Anti-Flt3/CD135 Antibody Picoband® Fluoro488 Conjugated
Product Specifications
Background
Cluster of differentiation antigen 135 (CD135) also known as fms like tyrosine kinase 3 (FLT-3), receptor-type tyrosine-protein kinase FLT3, or fetal liver kinase-2 (Flk2) is a protein that in humans is encoded by the 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.
Synonyms
Receptor-type tyrosine-protein kinase FLT3; 2.7.10.1; FL cytokine receptor; Fetal liver kinase 2; FLK-2; Fms-like tyrosine kinase 3; FLT-3; Tyrosine-protein kinase receptor flk-2; CD135; Flt3; Flk-2, Flt-3
Gene Name
Flt3
Gene ID
14255
UniProt
Q00342
Host
Rabbit
Reactivity
Mouse, Rat
Cross Reactivity
No cross-reactivity with other proteins.
Immunogen
E. coli-derived mouse Flt3 / CD135 recombinant protein (Position: E62-E295) .
Clonality
Polyclonal
Tissue Specificity
Hematopoietic stem and progenitor cell- enriched populations. Found in brain, placenta and testis.
Applications
Flow Cytometry
Field of Research
Angiogenesis, Cardiovascular, Cytokines, Immunology, Innate Immunity
Purification
Immunogen affinity purified.
Form
Liquid
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.
References & Citations
1. Verstraete K, Vandriessche G, Januar M, Elegheert J, Shkumatov AV, Desfosses A, Van Craenenbroeck K, Svergun DI, Gutsche I, Vergauwen B, Savvides SN (February 2011) . Structural insights into the extracellular assembly of the hematopoietic Flt3 signaling complex. Blood. 118 (1) : 60–68. 2. Yamamoto Y, Kiyoi H, Nakano Y, Suzuki R, Kodera Y, Miyawaki S, Asou N, Kuriyama K, Yagasaki F, Shimazaki C, Akiyama H, Saito K, Nishimura M, Motoji T, Shinagawa K, Takeshita A, Saito H, Ueda R, Ohno R, Naoe T (April 2001) . Activating mutation of D835 within the activation loop of FLT3 in human hematologic malignancies. Blood. 97 (8) : 2434–9.
Storage Conditions
At -20 ̊C for one year from date of receipt. Avoid repeated freezing and thawing. Protect from light.
Specificity
No cross reactivity with other proteins.
Applications Notes
6
Gene Name Synonym
FMS-like tyrosine kinase 3
Subcellular Location
Membrane; Constitutively activated mutant forms with internal tandem duplications are less efficiently transported to the cell surface and a significant proportion is retained in an immature form in the endoplasmic reticulum lumen. The activated kinase is rapidly targeted for degradation (By similarity) . .
Isotype
Rabbit IgG
Contents
Each vial contains 50% glycerol, 0.9% NaCl, 0.2% Na2HPO4, 0.02% NaN3.
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