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FLASH GENE
Symbol AXL contributors: mct/npt/pgu - updated : 25-01-2016
HGNC name AXL receptor tyrosine kinase
HGNC id 905
Location 19q13.2      Physical location : 41.725.107 - 41.767.670
Synonym name
  • AXL oncogene
  • AXL transforming sequence/gene
  • Synonym symbol(s) TYRO7, UFO, JTK11, ARK
    EC.number 2.7.10.1
    DNA
    TYPE functioning gene
    STRUCTURE 42.57 kb     20 Exon(s)
    10 Kb 5' upstream gene genomic sequence study
    MAPPING cloned Y linked   status provisional
    RNA
    TRANSCRIPTS type messenger
    identificationnb exonstypebpproduct
    ProteinkDaAAspecific expressionYearPubmed
    20 - 4716 - 885 - 2009 18840707
    full length isoform
    19 initiation site 4743 - 894 - 2009 18840707
  • lacking exon 10
  • otherwise similar to variant 1
  • 4128 - 17 - 626 - -
    EXPRESSION
    Type widely
       expressed in (based on citations)
    organ(s)
    SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
    Cardiovascularheart   highly Homo sapiens
    Reproductivefemale systemuteruscervix highly
    reproductivereproductive tract    
    tissue
    SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
    Lymphoid    
    cell lineage
    cell lines
    fluid/secretion
    at STAGE
    PROTEIN
    PHYSICAL PROPERTIES
    STRUCTURE
    motifs/domains
  • two Ig-like domains linked to two fibronectin,type III repeats
  • a cytoplamic region that contains an intrinsic protein tyrosine kinase domain
  • HOMOLOGY
    Homologene
    FAMILY
  • protein kinase superfamily
  • Tyr protein kinase family
  • AXL/UFO subfamily
  • CATEGORY enzyme , protooncogene , receptor membrane tyrosine
    SUBCELLULAR LOCALIZATION     plasma membrane
    text integral to plasma membrane
    basic FUNCTION
  • receptor tyrosine kinase
  • involved in the protection of neurons from apoptosis across neuronal migration
  • involved in the regulation of spermatogenesis, immunity, platelet function, cancer
  • enhances the expression of matrix metalloproteinase 9 MMP9, required for AXL-mediated invasion
  • promotes cell invasion by inducing MMP9 activity through activation of NF-kappaB and SMARCA4
  • with its ligand, GAS6, are involved in IL-15-mediated human NK differentiation from CD34(+) hematopoietic progenitor cells (HPCs)
  • regulates endothelial cell functions by modulation of signaling through angiopoietin/TIE2 and Dickkopf-homologue 3 (DKK3) pathways
  • its expression is required for metastasis of breast cancer cells to the lung
  • enhances endothelial tube formation by acting through the angiopoietin and DKK3 signaling system
  • GAS6/AXL-mediated signaling regulates dendritic cell activities, and identifies GAS6/AXL as a new dendritic cell chemotaxis pathway
  • unique epithelial-to-mesenchymal transition effector that is essential for breast cancer progression
  • is a key downstream target that drives YAP1-dependent oncogenic functions
  • regulates mesothelioma proliferation and invasiveness
  • contributes to carotid remodeling not only by inhibition of apoptosis but also via regulation of immune heterogeneity of vascular cells, cytokine/chemokine expression, and extracellular matrix remodeling
  • is a key TGFB1 effector
  • AXL in both hematopoietic and nonhematopoietic lineages contributes to the late phase of hypertension.
  • potential contribution of AXL-mediated phosphorylation dynamics to pluripotency-related signaling networks
  • contributes to cell migration and invasion, and promotes cell proliferation
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling signal transduction
    AXL/GAS6 pathway contributes to normal NK-cell development, at least in part via its regulatory effects on both the IL15 and c-Kit signaling
  • GAS6/AXL signaling plays an important role in vascular biology by modulating survival and migration of vascular smooth muscle cells and endothelial cells
  • a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • interacting with RANBP9
  • ligand GAS6
  • ability of TNK2 to modulate AXL and perhaps anaplastic lymphoma kinase (altered in anaplastic large cell lymphomas) might explain why TNK2 can promote metastatic and transformed behavior in a number of cancers
  • GAS6 in circulation is bound to AXL suggesting circulating GAS6 to be inhibited and incapable of stimulating the TAM receptors
  • interacting with MZF1 (binds to the AXL promoter, transactivates promoter activity, and enhances AXL-mRNA and protein expression in a dose-dependent manner
  • TULP1 interacts with TYRO3, AXL and MERTK of the TAM receptor tyrosine kinase subfamily, whereas tubby binds only to MERTK
  • AXL expression is induced by TGFB1 during Langerhans cells (LCs) differentiation and LC precursors acquire AXL early during differentiation
  • GAS6 interact with AXL in endothelial cells, inducing several signaling pathways involved in cell survival and proliferation
  • binding of AXL to YWHAZ, which is essentially required for AXL-mediated cell invasion, transendothelial migration, and resistance against TGFB1
  • ELMO2 scaffolds to be direct substrates and binding partners of AXL
  • GAS6-induced AXL signaling is a critical driver of pancreatic cancer progression
  • ARL2 inhibits the proliferation, migration and tumorigenicity of glioma cells by regulating the expression of AXL
  • cell & other
    REGULATION
    induced by IFN-alpha during human dendritic cell (DC) differentiation from monocytes
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral     --over  
    myelogenous leukemia
    tumoral     --over  
    lung carcinoma, invasion and progression
    tumoral     --over  
    colon carcinoma
    tumoral     --over  
    melanoma
    tumoral     --over  
    in both glioma and vascular cells and predict poor prognosis in glioblastoma multiformis patients
    tumoral     --over  
    in breast cancer independently predicts poor overall patient survival
    tumoral   amplification    
    in mesotheliomas
    tumoral     --over  
    in triple-negative/basal B cell lines of breast cancer compared with luminal or basal A cell lines
    constitutional     --over  
    myocardial expression and serum concentration of AXL is elevated in heart failure patients compared to controls
    constitutional     --over  
    plasma soluble AXL concentrations were higher in the preeclampsia patients, and plasma soluble AXL levels were correlated with the clinical parameters of severe preeclampsia
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
  • role of soluble AXL as a marker for NF1 related tumor burden
  • Therapy target
    SystemTypeDisorderPubmed
    cancerbrainglioma/neuroblstoma
    specific targeting of the Axl/Gas6 signaling pathway may represent a potential new approach for glioma treatment
    cancerangiogenesis 
    additive effect of AXL inhibition with anti-VEGF suggests that blocking AXL function might be a useful approach for enhancing antiangiogenic therapy and warrant further investigation
    cancerreproductivebreast
    detection and targeted treatment of AXL-expressing tumors represents an important new therapeutic strategy for breast cancer
    cancerhemopathy 
    unique target for chronic lymphocytic leukemia treatment
    cancerdigestiveliver
    potential therapeutic target for hepatocellular carcinoma
    cancerendocrinethyroid
    TYRO3/AXL-GAS6 autocrine circuit sustains the malignant features of thyroid cancer cells and targeting the circuit could offer a novel therapeutic approach in this cancer
    cancerlung 
    AXL inhibition suppressed mesothelioma anchorage-independent growth
    cancerendocrinepancreas
    GAS6 inhibition with low-dose warfarin or other AXL-targeting agents may improve outcome in patients with AXL-expressing tumors
    cancerreproductiveprostate
    role for AXL in prostate cancer tumorigenesis with implications for prostate cancer treatment
    ANIMAL & CELL MODELS
  • Axl /Tyro3 null mice have delayed first estrus and abnormal cyclicity due to developmental defects in GnRH neuron migration and survival