Description
This Human Receptor-Type Tyrosine-Protein Kinase FLT3 (CD135) ELISA Kit is intended for quantitative detection of human FLT3/FLK2 in cell culture supernates, lysates, tissue, serum and plasma (heparin, EDTA). Strip well format. Reagents for up to 96 tests.
This human FLT3/FLK2 ELISA Kit is based on standard sandwich enzyme-linked immune-sorbent assay technology. A monoclonal antibody from mouse specific for FLT3/FLK2 has been precoated onto 96-well plates. Standards (Expression system for standard: NSO, Immunogen sequence: N27-N541) and test samples are added to the wells, a biotinylated detection polyclonal antibody from goat specific for FLT3/FLK2 is added subsequently and then followed by washing with PBS or TBS buffer. Avidin-Biotin-Peroxidase Complex is added and unbound conjugates are washed away with PBS or TBS buffer. HRP substrate TMB are used to visualize HRP enzymatic reaction. TMB is catalyzed by HRP to produce a blue color product that changed into yellow after adding acidic stop solution. The density of yellow is proportional to the human FLT3/FLK2 amount of sample captured in plate.
The capture antibody is a monoclonal antibody from mouse, the detection antibody is a biotinylated polyclonal antibody from goat. Expression system for standard: 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. It is mapped to 13q12.2. 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. Mutations that result in the constitutive activation of this receptor result in acute myeloid leukemia and acute lymphoblastic leukemia