FMS related to Tyrosine Kinase 3 (FLT3, also called FLK2), is a member of the Type III Tyrosine Kinase receptor, which includes C-kit, PDGFR and M-CSF receptors. FLT3 is expressed in early independent granny cells and supports growth and differentiation in a hematopoietic system.
The FLT3 is activated after binding with Ligand FL, which produces tyrosine phosphorylation cascade and tyrosine phosphorylation from the downstream substrate. Subunit P85 of PI3 Kinase, SHP2, GRB2, and SHC everything has been reported to associate with FLT3 after FL stimulation. You can know more about FLT3 antibodies online via https://www.bosterbio.com/anti-flt3-cd135-picoband-trade-antibody-a00188-4-boster.html.
TYR589 / 591 is located in the Juxtamembrane FLT3 area and can play an important role in the regulation of the activity of FLT3 Tyrosine Kinase. The Somatic Mutation of FLT3 consisting of internal tandem duplication (ITDS) occurs in 20% of patients with acute myeloid leukemia. This gene encodes class III Tyrosine Kinase receptors that regulate hematopoiesis.
The receptor consists of an extracellular domain consisting of five domains such as immunoglobulin, one transmembrane area, and the cytoplasmic kinase domain is divided into two parts with the domain insert kinase. The receptor is activated by binding Tyrosine Kinase 3 ligands related to FMS to the extracellular domain, which induces the formation of homodimers in plasma membranes that lead to the autophosphorylation of the receptor.
Receptor kinases are activated subsequently in phosphory and activate several cytoplasmic effector molecules in the lane involved in apoptosis, proliferation, and differentiation of hematopoietic cells in the bone marrow. Mutations that resulted in the constitutional activation of this receptor produce acute myeloid leukemia and acute lymphoblastic leukemia.