Selected-GenAtlas references SOURCE GeneCards NCBI Gene Swiss-Prot Ensembl
HGNC UniGene Nucleotide OMIM UCSC
Home Page
Symbol LGALS9 contributors: mct - updated : 02-02-2016
HGNC name lectin, galactoside-binding, soluble, 9
HGNC id 6570
Location 17q11.2      Physical location : 25.958.173 - 25.976.585
Synonym name
  • oesinophil-activating factor
  • galectin 9
  • ecalectin
  • urate transporter/channel protein
  • tumor Ag HOM-HD-21
  • Synonym symbol(s) ECALECTIN, LEG9, UAT, HOM-HD-21, HUATA, MGC117375, MGC125973, MGC125974, LGALS9A
    TYPE functioning gene
    STRUCTURE 18.41 kb     11 Exon(s)
    10 Kb 5' upstream gene genomic sequence study
    MAPPING cloned Y linked N status provisional
    Physical map
    LOC390778 17 hypothetical gene supported by NM_021012 LOC388361 17 similar to PDZ and LIM domain 1 (elfin); carboxy terminal LIM domain protein 1; enigma homolog LOC388362 17 LOC388362 LOC253251 17q11.2 similar to 40S ribosomal protein S16 WSB1 17q11.2 SOCS box-containing WD protein SWiP-1 LOC390779 17 similar to ubiquitin specific protease 6; tre-2 oncogene; hyperpolymorphic gene 1 KSR 17q11.1 kinase suppressor of ras LGALS9 17q11.1 lectin, galactoside-binding, soluble, 9 (galectin 9) LOC390780 17 similar to ubiquitin specific protease 6; tre-2 oncogene; hyperpolymorphic gene 1 LOC390781 17 similar to galectin-9 NOS2A 17q11.2 nitric oxide synthase 2A (inducible, hepatocytes) LOC390782 17 similar to 60S ribosomal protein L10 (QM protein) (Tumor suppressor QM) (Laminin receptor homolog) NLK 17q11.2 nemo-like kinase PYY2 17q11.1-q11.2 peptide YY, 2 (seminalplasmin) PPY2 17q11.1-q11.2 pancreatic polypeptide 2 LOC339274 17q11.2 similar to Hypothetical protein KIAA0563 FLJ40504 17q11.2 hypothetical protein FLJ40504 MAC30 17q11.2 hypothetical protein FLJ40504 LOC90410 17q11.2 intraflagellar transport protein IFT20 TNFAIP1 17q11 tumor necrosis factor, alpha-induced protein 1 (endothelial) PDIP38 MGC45714 17q11.2 hypothetical protein MGC45714 VTN 17q11.2 vitronectin (serum spreading factor, somatomedin B, complement S-protein) SARM1 17q11 sterile alpha and TIR motif containing 1 MGC9564 17q11.2 similar to RIKEN cDNA 1110002C08 gene
    TRANSCRIPTS type messenger
    identificationnb exonstypebpproduct
    ProteinkDaAAspecific expressionYearPubmed
    10 - 1739 36 323 - 2009 19335620
  • isoform short
  • acting as an eosinophil chemoattractant
  • increasing E-selectin in LoVo colon carcinoma cells (Zhang 2009)
  • 11 - 1835 40 355 lymphoid tissues, spleen, peripheral blood lymphocytes 2009 19335620
  • isoform long
  • decreases E-selectin levels in LoVo colon carcinoma cells (Zhang 2009)
  • 9 splicing - - - - 2014 24333696
  • found to induce a small inhibitory effect on angiogenesis
  • endothelial cells regulate the expression and splicing of LGALS9 during angiogenesis
       expressed in (based on citations)
    SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
    blood / hematopoieticspleen   highly
    Nervousbrain   moderately
    Respiratorylung   moderately
    Urinarykidney   moderately
    SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
    SystemCellPubmedSpeciesStageRna symbol
    Lymphoid/ImmuneT cell Homo sapiens
    cell lineage
    cell lines
    at STAGE
  • N and C terminal carbohydrate-binding domains connected by a link peptide
  • four membrane spanning domains
  • two galectin domains
  • conjugated Other
    mono polymer monomer
    intraspecies homolog to sequences found in the SMS repeat gene clusters SMS-REPM,SMS-REPP (see symbols)
  • beta galactoside binding protein family (galophin family)
  • CATEGORY regulatory , secretory
    basic FUNCTION
  • cell adhesion
  • inflammation apoptosis and metastasis
  • T cell derived regulator of eosinophil recruitment in tissues during inflammatory reactions
  • eosinophil chemoattractant
  • induces osteoblast differentiation through the CD44/Smad signaling in the absence of BMPs (Tanikawa 2010)
  • increases alkaline phosphatase activities in osteoblasts and induces the phosphorylation of Smad1/5/8 and translocation of Smad4 tot he nucleus in the absence of BMPs (Tanikawa 2010)
  • also inducing binding of smad4 to the Id1 promoter and increases its activity (Tanikawa 2010)
  • involved in modulating cell-cell and cell-matrix interactions
  • might participate in the interaction between the hormone and receptor cells with their surrounding cells and might thus play a role in the pathogenesis of this disease and/or its associated immunodeficiency
  • may play a role in thymocyte-eptihelial interactions relevant to the biology of the thymus
  • inhibits cell proliferation
  • inducing Th1 death
  • ligand for HAVCR2/TIM3
  • inducing proliferation of osteoblasts through clustering lipid rafts on membrane and subsequent phosphorylation of the c-Src/ERK signaling pathway (Tanikawa 2008)
  • autocrine regulator of mast cell function to suppress excessive degranulation (niki 2009)
  • may have an immunoregulatory function during the ongoing cytotoxic response during a rejection episode (Naka 2009)
  • LPS-responsive factor that transactivates inflammatory cytokines gene in monocytes through direct interaction with CEBPB (Matsuura 2009)
  • regulates T helper cell function independently of HAVCR2
  • suppresses Th17 cell development in an IL2-dependent but HAVCR2-independent manner
  • LGALS9/HAVCR2 interactions inducing resistance of activated CD4(+) T cells to HIV-1 infection which suggest that LGALS9 may play a role in HIV-1 pathogenesis
  • LGALS9 engagement impairs the function of NK cells, including cytotoxicity and cytokine production
  • contributes to the inducible immunomodulatory functions of mesenchymal stromal cells (MSCs)
  • has likely dual properties as both a regulator and an activator of mast cells
  • exogenous LGALS9, in addition to being an effector molecule for Treg cells, acts synergistically with TGFB1 to enforce nduced regulatory T cells (iTreg) differentiation and maintenance
  • activation of CNS LGALS9 likely modulates neuroinflammatory processes in which TNF and IL6 contribute to either pathology or reparation
  • tandem repeat type of galectin, was originally identified as a chemotactic factor for eosinophils, and is also involved in the regulatory process of inflammation
  • possible involvement of the HAVCR2/LGALS9 system in the modulation of inflammatory bone destruction
  • CELLULAR PROCESS cell life, proliferation/growth
    a component S-type lectin
    small molecule
  • binding to CD44 and inducing the formation of a CD44/BMP receptor complex (Tanikawa 2010)
  • LGALS9 is a ligand for HAVCR2, a type I glycoprotein induced on T cells during chronic inflammation
  • HAVCR2 serves as a functional receptor in structural cells of the airways and via the ligand LGALS9 can modulate the inflammatory response
  • cell & other
  • high affinity for the Forssman pentasaccharide
    induced by by TNF in astrocytes via the JNK/JUN pathway and astrocyte-derived LGALS9 may function as an immunoregulatory protein in response to ongoing neuroinflammation
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral   insertion    
    in colorectal cancer
    constitutional     --low  
    in end-stage dilated cardiomyopathy (Colak 2009)
    tumoral     --over  
    overexpressed in Hodgkin's disease tissue
    Variant & Polymorphism
    Candidate gene
  • LGALS9-induced apoptosis of hyperproliferative rheumatoid arthritis (RA) fibroblast-like synoviocytes may play a role in the suppression of RA (Seki 2007)
  • decreased LGALS9 expression is inversely associated with malignant potential or differentiation of cervical intraepithelial neoplasia and cervical squamous cell carcinoma as a differentiation biomarker (Liang 2008)
  • Marker
    Therapy target
  • may have a beneficial utility fir the treatment of allergic disorders including asthma (Niki 2009)
  • blocking LGALS9-HAVCR2 interaction in vivo might alleviate the Th1-suppressive effect of NPC exosomes and sustain antitumoral T-cell responses and thereby improve clinical efficacy of immunotherapeutic approaches against nasopharyngeal carcinoma (Klibi 2009)