a receptor tyrosine kinase of the PDGFR family that binds the FL cytokine. FLT3 -/- mice have an impaired developmental capacity of primitive hematopoietic progenitor cells of all lineages with the greatest impact on lymphopoietic precursors. Activating mutations found in one third of cases of acute myeloid leukemia (AML), as well as in acute lymphoblastic leukemia, acute promyelocytic leukemia and myelodysplastic syndrome. Inhibitors: Sutent and PKC412. Note: This description may include information from UniProtKB.
Protein type: Kinase, protein; Protein kinase, tyrosine (receptor); Protein kinase, TK; EC 220.127.116.11; Membrane protein, integral; TK group; PDGFR family
Cellular Component: cell surface; integral to plasma membrane; endoplasmic reticulum lumen
Molecular Function: hematopoietin/interferon-class (D200-domain) cytokine receptor activity; vascular endothelial growth factor receptor activity; protein binding; protein homodimerization activity; phosphoinositide 3-kinase binding; transmembrane receptor protein tyrosine kinase activity; ATP binding
Biological Process: negative regulation of B cell differentiation; pro-B cell differentiation; lymphocyte proliferation; peptidyl-tyrosine phosphorylation; protein amino acid autophosphorylation; cytokine and chemokine mediated signaling pathway; positive regulation of phosphoinositide 3-kinase activity; regulation of apoptosis; positive regulation of phosphoinositide 3-kinase cascade; negative regulation of cell proliferation; positive regulation of MAP kinase activity; myeloid progenitor cell differentiation; positive regulation of tyrosine phosphorylation of STAT protein; positive regulation of MAPKKK cascade; B cell differentiation; positive regulation of cell proliferation; hemopoiesis; pro-T cell differentiation; transmembrane receptor protein tyrosine kinase signaling pathway; leukocyte homeostasis
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.