Invitrogen™ TNFRSF10B (DR5) Human ELISA Kit

Description

The Human Tumor Necrosis Factor Receptor SuperFamily 10 B/Death Receptor 5 (TNFRSF10B (DR5)) ELISA quantitates Hu DR5 in human serum, plasma, or cell culture medium. The assay will exclusively recognize both natural and recombinant Hu DR5. Principle of the method The Human DR5 solid-phase sandwich ELISA (enzyme-linked immunosorbent assay) is designed to measure the amount of the target bound between a matched antibody pair. A target-specific antibody has been pre-coated in the wells of the supplied microplate. Samples, standards, or controls are then added into these wells and bind to the immobilized (capture) antibody. The sandwich is formed by the addition of the second (detector) antibody, a substrate solution is added that reacts with the enzyme-antibody-target complex to produce measurable signal. The intensity of this signal is directly proportional to the concentration of target present in the original specimen. Rigorous validation Each manufactured lot of this ELISA kit is quality tested for criteria such as sensitivity, specificity, precision, and lot-to-lot consistency. See manual for more information on validation.

Apoptosis, or programmed cell death, occurs during normal cellular differentiation and development of multicellular organisms. Apoptosis is induced by certain cytokines including tumor necrosis factor (TNF) and Fas ligand in the TNF family through their death domain containing receptors, TNF receptor 1 (TNFR1) and Fas, respectively. Another member in the TNF family has been identified and designated TRAIL (for TNF related apoptosis inducing ligand) and Apo2L (for Apo2 ligand). Receptors for TRAIL include two death domain containing receptors, DR4 and DR5, as well as two decoy receptors, DcR1 and DcR2, lacking the intracellular signaling death domain. DR5 contains an intracellular death domain. This receptor can be activated by tumor necrosis factor related apoptosis inducing ligand (TNFSFS10/TEAIL/APO2L), and transduces apoptosis signal. Studies with FADD deficient mice suggested that FADD, a death domain containg adaptor protein, is required for the apoptosis mediated by this protein.