Affinage

SIGLEC9

Sialic acid-binding Ig-like lectin 9 · UniProt Q9Y336

Length
463 aa
Mass
50.1 kDa
Annotated
2026-06-10
78 papers in source corpus 38 papers cited in narrative 37 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SIGLEC9 encodes an inhibitory sialic-acid-binding immunoglobulin-like lectin expressed across myeloid cells, neutrophils, T cells, mast cells, and platelets that translates recognition of host and microbial sialoglycans into immunoregulatory signals (PMID:10801860, PMID:10801862, PMID:15827126, PMID:30988027, PMID:37100120). Its N-terminal V-set Ig domain binds both α2,3- and α2,6-linked sialic acids through a canonical site between the F and G β-strands, where a conserved domain-1 arginine (Arg120) is essential for ligand engagement, while a distinct C-C' loop region tunes glycan specificity (PMID:10801860, PMID:10801862, PMID:11741958, PMID:38321945); the same V-set domain independently recognizes high-molecular-weight hyaluronan at a separate, non-sialic-acid site (PMID:26411873). Upon ligand engagement and tyrosine phosphorylation of its cytoplasmic ITIM motifs, Siglec-9 recruits the phosphatase SHP-1 to dampen activating signaling, suppressing TCR/ZAP-70/NFAT signaling and T cell cytotoxicity, neutrophil oxidative burst and NET formation, and mast cell degranulation (PMID:15292262, PMID:30988027, PMID:37100120, PMID:19542910). The two cytoplasmic tyrosines transmit divergent outputs in macrophages, enhancing IL-10 while suppressing TNF-α upon TLR stimulation (PMID:18325328, PMID:24449467). Engagement is not uniformly inhibitory: certain cancer-associated ligands such as MUC1 bearing short sialylated O-glycans (MUC1-ST) bypass SHP recruitment to drive calcium flux and MEK-ERK activation, educating myeloid cells toward an immunosuppressive PD-L1-high tumor-associated macrophage phenotype (PMID:27595232, PMID:33627655, PMID:26540411). A broad spectrum of counter-receptors has been mapped, including host sialoglycoproteins that enforce neutrophil and platelet quiescence (glycophorin A, Tamm-Horsfall glycoprotein, GPIbα) and tumor-cell ligands (MUC16, DSG2, CD59) whose synthesis is driven principally by the α2,3-sialyltransferase ST3GAL4 (PMID:28416510, PMID:28829050, PMID:40204021, PMID:20497550, PMID:39813162, PMID:39436703, PMID:39551873). Sialylated bacterial capsules (group B and group A Streptococcus) and SARS-CoV-2 Omicron spike exploit Siglec-9 to evade phagocytic and neutrophil defenses, and Siglec-9 functions as an immune checkpoint whose genetic deletion or antibody blockade restores antitumor T cell and macrophage activity and synergizes with PD-1/PD-L1 blockade (PMID:19196661, PMID:26411873, PMID:38454157, PMID:37460871, PMID:37709296). Siglec-9 also serves as a non-immune leukocyte ligand for endothelial VAP-1/AOC3 at its enzymatic groove (PMID:21821708, PMID:29391504).

Mechanistic history

Synthesis pass · year-by-year structured walk · 25 steps
  1. 2000 High

    Establishing the molecular identity of Siglec-9 as a sialic-acid-binding inhibitory receptor was the foundational question, defining its domain architecture and ligand-binding determinants.

    Evidence cDNA cloning, COS-cell expression, recombinant binding assays, and mutagenesis of a conserved domain-1 arginine

    PMID:10801860 PMID:10801862

    Open questions at the time
    • Cytoplasmic signaling output not yet defined
    • Physiological ligands in vivo not identified
  2. 2001 High

    How Siglec family members achieve distinct glycan specificities was resolved by mapping the sequence region that discriminates α2,3- versus α2,8-linked sialosides.

    Evidence Reciprocal C-C' loop domain-swap chimeras of Siglec-7 and Siglec-9 with glyco-probe binding and modeling

    PMID:11741958

    Open questions at the time
    • Atomic-resolution structural basis not yet defined
    • Affinity for natural ligands not quantified
  3. 2004 High

    Whether Siglec-9 transmits inhibitory signals was answered by showing it suppresses TCR signaling via SHP-1 recruitment in an ITIM- and ligand-binding-dependent manner.

    Evidence Jurkat transfection, SHP-1 co-IP, phospho-ZAP-70 blots, NFAT reporter, Arg120Ala mutagenesis

    PMID:15292262

    Open questions at the time
    • Endogenous T cell context not addressed
    • Physiological ligand triggering inhibition unknown
  4. 2005 High

    The functional consequence of Siglec-9 ligation on neutrophils was defined as induction of two distinct ROS-dependent death pathways, establishing a role in neutrophil fate.

    Evidence Antibody ligation of primary and inflammatory human neutrophils with ROS scavenger and caspase inhibitor dissection

    PMID:15827126

    Open questions at the time
    • Natural ligands driving death in vivo not identified
    • Molecular link between ITIM signaling and ROS not mapped
  5. 2008 High

    How the two cytoplasmic tyrosines divide signaling labor was resolved by showing they differentially control IL-10 enhancement versus TNF-α suppression during TLR stimulation.

    Evidence Tyrosine-to-phenylalanine mutants in RAW264/THP-1 with TLR stimulation and cytokine ELISA

    PMID:18325328

    Open questions at the time
    • Downstream effectors of each tyrosine not identified
    • Endogenous ligand context not tested
  6. 2009 High

    Microbial subversion of Siglec-9 was established by showing GBS sialylated capsule engages neutrophil Siglec-9 in trans to blunt antibacterial functions.

    Evidence Sialoglycan binding, neutrophil oxidative burst/NET assays, neuraminidase and blocking-antibody controls

    PMID:19196661

    Open questions at the time
    • In vivo contribution to GBS pathogenesis not demonstrated
    • Host-pathogen specificity across Siglecs not delineated
  7. 2009 Medium

    The physical Siglec-9–SHP-1 complex was confirmed in primary neutrophils and shown to be developmentally regulated.

    Evidence Co-immunoprecipitation and phospho-Siglec-9 analysis in adult versus neonatal PMN with GM-CSF stimulation

    PMID:19542910

    Open questions at the time
    • Reciprocal validation of complex stoichiometry not shown
    • Functional consequence of neonatal differences not fully resolved
  8. 2010 High

    Identification of MUC16 (CA125) as a Siglec-9 ligand connected the receptor to tumor immune evasion on NK cells, B cells, and monocytes.

    Evidence Flow cytometry of primary immune cells, Jurkat-Siglec-9 transfection, MUC16 binding with neuraminidase control

    PMID:20497550

    Open questions at the time
    • Downstream signaling from MUC16 engagement not defined
    • Quantitative ligand affinity not measured
  9. 2011 High

    A non-immune adhesion function was uncovered by identifying Siglec-9 as a leukocyte ligand for endothelial VAP-1/AOC3, enabling inflammation imaging.

    Evidence Phage display, adhesion assays with mutants, modeling, and 68Ga-Siglec-9 peptide PET

    PMID:21821708

    Open questions at the time
    • Signaling consequences of VAP-1 engagement on leukocytes unknown
    • Sialic-acid dependence of this interaction not fully resolved
  10. 2013 High

    Siglec-9 engagement was shown to actively promote tumor cell growth by inducing MUC1–β-catenin signaling, expanding its role beyond immune inhibition.

    Evidence Soluble Siglec-9 and co-culture treatment of MUC1-transfected cells, β-catenin co-IP, nuclear fractionation, neuraminidase control

    PMID:24045940

    Open questions at the time
    • In vivo relevance to tumor progression not established
    • Receptor on the cancer-cell side beyond MUC1 not defined
  11. 2013 Medium

    A sialic-acid-independent counter-receptor mode was reported with prohibitins engaging Siglec-9 via an Arg120-dependent peptide interaction to inhibit ERK signaling.

    Evidence Arg120Ala mutant binding, bead co-immobilization with anti-CD3, phospho-ERK/c-Raf blots and IL-2 ELISA

    PMID:23567969

    Open questions at the time
    • Single-lab finding without reciprocal validation
    • Physiological relevance of sialic-acid-independent binding unclear
  12. 2013 Medium

    Siglec-9 engagement on astrocytoma cells was shown to drive calpain-mediated degradation of focal-adhesion proteins, linking it to tumor cell motility.

    Evidence Co-culture immunoblotting of FAK/Akt/paxillin/p130Cas with calpain inhibitor rescue and invasion assays

    PMID:24145038

    Open questions at the time
    • Single-lab finding requiring independent confirmation
    • Signaling link from Siglec-9 to calpain activation unmapped
  13. 2014 Medium

    Subcellular regulation of signaling was addressed by showing lectin-activity-dependent redistribution of Siglec-9 into lipid rafts contributes to IL-10 enhancement.

    Evidence Detergent-insoluble membrane fractionation, lectin-defective and ITIM mutants, cholesterol oxidase, cytokine ELISA

    PMID:24449467

    Open questions at the time
    • Direct partners within rafts not identified
    • Single-lab observation
  14. 2015 High

    The first non-sialic-acid glycan ligand was identified, showing HMW-HA engages a distinct V-set site to suppress neutrophil functions, a route exploited by GAS.

    Evidence HMW-HA binding to a separate site, neutrophil functional assays, GAS capsule-dependent blocking

    PMID:26411873

    Open questions at the time
    • Structural definition of the HA-binding site not resolved
    • Relative contribution of HA versus sialic-acid ligands in vivo unknown
  15. 2015 Medium

    Siglec-9 was shown to modulate alternative macrophage activation by enhancing IL-4-induced Arg1 through MEK-ERK rather than PI-3K.

    Evidence ITIM mutants in RAW264, IL-4 stimulation, pathway-selective inhibitors, phospho-ERK/Akt blots

    PMID:26540411

    Open questions at the time
    • Single-lab finding
    • Ligand triggering this polarization in vivo not defined
  16. 2016 High

    A distinct activating signaling mode was established when tumor MUC1-ST was shown to drive Siglec-9 calcium flux and MEK-ERK activation, educating immunosuppressive TAMs.

    Evidence MUC1-ST binding, phosphatase assays (SHP-1/2 negative), calcium flux, MEK-ERK blots, PD-L1 flow cytometry

    PMID:27595232

    Open questions at the time
    • Mechanistic switch between inhibitory and activating outputs not fully defined
    • Receptor proximal adaptor for calcium flux unknown
  17. 2016 Medium

    Loss-of-function and knockdown studies established that constitutively expressed Siglec-9 sets macrophage polarization responses and inflammatory cytokine balance.

    Evidence Siglec-9 siRNA knockdown with LPS/IFN-γ and IL-4 stimulation, CCR7/CD200R readouts; soluble Siglec-9 NF-κB inhibition with CIA model; SNP-variant cytokine assay

    PMID:26923638 PMID:27267914 PMID:27878892

    Open questions at the time
    • Soluble versus membrane Siglec-9 mechanisms not unified
    • Genetic-variant functional impact tested only in vitro
  18. 2017 High

    Host 'self' sialoglycoproteins were identified as tonic suppressors of neutrophil activation, defining a sialic-acid-based self-recognition system.

    Evidence Glycophorin A and Tamm-Horsfall protein binding, periodate/neuraminidase modification, neutrophil activation rescue, THP-null mouse urinalysis

    PMID:28416510 PMID:28829050

    Open questions at the time
    • Quantitative contribution of each self-ligand in vivo not weighted
    • Mechanism integrating multiple self-ligands unresolved
  19. 2018 Medium

    Src-family-kinase-dependent phosphorylation of Siglec-9 was shown to restrain dendritic-cell migration, and soluble Siglec-9/MCP-1 to drive reparative M2 macrophages.

    Evidence Dasatinib/SFK inhibitor and blocking-antibody migration assays; CCR2-blocking M2 differentiation and ALF rat model with M2 depletion

    PMID:24882272 PMID:28272428

    Open questions at the time
    • Single-lab findings
    • Endogenous ligand driving DC restraint not identified
  20. 2018 Medium

    The Siglec-9–VAP-1 interaction was further characterized as occurring at the amine-oxidase catalytic site and capable of triggering enzymatic activity.

    Evidence Amine oxidase activity assay, inhibitor competition, Arg/Ala mutant peptide, molecular docking

    PMID:29391504

    Open questions at the time
    • Physiological consequence of triggering VAP-1 activity unknown
    • Single-lab finding
  21. 2019 High

    Siglec-9 was defined as a T-cell inhibitory checkpoint in melanoma, expanding its checkpoint role to the adaptive immune compartment.

    Evidence Flow cytometry of tumor-infiltrating T cells, ligand/antibody engagement, cytotoxicity and cytokine assays, SHP-1-specific phosphorylation

    PMID:30988027

    Open questions at the time
    • Identity of melanoma ligands not defined here
    • In vivo therapeutic blockade not tested in this study
  22. 2021 High

    The cancer-cell glycan machinery generating Siglec-9 ligands was traced to α2,3-sialyltransferases, and synthetic agonists confirmed pharmacological control of neutrophil NETosis.

    Evidence ST3GAL1/ST3GAL4 transcriptomics with Siglec-9 triggering on macrophages; synthetic glycopolymer agonists in COVID-19 neutrophil NETosis assays

    PMID:33627655 PMID:34056095

    Open questions at the time
    • Single dominant sialyltransferase across cancers not generalized
    • In vivo efficacy of agonists/antagonists not established here
  23. 2023 High

    Genetic and antibody studies established Siglec-9 as a targetable macrophage checkpoint in glioblastoma and ovarian cancer that synergizes with PD-1/PD-L1 blockade, and as an inhibitory mast-cell receptor.

    Evidence Siglece-KO mouse GBM models with scRNA-seq; ovarian TAM blockade with phospho-SHP-1 and CD8 cytotoxicity assays; CRISPR SIGLEC9 knockout in primary mast cells with ligand gain-of-function

    PMID:37100120 PMID:37460871 PMID:37709296

    Open questions at the time
    • Murine Siglece versus human Siglec-9 correspondence not fully resolved
    • Combination dosing and ligand-specific responses not optimized
  24. 2024 High

    New ligands and structural/glycan determinants were defined, and viral exploitation of Siglec-9 by SARS-CoV-2 Omicron spike was demonstrated.

    Evidence NMR/MD of the V-set domain; ST3GAL4 CRISPR screen and mass spectrometry in AML; CD59 CRISPRi screen; Omicron F375S spike mutagenesis with phagocytosis/antigen-presentation rescue

    PMID:38321945 PMID:38454157 PMID:39436703 PMID:39551873

    Open questions at the time
    • CD59 as a ligand not independently confirmed
    • In vivo relevance of viral exploitation to disease severity not established
  25. 2025 Medium

    Additional counter-receptors were mapped, including DSG2 in melanoma and a cis self-modulatory GPIbα–Siglec-9 interaction that brakes platelet activation.

    Evidence Proximity-labeling/CRISPR screen identifying DSG2 with phagocytosis assays; platelet-specific Siglec-E conditional KO with cis/trans GPIbα binding assays

    PMID:39813162 PMID:40204021

    Open questions at the time
    • DSG2 finding from single lab
    • Mechanistic distinction between cis and trans ligand engagement not fully generalized

Open questions

Synthesis pass · forward-looking unresolved questions
  • How a single V-set domain integrates competing host self-ligands, microbial mimics, and HMW-HA to switch between SHP-1-dependent inhibition and calcium/MEK-ERK activation in a given cell type remains unresolved.
  • No unified rule predicting inhibitory versus activating output from ligand structure
  • Quantitative ligand competition in vivo not modeled
  • Proximal adaptor mediating activating calcium flux unidentified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 4 GO:0060089 molecular transducer activity 4 GO:0098772 molecular function regulator activity 4 GO:0060090 molecular adaptor activity 2 GO:0008289 lipid binding 1 GO:0038024 cargo receptor activity 1
Localization
GO:0005886 plasma membrane 3 GO:0005634 nucleus 1
Pathway
R-HSA-168256 Immune System 5 R-HSA-162582 Signal Transduction 4 R-HSA-1643685 Disease 4 R-HSA-109582 Hemostasis 1 R-HSA-5357801 Programmed Cell Death 1
Partners
AOC3CD59DSG2GP1BAGYPAMUC1MUC16PTPN6

Evidence

Reading pass · 37 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 Siglec-9 is a type I transmembrane protein with three extracellular Ig-like domains (N-terminal V-set + two C2-set), a transmembrane region, and a cytoplasmic tail containing two tyrosine-based signaling motifs including a canonical ITIM. Expression of full-length cDNA in COS cells induced sialic-acid-dependent erythrocyte binding. Recombinant soluble extracellular domain binds α2-3 and α2-6-linked sialic acids; the carboxyl group and side chain of sialic acid are essential, and mutation of a critical arginine residue in domain 1 abrogates binding. cDNA cloning, COS cell expression, recombinant protein binding assays, site-directed mutagenesis of conserved Arg The Journal of biological chemistry High 10801860 10801862
2001 The C-C' loop region (residues Asn70–Lys75) in the V-set sugar-binding domain of Siglec-7 determines its preference for α2,8-disialyl and branched α2,6-sialyl residues (GD3, LSTb), whereas the equivalent region in Siglec-9 confers preference for α2,3-linked (LSTc, GD1a) structures. Swapping this small region between Siglec-7 and Siglec-9 chimeras transferred binding specificity accordingly. Chimeric protein expression in CHO cells, polyvalent streptavidin-based glyco-probe binding assays, molecular modeling The Journal of biological chemistry High 11741958
2004 Siglec-9 negatively regulates T cell receptor (TCR) signaling: following pervanadate stimulation or TCR engagement, Siglec-9 undergoes tyrosine phosphorylation and recruits SHP-1; it reduces phosphorylation of ZAP-70 Tyr319 and decreases NFAT transcriptional activity. Mutation of the conserved Arg120 in the ligand-binding site reduces inhibitory function, indicating ligand binding is required for optimal TCR inhibition. Stable/transient transfection of Jurkat T cells with Siglec-9, pervanadate/TCR stimulation, co-immunoprecipitation of SHP-1, phospho-ZAP-70 western blot, NFAT-luciferase reporter assay, Arg120Ala mutagenesis The Journal of biological chemistry High 15292262
2005 Siglec-9 ligation on normal neutrophils induces caspase-dependent, ROS-dependent apoptosis. In neutrophils primed with GM-CSF, IFN-α, or IFN-γ, Siglec-9 ligation triggers a caspase-independent, ROS-dependent cell death with cytoplasmic vacuolization. Both death pathways are abrogated by ROS scavengers or in neutrophils unable to generate ROS. Siglec-9 antibody ligation on primary human neutrophils and inflammatory neutrophils (sepsis, RA patients), ROS scavenger experiments, caspase inhibitor experiments, cytology Blood High 15827126
2008 Siglec-9 expression in macrophages (RAW264 and THP-1) strongly enhances IL-10 production and reduces TNF-α upon TLR stimulation (LPS, peptidoglycan, CpG, dsRNA). These effects require both cytoplasmic tyrosine residues: mutation of both to phenylalanine abrogates IL-10 enhancement and TNF-α suppression. A membrane-proximal ITIM mutant partially retains TNF-α inhibition but loses IL-10 enhancement, indicating divergent signaling via the two tyrosines. Stable transfection of Siglec-9 and ITIM tyrosine mutants in RAW264/THP-1, TLR stimulation assays, ELISA for cytokines Biochemical and biophysical research communications High 18325328
2009 Bacterial group B Streptococcus (GBS) sialylated capsular polysaccharide (CPS) presenting terminal Sialα2-3Galβ1-4GlcNAc engages neutrophil Siglec-9 in trans, dampening neutrophil oxidative burst, NET formation, and enabling bacterial survival. These effects are Sia- and Siglec-9-dependent (abrogated by neuraminidase treatment of GBS or by blocking Siglec-9). Immobilized sialoglycan binding assays, GBS CPS binding to isolated human neutrophils, oxidative burst assays, NET formation assays, bacterial survival assays, neuraminidase treatment, Siglec-9 blocking antibodies Blood High 19196661
2010 Siglec-9 is identified as the receptor for MUC16 (CA125) on NK cells, B cells, and monocytes. Siglec-9-transfected Jurkat cells and monocytes from healthy donors bind to ovarian tumor cells via Siglec-9–csMUC16 interaction; neuraminidase treatment of immune cells releases sMUC16, confirming sialic acid dependence. Flow cytometry of primary immune cells, Siglec-9 transfection into Jurkat cells, MUC16 binding assays, neuraminidase treatment, co-culture adhesion assays Molecular cancer High 20497550
2011 Siglec-9 is a novel leukocyte ligand for vascular adhesion protein-1 (VAP-1/AOC3). The interaction was identified by phage display and confirmed by in vitro and ex vivo adhesion assays. Interaction occurs at the enzymatic groove of VAP-1 and is only partially dependent on VAP-1 enzymatic activity. A 68Ga-labeled Siglec-9 peptide specifically detects VAP-1 at sites of inflammation and cancer by PET. Phage display, in vitro/ex vivo adhesion assays with mutated proteins, molecular modeling, PET imaging with 68Ga-labeled Siglec-9 peptide Blood High 21821708
2013 Siglec-9 binds MUC1 on cancer cells in a sialic acid-dependent manner, inducing recruitment of β-catenin to the MUC1 C-terminal domain in a dose- and time-dependent manner. Recruited β-catenin translocates to the nucleus, promoting cell growth. Neuraminidase treatment abolishes Siglec-9-induced signaling. Recombinant soluble Siglec-9 treatment of MUC1-transfected 3T3 and HCT116 cells, co-culture with Siglec-9-expressing HEK293 cells, co-immunoprecipitation of β-catenin with MUC1, nuclear fractionation, neuraminidase treatment, proliferation assays The Journal of biological chemistry High 24045940
2013 Prohibitin-1 and prohibitin-2 expressed on the surface of T cell leukemia lines and activated T lymphocytes serve as counter-receptors for Siglec-9 on macrophages and dendritic cells, in a sialic acid-independent but Arg120-dependent ionic peptide–peptide interaction. Engagement of prohibitins via Siglec-9 (co-immobilized with anti-CD3) inhibits ERK1/2 phosphorylation, c-Raf phosphorylation, and IL-2 production in Jurkat cells. Binding assays with Siglec-9 Arg120Ala mutant, co-immobilization of Siglec-9 and anti-CD3 on beads, phospho-ERK1/2 and phospho-c-Raf western blot, IL-2 ELISA Biochemical and biophysical research communications Medium 23567969
2013 Siglec-9 binding to sialylglycoconjugates on astrocytoma (AS) cells induces rapid calpain-mediated degradation of focal adhesion kinase (FAK), Akt, paxillin, and p130Cas, leading to cell detachment and increased motility/invasiveness. Despite degradation of total Akt, phospho-Akt was increased at the leading cytoplasmic edge, consistent with enhanced motility. Co-culture of Siglec-9-expressing and Siglec-9-deficient cells with AS astrocytoma cells, immunoblotting for FAK/Akt/paxillin/p130Cas degradation, calpain inhibitor experiments, motility and invasion assays The Journal of biological chemistry Medium 24145038
2014 Upon TLR2 stimulation, a portion of Siglec-9 redistributes into lipid raft (detergent-insoluble microdomain) fractions with kinetics mirroring TLR2 redistribution (peak 3–10 min). This raft localization is lectin-activity-dependent: a lectin-defective Siglec-9 mutant fails to enter lipid rafts, whereas a double-ITIM tyrosine mutant still translocates. IL-10 production is partially reduced by disrupting lipid raft organization with cholesterol oxidase, suggesting raft localization contributes to IL-10 enhancement. Membrane fractionation (detergent-insoluble microdomains), lectin-defective and ITIM tyrosine mutant transfection, cholesterol oxidase treatment, cytokine ELISA Cytotechnology Medium 24449467
2015 High-molecular-weight hyaluronan (HMW-HA) is recognized by Siglec-9 through a site in its V-set domain distinct from the sialic acid-binding site, representing the first non-sialic-acid glycan ligand for a CD33-related Siglec. HMW-HA engagement of Siglec-9 limits NET formation, oxidative burst, and apoptosis in human neutrophils. Group A Streptococcus (GAS) exploits its own HMW-HA capsule to engage Siglec-9, blocking these neutrophil functions and promoting bacterial survival. Binding assays with Siglec-9 and HMW-HA, neutrophil functional assays (NET formation, oxidative burst, apoptosis), GAS capsule-dependent blocking experiments Journal of molecular medicine (Berlin, Germany) High 26411873
2016 MUC1 carrying cancer-specific short sialylated O-linked glycans (MUC1-ST) binds Siglec-9 on myeloid cells without activating SHP-1 or SHP-2, but instead induces calcium flux leading to MEK-ERK kinase activation, educating myeloid cells toward a tumor-associated macrophage-like phenotype with increased PD-L1 expression. MUC1-ST binding assays, phosphatase activation assays (SHP-1/SHP-2), calcium flux measurement, MEK-ERK phosphorylation western blot, PD-L1 expression by flow cytometry, macrophage phenotyping Nature immunology High 27595232
2016 A SIGLEC9 GA haplotype (rs2075803 G/rs2258983 A) encodes a Siglec-9 protein variant that is less effective at suppressing inflammatory TNF-α production in a myeloid cell line compared to the other major haplotype variant, as measured by in vitro cytokine assays. In vitro myeloid cell line transfection with variant Siglec-9 constructs, TNF-α ELISA after stimulation Respirology (Carlton, Vic.) Medium 27878892
2016 Soluble Siglec-9 (sSiglec-9) suppresses M1 macrophage activation by inhibiting NF-κB p65 phosphorylation in RAW264.7 cells, reducing M1 marker expression (TNF-α, IL-6, iNOS) without affecting M2 markers. In a murine collagen-induced arthritis model, sSiglec-9 attenuated arthritis severity, decreased serum TNF-α, and increased Foxp3+ Treg cell proportions. RAW264.7 macrophage culture with sSiglec-9, western blot for NF-κB p65 phosphorylation, NF-κB chemical blockade, cytokine ELISA, DBA/1J mouse CIA model, histology, flow cytometry for Tregs Arthritis research & therapy Medium 27267914
2017 Glycophorin A, the most abundant sialoglycoprotein on erythrocytes, engages neutrophil Siglec-9 to suppress neutrophil activation in vitro and ex vivo. Mild periodate oxidation of erythrocyte sialic acid side chains (with aldehyde quenching) reduces erythrocyte binding to Siglec-9 and restores neutrophil activation (l-selectin shedding, oxidative burst, chemotaxis, NET formation, apoptosis), demonstrating a sialic acid-based 'self' signal that maintains neutrophil quiescence in blood. ELISA and immunofluorescence for glycophorin A–Siglec-9 interaction, sodium metaperiodate oxidation of erythrocyte sialic acids, ex vivo and in vitro neutrophil activation assays Blood High 28416510
2017 Tamm-Horsfall glycoprotein (THP) engages neutrophil Siglec-9 (and its mouse ortholog Siglec-E) via N-glycan sialic acid moieties, suppressing neutrophil ROS generation, chemotaxis, and killing of uropathogenic E. coli. THP-null mice have significantly more neutrophils in urine than wild-type mice. THP–neutrophil binding assays, neuraminidase treatment, Siglec-9 blocking antibody, ROS/chemotaxis/bacterial killing assays, THP-null mouse urinalysis Immunology and cell biology High 28829050
2017 MCP-1 and secreted ectodomain of Siglec-9 (sSiglec-9) synergistically promote M2 macrophage differentiation from bone marrow-derived macrophages via CCR2, producing liver-regenerating factors that suppress hepatocyte apoptosis and promote proliferation. In a rat acute liver failure model, combined MCP-1/sSiglec-9 treatment improved survival and induced anti-inflammatory M2 macrophages; depletion of M2 macrophages (mannosylated clodronate liposomes) abolished recovery. In vitro M2 differentiation assay with bone marrow-derived macrophages, CCR2 blocking, D-galactosamine rat ALF model, M2-depletion with mannosylated clodronate liposomes, hepatocyte apoptosis/proliferation assays Scientific reports Medium 28272428
2018 Dasatinib dephosphorylates Siglec-9 (and Siglec-3) in human monocyte-derived dendritic cells by inhibiting SRC-family kinases, which more than doubles the number of moDCs migrating toward a CCL19 gradient. Specific blocking of Siglec-9 also enhanced DC migration, confirming that SFK-dependent Siglec-9 phosphorylation restrains DC migration. Dasatinib and SRC inhibitor 1 treatment of moDCs, phosphorylation assays for Siglec-9 and SFKs, CCL19 gradient migration assays, specific Siglec-9 blocking antibody Experimental hematology Medium 24882272
2018 Siglec-9 is an inhibitory receptor on human primary amine oxidase (hAOC3/VAP-1). The Siglec-9 peptide binds to hAOC3 and triggers its amine oxidase enzymatic activity toward benzylamine. hAOC3 inhibitors (semicarbazide and imidazole) reduce binding of wild-type and Arg/Ala mutated Siglec-9 peptides to hAOC3, and molecular docking shows the R3 residue of the Siglec-9 peptide interacts in the catalytic site when topaquinone is in the non-catalytic on-copper conformation. Amine oxidase activity assay, competitive binding with hAOC3 inhibitors, Arg/Ala mutant peptide, molecular docking Scientific reports Medium 29391504
2019 Siglec-9 is expressed on intratumoral CD8+ effector memory T cells in melanoma and functions as an inhibitory checkpoint: engagement of Siglec-9 by its ligands or specific antibodies suppresses TCR signaling, cytotoxicity, and cytokine production. Inhibition is associated with phosphorylation of SHP-1 but not SHP-2. Cognate Siglec-9 ligands are expressed on the majority of primary and metastatic melanoma tumor cells. Flow cytometry of tumor-infiltrating vs. peripheral T cells, Siglec-9 ligand engagement/antibody stimulation assays, cytotoxicity assays, cytokine production, phospho-SHP-1/SHP-2 assays Cancer immunology research High 30988027
2021 Pancreatic ductal adenocarcinoma cells express increased sialylation driven primarily by α2,3-sialyltransferases ST3GAL1 and ST3GAL4, producing ligands recognized by Siglec-9 (and Siglec-7) on myeloid cells. Triggering Siglec-9 in macrophages reduces inflammatory programmes and increases PD-L1 and IL-10 expression, directing monocyte-to-macrophage differentiation toward an immunosuppressive phenotype. ST3GAL1/ST3GAL4 identification by transcriptomics, Siglec-9 binding assays, Siglec-9 triggering on macrophages, PD-L1/IL-10 expression assays, single-cell and bulk transcriptomics Nature communications High 33627655
2021 Synthetic glycopolymers designed as Siglec-9 agonists suppress NETosis in human neutrophils induced by viral TLR agonists and plasma from severe COVID-19 patients, confirming Siglec-9 as a functional checkpoint receptor that can be pharmacologically activated to suppress neutrophil extracellular trap formation. Synthetic glycopolymer synthesis, neutrophil NETosis assays with TLR agonists and COVID-19 patient plasma, Siglec-9 agonism confirmed by receptor engagement ACS central science Medium 34056095
2023 Siglec-9 is expressed on human mast cells and functions as an inhibitory receptor. CRISPR/Cas9 disruption of SIGLEC9 increases baseline activation marker expression and enhances responsiveness to IgE-dependent and -independent stimulation. Glycophorin A and HMW-HA (native Siglec-9 ligands), as well as Siglec-9 co-engagement with FcεRI, reduce mast cell degranulation, arachidonic acid production, and chemokine release. CRISPR/Cas9 SIGLEC9 knockout, flow cytometry for activation markers, degranulation assays, arachidonic acid measurement, chemokine ELISA, native ligand pretreatment, FcεRI co-engagement The Journal of allergy and clinical immunology High 37100120
2023 Siglec-9 functions as an immune-checkpoint molecule on macrophages in glioblastoma. Deletion of Siglece (murine Siglec-9 homolog) restrained tumor development and prolonged survival in mouse GBM models. Mechanistically, Siglece deletion directly activated both CD4+ and CD8+ T cells through antigen presentation, secreted chemokines, and co-stimulatory factor interactions. Siglece deletion synergized with anti-PD-1/PD-L1 treatment. Siglece knockout mouse GBM models, survival analysis, single-cell RNA-seq, spatial transcriptomics, T cell activation assays (antigen presentation, chemokines, co-stimulatory factors) Nature cancer High 37460871
2023 Blockade of Siglec-9 in ovarian cancer suppresses phosphorylation of SHP-1, repolarizes TAMs toward an antitumorigenic phenotype, and restores cytotoxic CD8+ T cell activity in vitro and ex vivo. Siglec-9 blockade synergizes with anti-PD-1 antibody to enhance CD8+ T cell cytotoxicity. Siglec-9 blocking antibody treatment of primary ovarian cancer TAMs, phospho-SHP-1 assay, macrophage phenotyping by flow cytometry, CD8+ T cell cytotoxicity assays (in vitro and ex vivo), anti-PD-1 combination Journal for immunotherapy of cancer Medium 37709296
2024 SARS-CoV-2 Omicron spike sequence FAPFFAF (positions 371–377) confers enhanced binding to Siglec-9 on macrophages, impairing phagocytosis and antigen presentation. A phenylalanine-to-serine mutation at position 375 (F375S) reverts this to the ancestral-strain sequence, abolishes enhanced Siglec-9 binding, and restores macrophage uptake and immunogenicity of Omicron RBD nanoparticles. Reverse mutagenesis (F375S) in Omicron spike, Siglec-9 binding assays, macrophage phagocytosis assays, antigen presentation assays, RBD nanoparticle immunization in mice/rabbits/macaques Nature immunology High 38454157
2024 ST3GAL4 is identified as the main driver of Siglec-9 ligand synthesis in AML cells by integrated CRISPR genomic screening and bioinformatics. CRISPR-Cas9 KO of ST3GAL4 dramatically reduces Siglec-9 ligand expression. Mass spectrometry shows Siglec-9 primarily binds N-linked sialoglycans on AML cells. ST3GAL4 KO enhances AML cell sensitivity to phagocytosis by Siglec-9-expressing macrophages. CRISPR genomic screen, ST3GAL4 CRISPR-Cas9 KO, Siglec-9 ligand expression assays, mass spectrometry of cell-surface glycosylation, macrophage phagocytosis assay Leukemia High 39551873
2024 NMR spectroscopy and molecular dynamics revealed that Neu5Ac is accommodated between the F and G β-strands at the canonical sialic acid binding site of the Siglec-9 V-set domain. Synthetic sialoglycan modifications at C9 (MTTS scaffold) generate new interactions with hydrophobic residues at the G-G' loop and N-terminal region; C5 modifications (BTC scaffold) stabilize the B'-C loop, explaining enhanced affinity of these modified ligands. Triple-resonance 3D NMR backbone assignment of Siglec-9 V-set domain, NMR chemical shift perturbation mapping, molecular dynamics simulation ACS chemical biology High 38321945
2024 CD59 is identified as a candidate Siglec-9 ligand on prostate cancer cells by CRISPRi screen and mass spectrometry. Blocking Siglec-7/9–sialic acid interactions inhibited prostate cancer xenograft growth and increased immune cell infiltration in humanized mice. CRISPRi screen, mass spectrometry, Siglec-9 blocking in humanized mouse xenograft model The Journal of clinical investigation Medium 39436703
2025 DSG2 (Desmoglein 2) is identified as a dominant counter receptor of Siglec-9 in melanoma cells, with the interaction mediated primarily by sialic acid-bearing N-glycans on DSG2. Blocking DSG2–Siglec-9 trans-interaction significantly enhances macrophage phagocytosis of melanoma cells. Proximity labeling combined with CRISPR knockout screening, sialic acid dependency assays, macrophage phagocytosis assays Advanced science (Weinheim, Baden-Wurttemberg, Germany) Medium 39813162
2025 GPIbα mucin-like region carries O-linked glycans with α2,3-linked sialic acid that bind Siglec-9 in cis on platelets, acting as a 'parking brake' to suppress platelet activation. Siglec-E conditional knockout (platelet factor 4-Cre) significantly increases platelet coagulation activity in vivo and in vitro. The GPIbα ligand does not engage Siglec-9 in trans on other cells, indicating a self-modulation mechanism. Platelet factor 4-Cre:Siglec-E conditional KO mice, in vitro human platelet culture, recombinant GPIbα glycoprotein, cis vs. trans binding assays, neuraminidase treatment, platelet activation assays Journal of thrombosis and haemostasis : JTH High 40204021
2009 Siglec-9 and SHP-1 physically interact in human neutrophils as shown by co-immunoprecipitation. Neonatal PMN express diminished Siglec-9 with basal phosphorylation, and GM-CSF differentially regulates Siglec-9 phosphorylation in neonatal vs. adult PMN (decreasing it in neonates, increasing it in adults), with distinct downstream survival signaling consequences. Co-immunoprecipitation of Siglec-9 and SHP-1, flow cytometry, western blot for phospho-Siglec-9, GM-CSF stimulation assays in adult and neonatal PMN Pediatric research Medium 19542910
2006 Siglec-9 mediates rapid endocytosis of anti-Siglec-9 monoclonal antibody in AML cells and transfected rat basophilic leukemia cells, identifying it as an endocytic receptor on myeloid leukemia cells absent from normal bone marrow myeloid progenitors. Anti-Siglec-9 mAb internalization assay in primary AML cells and transfected RBL cells, flow cytometry Leukemia research Medium 16828866
2015 Siglec-9 modulates IL-4-stimulated macrophage signaling: Siglec-9 expression enhances induction of arginase-1 (Arg1) by IL-4 through the MEK-ERK pathway (not the PI-3K pathway), as ITIM tyrosine mutations abolish the Arg1 enhancement, and MEK inhibitors but not PI-3K inhibitors block the effect. Siglec-9 also enhances IL-4-induced Akt phosphorylation and ERK phosphorylation without IL-4. Stable transfection with Siglec-9 and ITIM mutants in RAW264, IL-4 stimulation, Arg1 expression assay, MEK and PI-3K inhibitors, phospho-Akt and phospho-ERK western blots Bioscience, biotechnology, and biochemistry Medium 26540411
2016 Siglec-9 knockdown in human macrophages enhances LPS- and LPS/IFN-γ-induced CCR7 expression and decreases IL-4-induced CD200R expression, demonstrating that constitutively expressed Siglec-9 modulates macrophage polarization responses. Siglec-9 siRNA knockdown in primary human monocyte-derived macrophages, LPS/IFN-γ and IL-4 stimulation, CCR7 and CD200R expression by qRT-PCR and flow cytometry Bioscience, biotechnology, and biochemistry Medium 26923638

Source papers

Stage 0 corpus · 78 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 Molecular mimicry of host sialylated glycans allows a bacterial pathogen to engage neutrophil Siglec-9 and dampen the innate immune response. Blood 316 19196661
2016 The mucin MUC1 modulates the tumor immunological microenvironment through engagement of the lectin Siglec-9. Nature immunology 312 27595232
2021 Sialic acids in pancreatic cancer cells drive tumour-associated macrophage differentiation via the Siglec receptors Siglec-7 and Siglec-9. Nature communications 256 33627655
2023 Siglec-9 acts as an immune-checkpoint molecule on macrophages in glioblastoma, restricting T-cell priming and immunotherapy response. Nature cancer 190 37460871
2000 Siglec-9, a novel sialic acid binding member of the immunoglobulin superfamily expressed broadly on human blood leukocytes. The Journal of biological chemistry 190 10801862
2005 Siglec-9 transduces apoptotic and nonapoptotic death signals into neutrophils depending on the proinflammatory cytokine environment. Blood 181 15827126
2010 Identification of Siglec-9 as the receptor for MUC16 on human NK cells, B cells, and monocytes. Molecular cancer 172 20497550
2001 A small region of the natural killer cell receptor, Siglec-7, is responsible for its preferred binding to alpha 2,8-disialyl and branched alpha 2,6-sialyl residues. A comparison with Siglec-9. The Journal of biological chemistry 168 11741958
2004 Negative regulation of T cell receptor signaling by Siglec-7 (p70/AIRM) and Siglec-9. The Journal of biological chemistry 163 15292262
2000 Cloning, characterization, and phylogenetic analysis of siglec-9, a new member of the CD33-related group of siglecs. Evidence for co-evolution with sialic acid synthesis pathways. The Journal of biological chemistry 132 10801860
2019 Siglec-9 Regulates an Effector Memory CD8+ T-cell Subset That Congregates in the Melanoma Tumor Microenvironment. Cancer immunology research 130 30988027
2011 Siglec-9 is a novel leukocyte ligand for vascular adhesion protein-1 and can be used in PET imaging of inflammation and cancer. Blood 104 21821708
2017 Erythrocyte sialoglycoproteins engage Siglec-9 on neutrophils to suppress activation. Blood 87 28416510
2008 Siglec-9 enhances IL-10 production in macrophages via tyrosine-based motifs. Biochemical and biophysical research communications 87 18325328
2017 Siglec-8 and Siglec-9 binding specificities and endogenous airway ligand distributions and properties. Glycobiology 81 28369504
2015 Host and pathogen hyaluronan signal through human siglec-9 to suppress neutrophil activation. Journal of molecular medicine (Berlin, Germany) 73 26411873
2013 Binding of the sialic acid-binding lectin, Siglec-9, to the membrane mucin, MUC1, induces recruitment of β-catenin and subsequent cell growth. The Journal of biological chemistry 66 24045940
2010 Immunomodulation of monocyte-derived dendritic cells through ligation of tumor-produced mucins to Siglec-9. Biochemical and biophysical research communications 66 20971061
2021 Synthetic Siglec-9 Agonists Inhibit Neutrophil Activation Associated with COVID-19. ACS central science 55 34056095
2015 Expression of ligands for Siglec-8 and Siglec-9 in human airways and airway cells. The Journal of allergy and clinical immunology 52 25747723
2006 Analysis of the CD33-related siglec family reveals that Siglec-9 is an endocytic receptor expressed on subsets of acute myeloid leukemia cells and absent from normal hematopoietic progenitors. Leukemia research 51 16828866
2020 The Roles of Siglec7 and Siglec9 on Natural Killer Cells in Virus Infection and Tumour Progression. Journal of immunology research 46 32322597
2024 Sialylated glycoproteins suppress immune cell killing by binding to Siglec-7 and Siglec-9 in prostate cancer. The Journal of clinical investigation 39 39436703
2021 Development of Siglec-9 Blocking Antibody to Enhance Anti-Tumor Immunity. Frontiers in oncology 39 34869028
2016 Soluble Siglec-9 suppresses arthritis in a collagen-induced arthritis mouse model and inhibits M1 activation of RAW264.7 macrophages. Arthritis research & therapy 35 27267914
2000 Identification and molecular characterization of a novel member of the siglec family (SIGLEC9). Genomics 33 10903842
2018 Decreased Siglec-9 Expression on Natural Killer Cell Subset Associated With Persistent HBV Replication. Frontiers in immunology 32 29899741
2017 Secreted Ectodomain of SIGLEC-9 and MCP-1 Synergistically Improve Acute Liver Failure in Rats by Altering Macrophage Polarity. Scientific reports 31 28272428
2023 LINC01004-SPI1 axis-activated SIGLEC9 in tumor-associated macrophages induces radioresistance and the formation of immunosuppressive tumor microenvironment in esophageal squamous cell carcinoma. Cancer immunology, immunotherapy : CII 29 36688997
2017 Tamm-Horsfall glycoprotein engages human Siglec-9 to modulate neutrophil activation in the urinary tract. Immunology and cell biology 29 28829050
2017 Increased expression of Siglec-9 in chronic obstructive pulmonary disease. Scientific reports 28 28860481
2016 Influence of SIGLEC9 polymorphisms on COPD phenotypes including exacerbation frequency. Respirology (Carlton, Vic.) 27 27878892
2023 Siglec-9+ tumor-associated macrophages delineate an immunosuppressive subset with therapeutic vulnerability in patients with high-grade serous ovarian cancer. Journal for immunotherapy of cancer 26 37709296
2016 Regulation of airway inflammation by Siglec-8 and Siglec-9 sialoglycan ligand expression. Current opinion in allergy and clinical immunology 26 26694037
2018 Targeting Neutrophils in Severe Asthma via Siglec-9. International archives of allergy and immunology 23 29306942
2014 A soluble form of Siglec-9 provides an antitumor benefit against mammary tumor cells expressing MUC1 in transgenic mice. Biochemical and biophysical research communications 22 24924635
2021 Siglec-9 defines and restrains a natural killer subpopulation highly cytotoxic to HIV-infected cells. PLoS pathogens 20 34762717
2009 Siglec-9 and SHP-1 are differentially expressed in neonatal and adult neutrophils. Pediatric research 20 19542910
2024 The glycosyltransferase ST3GAL4 drives immune evasion in acute myeloid leukemia by synthesizing ligands for the glyco-immune checkpoint receptor Siglec-9. Leukemia 19 39551873
2023 Siglec-9 is an inhibitory receptor on human mast cells in vitro. The Journal of allergy and clinical immunology 19 37100120
2022 Siglec-9, a Putative Immune Checkpoint Marker for Cancer Progression Across Multiple Cancer Types. Frontiers in molecular biosciences 18 35372497
2016 Feasibility of (68)Ga-labeled Siglec-9 peptide for the imaging of acute lung inflammation: a pilot study in a porcine model of acute respiratory distress syndrome. American journal of nuclear medicine and molecular imaging 18 27069763
2019 Decreased erythrocyte binding of Siglec-9 increases neutrophil activation in sickle cell disease. Blood cells, molecules & diseases 16 31901888
2016 A soluble form of Siglec-9 provides a resistance against Group B Streptococcus (GBS) infection in transgenic mice. Microbial pathogenesis 16 27544323
2024 The receptor binding domain of SARS-CoV-2 Omicron subvariants targets Siglec-9 to decrease its immunogenicity by preventing macrophage phagocytosis. Nature immunology 15 38454157
2017 Siglec-9 is upregulated in rheumatoid arthritis and suppresses collagen-induced arthritis through reciprocal regulation of Th17-/Treg-cell differentiation. Scandinavian journal of immunology 15 28273363
2023 Siglec-9 Restrains Antibody-Dependent Natural Killer Cell Cytotoxicity against SARS-CoV-2. mBio 14 36728420
2016 Constitutively expressed Siglec-9 inhibits LPS-induced CCR7, but enhances IL-4-induced CD200R expression in human macrophages. Bioscience, biotechnology, and biochemistry 14 26923638
2020 Soluble Siglec-9 alleviates intestinal inflammation through inhibition of the NF-κB pathway. International immunopharmacology 13 32570035
2015 Siglec-9 modulated IL-4 responses in the macrophage cell line RAW264. Bioscience, biotechnology, and biochemistry 13 26540411
2013 Binding of a sialic acid-recognizing lectin Siglec-9 modulates adhesion dynamics of cancer cells via calpain-mediated protein degradation. The Journal of biological chemistry 12 24145038
2024 Unraveling Molecular Recognition of Glycan Ligands by Siglec-9 via NMR Spectroscopy and Molecular Dynamics Modeling. ACS chemical biology 11 38321945
2013 Prohibitins function as endogenous ligands for Siglec-9 and negatively regulate TCR signaling upon ligation. Biochemical and biophysical research communications 10 23567969
2024 Expression of Siglec-9 in peripheral blood neutrophils was increased and associated with disease severity in patients with AECOPD. Cytokine 9 38412768
2024 Targeting Tumor-Associated Sialic Acids Using Chimeric Switch Receptors Based on Siglec-9 Enhances the Antitumor Efficacy of Engineered T Cells. Cancer immunology research 9 39037052
2023 Sialic Acids on Tumor Cells Modulate IgA Therapy by Neutrophils via Inhibitory Receptors Siglec-7 and Siglec-9. Cancers 9 37444515
2022 Development of Effective Siglec-9 Antibodies Against Cancer. Current oncology reports 9 36445569
2014 Dasatinib enhances migration of monocyte-derived dendritic cells by reducing phosphorylation of inhibitory immune receptors Siglec-9 and Siglec-3. Experimental hematology 8 24882272
2024 Siglec-7 and Siglec-9 expression in primary triple negative and oestrogen receptor positive breast cancer and in vitro signalling. Clinical & translational immunology 7 39246414
2014 Lectin-dependent localization of cell surface sialic acid-binding lectin Siglec-9. Cytotechnology 7 24449467
2025 Proximity Labeling and Genetic Screening Reveal that DSG2 is a Counter Receptor of Siglec-9 and Suppresses Macrophage Phagocytosis. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 6 39813162
2010 A novel function of Siglec-9 A391C polymorphism on T cell receptor signaling. International archives of allergy and immunology 6 20733319
2025 Tumor-expressed GPNMB orchestrates Siglec-9+ TAM polarization and EMT to promote metastasis in triple-negative breast cancer. Proceedings of the National Academy of Sciences of the United States of America 5 40892920
2023 The change of Siglec-9 expression in peripheral blood NK cells of SFTS patients can affect the function of NK cells. Immunology letters 5 37865296
2020 Synthetic Siglec-9 Agonists Inhibit Neutrophil Activation Associated with COVID-19. ChemRxiv : the preprint server for chemistry 5 33469569
2018 Mapping the interaction site and effect of the Siglec-9 inflammatory biomarker on human primary amine oxidase. Scientific reports 5 29391504
2014 Enhanced lentiviral vector production in 293FT cells expressing Siglec-9. Cytotechnology 4 24464124
2024 Association of SIGLEC9 Expression with Cytokine Expression, Tumor Grading, KRAS, NRAS, BRAF, PIK3CA, AKT Gene Mutations, and MSI Status in Colorectal Cancer. Current issues in molecular biology 3 39727942
2026 Synthetic SIGLEC9-based chimeric switch receptor augments the efficacy of CAR macrophages against glioblastoma. Proceedings of the National Academy of Sciences of the United States of America 2 41843671
2025 Sialylated glycoproteins bind to Siglec-9 in a cis manner on platelets to suppress platelet activation. Journal of thrombosis and haemostasis : JTH 2 40204021
2024 Effect of Hypoxia on Siglec-7 and Siglec-9 Receptors and Sialoglycan Ligands and Impact of Their Targeting on NK Cell Cytotoxicity. Pharmaceuticals (Basel, Switzerland) 2 39598355
2024 Transforming the Dark into Light: A Siglec-9 Switch. Cancer immunology research 1 39037058
2026 Chemoradiotherapy facilitates siglec-10+/siglec-9+ macrophage-mediated impairment of CD24+/MUC16+ tumor cell elimination and enhances PD-L2 dependent immunosuppression in cervical cancer. Cancer immunology, immunotherapy : CII 0 41801406
2026 Targeting PD-L1 and disrupting Siglec-9 cooperatively potentiate macrophage phagocytosis of breast cancer via a trispecific macrophage engager (TriME). Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 0 42259136
2025 [Preliminary study on the role of siglec-9 expression in peripheral blood of acute respiratory distress syndrome patients]. Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases 0 39914835
2025 Rational design of FVIII sialylated peptides to target Siglec-3 and Siglec-9 and improve peptide formulations for reverse vaccines. Frontiers in bioengineering and biotechnology 0 40276034
2025 Soluble Siglec-9 Improves Intestinal Barrier Function in a Mouse Model of Metabolic Dysfunction-Associated Steatohepatitis. Metabolites 0 40559390
2025 Siglec-9 acts as an immune checkpoint marker on MDSCs in brucella infection. Frontiers in cellular and infection microbiology 0 41234517

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