Aliases for FLT3 Gene
External Ids for FLT3 Gene
This gene encodes a class III receptor tyrosine kinase that regulates hematopoiesis. This receptor is activated by binding of the fms-related tyrosine kinase 3 ligand to the extracellular domain, which induces homodimer formation in the plasma membrane leading to autophosphorylation of the receptor. The activated receptor kinase subsequently phosphorylates and activates multiple cytoplasmic effector molecules in pathways involved in apoptosis, proliferation, and differentiation of hematopoietic cells in bone marrow. Mutations that result in the constitutive activation of this receptor result in acute myeloid leukemia and acute lymphoblastic leukemia. [provided by RefSeq, Jan 2015]
GeneCards Summary for FLT3 Gene
FLT3 (Fms-Related Tyrosine Kinase 3) is a Protein Coding gene. Diseases associated with FLT3 include minimally differentiated acute myeloblastic leukemia and lymphoblastic leukemia. Among its related pathways are GPCR Pathway and Pathways in cancer. GO annotations related to this gene include protein homodimerization activity and phosphatidylinositol 3-kinase binding. An important paralog of this gene is FGFR3.
UniProtKB/Swiss-Prot for FLT3 Gene
Tyrosine-protein kinase that acts as cell-surface receptor for the cytokine FLT3LG and regulates differentiation, proliferation and survival of hematopoietic progenitor cells and of dendritic cells. Promotes phosphorylation of SHC1 and AKT1, and activation of the downstream effector MTOR. Promotes activation of RAS signaling and phosphorylation of downstream kinases, including MAPK1/ERK2 and/or MAPK3/ERK1. Promotes phosphorylation of FES, FER, PTPN6/SHP, PTPN11/SHP-2, PLCG1, and STAT5A and/or STAT5B. Activation of wild-type FLT3 causes only marginal activation of STAT5A or STAT5B. Mutations that cause constitutive kinase activity promote cell proliferation and resistance to apoptosis via the activation of multiple signaling pathways.
FMS-like receptor tyrosine kinase-3 (FLT3) is a member of the class III RTK (receptor tyrosine kinase) family and is expressed primarily in hematopoietic progenitor cells. The expression within these cells demonstrates that FLT3 has an important role in the pathogenesis of AML (acute myelogenous leukemia), under which conditions wild type receptors are overexpressed or mutated forms of the receptor are present. Inhibitors of both mutated and wild type receptors are therefore of interest in a therapeutic context.