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Symbol FLT3 contributors: mct/npt/pgu - updated : 08-02-2016
HGNC name fms-related tyrosine kinase 3
HGNC id 3765
  • five immunoglobulin-like C2-type domains in the extracellular region
  • a signal peptide domain
  • a catalytic domain interrupted in two part by a specific hydrophilic "interkinase" sequence
  • a juxtamembrane domain (in ETV6/FLT3 fusion protein is critical for cell proliferation and PIM1 up-regulation that might be independent of a requirement for signaling through STAT5, MAPK, and AKT pathways)
  • conjugated GlycoP , PhosphoP
    mono polymer homomer , dimer
    interspecies homolog to murine Flt3
    homolog to C.elegans F59F3.5
  • protein kinase superfamily
  • Tyr protein kinase family
  • CSF-1/PDGF receptor subfamily
  • CATEGORY enzyme , protooncogene , receptor membrane tyrosine kinase
    SUBCELLULAR LOCALIZATION     plasma membrane
    intracellular,cytoplasm,organelle,endoplasmic reticulum
    text type I membrane protein, localized primarily at the cell surface (
    basic FUNCTION
  • receptor for the FL cytokine
  • having tyrosine-protein kinase activity
  • involved in proliferative events of hematopoietic stem cells
  • activated at the late stages of liver regeneration and participates in the proliferation response that is observed during progenitor-dependent liver regeneration
  • plays a critical role in maintenance of hematopoietic homeostasis
  • FLT3 signaling might play an important role in cell survival, especially at stem and progenitor cells that are critical cellular targets for acute myelogenous leukemia transformation
  • FLT3-mediated MAPK14 activation participates in the control of megakaryopoiesis in primary myelofibrosis
  • HOXA9 and FLT3 signaling are individually important for the generation of lymphoid lineage precursors from multipotent hematopoietic progenitors (MPP) in bone marrow
  • FLT3 signaling plays a crucial role in regulating the survival and differentiation of lymphoid progenitors into B cell precursors (BCPs) in bone marrow
  • regulates the proliferation, survival, and maintenance of developmental stage-specific hematopoietic progenitors that give rise to BCPs
  • FYN cooperates with oncogenic FLT3-ITD (internal tandem duplication) in cellular transformation by selective activation of the STAT5 pathway
  • CELLULAR PROCESS cell life, proliferation/growth
    text positive control of cell proliferation
    FLT3 signaling regulates the proliferation, survival, and maintenance of multipotent hematopoietic progenitors that generate B cell precursors
    a component
    small molecule nucleotide,
  • ATP
  • protein
  • binding to the FL cytokine
  • PTPRJ is negatively regulating FLT3 signaling activity and its loss may contribute to but is not sufficient for leukemogenic cell transformation
  • SOCS6 negatively regulates FLT3 activation, the downstream Erk signaling pathway, and cell proliferation
  • FLT3-mediated inhibition of hematopoiesis in KMT2A-AFF1-expressing hESCs, which is associated with large transcriptional changes and downregulation of genes involved in hematopoietic system development and function
  • SOCS2 negatively regulates FLT3 signaling by blocking activation of Erk 1/2 and STAT5
  • direct interaction of PTPRJ with the hematopoietic receptor-tyrosine kinase Fms-like tyrosine kinase-3 (FLT3), and interaction occurs mainly via an enzyme-substrate complex formation triggered by FLT3 ligand stimulation
  • BCL11A is required for expression of I7 receptor (IL7RA) and FLT3 in early hematopoietic progenitor cells
  • promotes FLT3 receptor activation in acute myeloid leukemia cells
  • CBFB is essential for the development of FLT3(+) macrophage-dendritic cell (DC) progenitors in the bone marrow and all DC subsets in the periphery
  • HES1 directly bound to the promoter region of the FMS-like tyrosine kinase 3 (FLT3) gene and downregulated the promoter activity
  • ITD-FLT3 increases cell migration toward CXCL12 by antagonizing the down-regulation of ROCK1 expression
  • cell & other
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral   amplification    
    in childhood acute myeloid leukemia
    tumoral somatic mutation      
    duplication mutations within the juxtamembrane domain in adult de novo acute myeloid leukemia
    tumoral somatic mutation      
    in high hyperdiploid childhood acute lymphoblastic leukemia
    tumoral somatic mutation      
    an internal tandem duplication (FLT3/ITD) is associated with poor prognosis in acute myeloid leukemia (AML), interaction with NPM1 mutations identify 3 prognostic groups: good (FLT3/ITD(-)NPM1(+)), intermediate (FLT3/ITD(-)NPM1(-) or FLT3/ITD(+)NPM1(+)), and poor (FLT3/ITD(+)NPM1(-))
    constitutional       gain of function
    activating mutations in FLT3 induce ligand-independent downstream signaling that promotes oncogenesis through pathways involved in proliferation, differentiation, and survival
      fusion translocation    
    ETV6/FLT3 (EF) fusion proteins in a patient with myeloproliferative disorder (MPD) and a t(12;13)(p13;q12) translocation
    Variant & Polymorphism
    Candidate gene
    Therapy target
    activated FLT3 is a promising molecular target for AML therapies
    model of APL-like disease in mice