces luciferase reporter activity to ~36% of mock-methylated controls, directly demonstrating that DNA methylation represses FCER1G transcription. Patch-methylation luciferase reporter assay with full vs. mock methylated FCER1G promoter constructs Zhong nan da xue xue bao. Yi xue ban Medium 23456064
2014 Type II phosphatidylinositol 4-kinases (PtdIns 4-kinases) physically associate with the FcεRIγ subunit; this association increases threefold upon FcεRI ligation, and mutation of both canonical ITAM tyrosines (Y65 and Y76) abolishes the interaction, demonstrating that ITAM tyrosines are required for PtdIns 4-kinase coupling to FcεRIγ. Anti-FcεRIγ immunoprecipitation with PtdIns 4-kinase activity assay, ITAM tyrosine point mutants (Y65F, Y76F), RBL-2H3 cells Molecular and cellular biochemistry Medium 24481753
2017 FcεRIγ (Fcer1g) on non-B myeloid APCs negatively regulates B cell responses; mice lacking Fcer1g showed a markedly enhanced and prolonged extrafollicular plasmablast response, and this enhancement was CD40L-dependent, placing FcεRIγ on myeloid APCs in a pathway that downregulates T cell help. Adoptive transfer into Fcer1g-/- and Myd88-/- recipient mice, flow cytometry, antibody response quantification, CD40L blockade epistasis Journal of immunology Medium 28659358
2018 FcεRIγ is required for NKp30 cell-surface expression and function in IL-15-induced NKp30+CD8+ T cells; concomitant induction of FcεRIγ (via promoter demethylation) and NKp30 occurs, and FcεRIγ acquisition correlates with Syk and PLZF expression, enabling NK-like antitumor cytotoxicity. IL-15 stimulation of CD8+ T cells, flow cytometry, promoter demethylation analysis, in vitro cytotoxicity assays, xenograft mouse model Proceedings of the National Academy of Sciences of the United States of America Medium 29895693
2019 FcεRIγ on NK cells stabilizes NKp46 surface expression and limits NK cell ability to restrain virus-specific CD8+ T cells during LCMV infection; Fcer1g-/- mice showed enhanced CD8+ T cell responses and rapid viral control. FcεRIγ did not affect NKp46 mRNA but specifically stabilized its surface protein. Fcer1g-/- mice (genetic KO), flow cytometry for NKp46 and other activating receptors, viral load quantification, CD8+ T cell expansion measurement during LCMV infection PLoS pathogens High 31220194
2019 DCAR1, a C-type lectin receptor on rat myeloid cells, associates with FcεRIγ as its activating adaptor protein, enabling efficient phagocytosis of antibody-coated beads and reactive oxygen species production upon DCAR1 crosslinking on eosinophils. Co-immunoprecipitation, phagocytosis assay, ROS assay, monoclonal antibody-based characterization Frontiers in immunology Medium 31134097
2019 Syk recruitment to FcεRIγ involves multivalent cis and trans docking configurations on γ homodimers; multivalent interactions improve cis-oriented binding by ~1000-fold. Autophosphorylation of Syk Y130 in interdomain A alters the bias for cis binding. Short distances between paired γ ITAM pairs are required for trans docking, as demonstrated in γ-KO cells reconstituted with disulfide-linked γ subunits or monomeric ITAM/hemITAM γ-chimeras. Molecular dynamics simulation, hybrid MD/worm-like chain polymer modeling, live cell imaging, reconstitution in γ-KO cells with disulfide-linked γ and chimeric ITAM constructs, phosphomimetic Y130E Syk mutant Molecular biology of the cell High 31216232
2021 Rhesus macaque activating KIR (KIR3DS05), which contains a positively charged arginine in its transmembrane domain, associates with FcεRIγ (not DAP12) as its signal-transducing adaptor; this association results in increased and stabilized KIR3DS05 surface expression. Ligand binding (Mamu-A1*001 and A1*011) triggers signal transduction in the presence of FcεRIγ but not DAP12. Co-immunoprecipitation of transfected and primary cells, flow cytometry, signaling assays with specific MHC-I ligands Frontiers in immunology Medium 33968088
2022 FcεRIγ (FcRγ) upregulation in NK cells is dependent on cell proliferation driven by IL-2, IL-15, or IL-12, sensitive to mTOR suppression, and inhibited by TGFβ or IFNα; diminished proliferation (e.g., rapamycin treatment) leads to adaptive-like FcRγ-/low NK cell phenotype. Lower FcRγ protein expression was observed in NK cells during rapamycin treatment in vivo. Flow cytometry in lung transplant patients on rapamycin, cytokine stimulation experiments, mTOR inhibitor treatment, TGFβ/IFNα treatment of NK cells The Journal of experimental medicine Medium 36066491
2024 Covalent small molecules identified by HTS disrupt the interaction between the FCER1G phospho-ITAM and the SYK tandem SH2 domains (SYK-tSH2) by covalently modifying SYK-tSH2; the FCER1G p-ITAM interaction with SYK-tSH2 enables SYK activation via phosphorylation. High-throughput screen, TR-FRET binding assay, orthogonal protein-protein interaction assay, biochemical and biophysical characterization of inhibitor binding PloS one Medium 38359047
2025 USP5 deubiquitylase interacts with FcεRIγ in mast cells, reverses K48-linked polyubiquitylation of FcεRIγ (added by E3 ligase Cbl-b), and thereby stabilizes FcεRIγ protein. USP5 knockdown increases Cbl-b binding to FcεRIγ, enhancing its polyubiquitylation and degradation, and attenuates IgE-induced mast cell activation (β-hexosaminidase/histamine release) and allergic inflammation in mice. Co-immunoprecipitation, ubiquitylation assays (K48-linkage specific), siRNA knockdown of USP5 in mast cells and HEK293T cells, USP5 inhibitor WP1130, in vivo mouse allergy models Science signaling High 40729432
2026 In double-negative T (DNT) cells, FcεRIγ mediates IgG1-stimulated antibody-dependent cellular cytotoxicity (ADCC) against tumor cells via the FcεRIγ/Syk/AKT/NF-κB signaling pathway; Fcer1g-deficient DNT cells failed to respond to IgG1 stimulation, and Syk inhibition reduced cytotoxicity and phosphorylation of AKT and NF-κB. Combined DNT cells + tumor antibody therapy was abolished by Fcer1g deficiency in subcutaneous tumor models. Fcer1g knockout DNT cells, in vitro cytotoxicity assays, Syk inhibitor, Western blot for pathway phosphorylation (AKT, NF-κB), subcutaneous mouse tumor model Journal of molecular cell biology Medium 41481135

Source papers

Stage 0 corpus · 40 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 91 23921530
2011 Demethylation of the FCER1G promoter leads to FcεRI overexpression on monocytes of patients with atopic dermatitis. Allergy 65 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 62 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
2019 NK cell-intrinsic FcεRIγ limits CD8+ T-cell expansion and thereby turns an acute into a chronic viral infection. PLoS pathogens 44 31220194
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
2022 Diminished cell proliferation promotes natural killer cell adaptive-like phenotype by limiting FcεRIγ expression. The Journal of experimental medicine 37 36066491
2021 FcεRIγ-negative NK cells persist in vivo and enhance efficacy of therapeutic monoclonal antibodies in multiple myeloma. Blood advances 31 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
2019 Phenotypic and Functional Analysis of Human NK Cell Subpopulations According to the Expression of FcεRIγ and NKG2C. Frontiers in immunology 22 31867015
2012 Altered expression of the TCR signaling related genes CD3 and FcεRIγ in patients with aplastic anemia. Journal of hematology & oncology 22 22401598
2021 FCER1G and PTGS2 Serve as Potential Diagnostic Biomarkers of Acute Myocardial Infarction Based on Integrated Bioinformatics Analyses. DNA and cell biology 20 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 9 38359047
2022 FCER1G Gene Hypomethylation in Patients with Rheumatoid Arthritis. Journal of clinical medicine 9 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 7 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
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 5 23456064
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
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 4 35711924
2024 FCER1G as a novel immune-associated blood biomarker in cardiogenic stroke. Heliyon 3 39071704
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
2025 USP5 deubiquitylates and stabilizes FcεRIγ to enhance IgE-induced mast cell activation and allergic inflammation. Science signaling 2 40729432
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 Comprehensive analysis reveals the tumor suppressor role of macrophage signature gene FCER1G in hepatocellular carcinoma. Scientific reports 1 39893200
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
2026 Integration of single-cell RNA-sequencing and machine learning identifies GRN and FCER1G as potential peroxisomal targets in influenza pathogenesis. BMC infectious diseases 0 42185776
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

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