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Product Name FLT3 Chinese Name FMS样酪氨酸激酶3 Alias Receptor-type tyrosine-protein kinase FLT3; CD135 antigen; Fetal liver kinase 2; FL cytokine receptor; Flk 2; Flk2; Flt 3; FLT-3; FMS like tyrosine kinase 3; Fms related tyrosine kinase 3; Growth factor receptor tyrosine kinase type III; Stem cell tyrosine kinase 1; Stk 1; Stk1; Tyrosine protein kinase receptor FLT3; FLT3_HUMAN. Research Area Kinases and Phosphatases Immunogen Species Rabbit Clonality Polyclonal React Species Human, Mouse, Rat, Applications WB=1:500-2000 ELISA=1:5000-10000 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:100-500 (Paraffin sections need antigen repair)
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.Theoretical molecular weight 109kDa Cellular localization cytoplasmic The cell membrane Form Liquid Concentration 1mg/ml immunogen KLH conjugated synthetic peptide derived from human FLT-3: 551-650/993 <Cytoplasmic> Lsotype IgG Purification affinity purified by Protein A Buffer Solution 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. Storage Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. Attention This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. PubMed PubMed Product Detail 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.
Function:
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.
Subunit:
Monomer in the absence of bound FLT3LG. Homodimer in the presence of bound FLT3LG. One homodimer interacts with one FLT3LG molecule. Interacts with FIZ1 following ligand activation (By similarity). Interacts with FES, FER and GRB2. Interacts with PTPRJ/DEP-1 and PTPN11/SHP2.
Subcellular Location:
Membrane; Single-pass type I membrane protein. Endoplasmic reticulum lumen.
Tissue Specificity:
Detected in bone marrow, in hematopoietic stem cells, in myeloid progenitor cells and in granulocyte/macrophage progenitor cells (at protein level). Detected in bone marrow, liver, thymus, spleen and lymph node, and at low levels in kidney and pancreas. Highly expressed in T-cell leukemia.
Post-translational modifications:
N-glycosylated, contains complex N-glycans with sialic acid.
Autophosphorylated on several tyrosine residues in response to FLT3LG binding. FLT3LG binding also increases phosphorylation of mutant kinases that are constitutively activated. Dephosphorylated by PTPRJ/DEP-1, PTPN1, PTPN6/SHP-1, and to a lesser degree by PTPN12. Dephosphorylation is important for export from the endoplasmic reticulum and location at the cell membrane.
DISEASE:
Defects in FLT3 are a cause of acute myelogenous leukemia (AML) [MIM:601626]. AML is a malignant disease in which hematopoietic precursors are arrested in an early stage of development. Note=Somatic mutations that lead to constitutive activation of FLT3 are frequent in AML patients. These mutations fall into two classes, the most common being in-frame internal tandem duplications of variable length in the juxtamembrane region that disrupt the normal regulation of the kinase activity. Likewise, point mutations in the activation loop of the kinase domain can result in a constitutively activated kinase.
Similarity:
Belongs to the protein kinase superfamily. Tyr protein kinase family. CSF-1/PDGF receptor subfamily.
Contains 1 Ig-like C2-type (immunoglobulin-like) domain.
Contains 1 protein kinase domain.
SWISS:
P36888
Gene ID:
2322
Database links:Entrez Gene: 2322 Human
Entrez Gene: 14255 Mouse
Omim: 136351 Human
SwissProt: P36888 Human
SwissProt: Q00342 Mouse
Unigene: 507590 Human
Unigene: 194 Mouse
Unigene: 6774 Rat
Product Picture Sample:
Lane 1: Mouse Cerebrum tissue lysates
Lane 2: Mouse Placenta tissue lysates
Lane 3: Mouse Testis tissue lysates
Lane 4: Rat Cerebrum tissue lysates
Lane 5: Rat Placenta tissue lysates
Lane 6: Human THP-1 cell lysates
Primary: Anti-FLT3 (SL2767R) at 1/1000 dilution
Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
Predicted band size: 109 kDa
Observed band size: 160 kDa
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