Recombinant human Flt3 / CD135 protein (L610_E611insCSSDNEYFYVDFREYEYDLKWEF-PRENL) (Active) is a Human Fragment protein, in the 571 to 993 aa range, expressed in Baculovirus infected Sf9, with >70% purity and suitable for SDS-PAGE, FuncS.
Application | Reactivity | Dilution info | Notes |
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Application SDS-PAGE | Reactivity Reacts | Dilution info - | Notes - |
Application FuncS | Reactivity Reacts | Dilution info - | Notes - |
Tyrosine-protein kinase that acts as a 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.
CD135, FLK2, STK1, FLT3, Receptor-type tyrosine-protein kinase FLT3, FL cytokine receptor, Fetal liver kinase-2, Fms-like tyrosine kinase 3, Stem cell tyrosine kinase 1, FLK-2, FLT-3, STK-1
Recombinant human Flt3 / CD135 protein (L610_E611insCSSDNEYFYVDFREYEYDLKWEF-PRENL) (Active) is a Human Fragment protein, in the 571 to 993 aa range, expressed in Baculovirus infected Sf9, with >70% purity and suitable for SDS-PAGE, FuncS.
pH: 7.5
Constituents: 25% Glycerol (glycerin, glycerine), 0.87% Sodium chloride, 0.79% Tris HCl, 0.31% Glutathione, 0.004% (R*,R*)-1,4-Dimercaptobutan-2,3-diol, 0.003% EDTA, 0.002% PMSF
Affinity purified.
Tyrosine-protein kinase that acts as a 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.
Belongs to the protein kinase superfamily. Tyr protein kinase family. CSF-1/PDGF receptor subfamily.
N-glycosylated, contains complex N-glycans with sialic acid.
This product is an active protein and may elicit a biological response in vivo, handle with caution.
Flt3 also known as CD135 or FLT3 tyrosine kinase is a receptor tyrosine kinase that belongs to the class III receptor tyrosine kinase family. It has a molecular weight of approximately 160 kDa. This protein plays an important role in the development of hematopoietic stem and progenitor cells. Flt3 is expressed mainly in early progenitor cells within the bone marrow. Additionally it is present in some populations of mature cells in the peripheral blood and lymphoid organs.
Flt3 functions as a receptor that is activated by binding to its ligand FLT3 ligand (FLT3L). This interaction stimulates the associated tyrosine kinase activity leading to auto-phosphorylation of Flt3 and subsequent downstream signaling. Flt3 does not form a heterocomplex rather it dimerizes upon ligand binding to initiate signaling cascades. These cascades promote cell proliferation differentiation and survival particularly impacting hematopoiesis and immune responses.
Flt3 signaling impacts the internal signaling networks involving the MAPK/ERK and PI3K/AKT pathways both central to cell cycle regulation and apoptosis. Flt3 interacts functionally with proteins such as SHP2 and GRB2 in these pathways aiding signal transduction. The Flt3 receptor also shares functional motifs with KIT and PDGF receptors indicating shared regulatory mechanisms involved in cellular proliferation.
Flt3 mutations especially internal tandem duplications in Flt3/ITD are significant in acute myeloid leukemia (AML) leading to abnormal cell growth and survival. These mutations often co-occur with other genetic anomalies such as NPM1 mutations contributing to the oncogenic process. The abnormal activation of Flt3 kinase activity also has ramifications in myelodysplastic syndromes making it a target for therapeutic intervention with drugs such as anti-FLT3 inhibitors in the treatment regime.
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SDS-PAGE analysis of ab268586.
The specific activity of Flt3 / CD135 was determined to be 12 nmol/min/mg in a kinase assay using MBP substrate.
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