ELISA/assay

Rabbit Fas/APO-1 ELISA Kit

MBS733022

48-Strip-Wells

470 USD

ELISA Kit

Rabbit Fas/APO-1 ELISA Kit

Fas/APO-1

Fas/Apo-1/CD95; Tumor necrosis factor receptor superfamily member 6; tumor necrosis factor receptor superfamily member 6; Fas AMA; FAS 827dupA; CD95 antigen; FASLG receptor; apoptosis antigen 1; Delta Fas/APO-1/CD95; FAS receptor variant 9; APO-1 cell surface antigen; TNF receptor superfamily member 6; apoptosis-mediating surface antigen FAS; Fas (TNF receptor superfamily, member 6); tumor necrosis factor receptor superfamily, member 6; Fas cell surface death receptor; Apo-1 antigen; Apoptosis-mediating surface antigen FAS; FASLG receptor; CD_antigen: CD95

Fas/APO-1

FAS; FAS; APT1; CD95; FAS1; APO-1; FASTM; ALPS1A; TNFRSF6; APT1; FAS1; TNFRSF6

TNR6_HUMAN

Rabbit

This assay has high sensitivity and excellent specificity for detection of FAS/APO-1. No significant cross-reactivity or interference between FAS/APO-1 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between FAS/APO-1 and all the analogues, therefore, cross reaction may still exist in some cases.

Store all reagents at 2-8 degree C.

Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Assay Type: Competitive. Sensitivity: 1.0 pg/mL.

Intended Uses: This FAS/APO-1 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Rabbit FAS/APO-1. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Cell Biology

Principle of the assay: FAS/APO-1 ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-FAS/APO-1 antibody and an FAS/APO-1-HRP conjugate. The assay sample and buffer are incubated together with FAS/APO-1-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the FAS/APO-1 concentration since FAS/APO-1 from samples and FAS/APO-1-HRP conjugate compete for the anti-FAS/APO-1 antibody binding site. Since the number of sites is limited, as more sites are occupied by FAS/APO-1 from the sample, fewer sites are left to bind FAS/APO-1-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The FAS/APO-1 concentration in each sample is interpolated from this standard curve.

887458

CAA61473.1

P25445

24,781 Da

Adipogenesis Pathway (198832); African Trypanosomiasis Pathway (194384); African Trypanosomiasis Pathway (194323); Allograft Rejection Pathway (920963); Allograft Rejection Pathway (83123); Allograft Rejection Pathway (535); Alzheimer's Disease Pathway (83097); Alzheimer's Disease Pathway (509); Alzheimers Disease Pathway (672448); Apoptosis Pathway (198797)

The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor contains a death domain. It has been shown to play a central role in the physiological regulation of programmed cell death, and has been implicated in the pathogenesis of various malignancies and diseases of the immune system. The interaction of this receptor with its ligand allows the formation of a death-inducing signaling complex that includes Fas-associated death domain protein (FADD), caspase 8, and caspase 10. The autoproteolytic processing of the caspases in the complex triggers a downstream caspase cascade, and leads to apoptosis. This receptor has been also shown to activate NF-kappaB, MAPK3/ERK1, and MAPK8/JNK, and is found to be involved in transducing the proliferating signals in normal diploid fibroblast and T cells. Several alternatively spliced transcript variants have been described, some of which are candidates for nonsense-mediated mRNA decay (NMD). The isoforms lacking the transmembrane domain may negatively regulate the apoptosis mediated by the full length isoform. [provided by RefSeq, Mar 2011]

FAS: Receptor for TNFSF6/FASLG. The adapter molecule FADD recruits caspase-8 to the activated receptor. The resulting death- inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) mediating apoptosis. FAS- mediated apoptosis may have a role in the induction of peripheral tolerance, in the antigen-stimulated suicide of mature T-cells, or both. The secreted isoforms 2 to 6 block apoptosis (in vitro). Binds DAXX. Interacts with HIPK3. Part of a complex containing HIPK3 and FADD. Binds RIPK1 and FAIM2. Interacts with BRE and FEM1B. Interacts with FADD. Isoform 1 and isoform 6 are expressed at equal levels in resting peripheral blood mononuclear cells. After activation there is an increase in isoform 1 and decrease in the levels of isoform 6. 6 isoforms of the human protein are produced by alternative splicing. Protein type: Membrane protein, integral; Cell surface; Apoptosis; Receptor, cytokine. Chromosomal Location of Human Ortholog: 10q24.1. Cellular Component: cell surface; cytoplasm; integral to membrane; plasma membrane; CD95 death-inducing signaling complex; nucleus; cytosol; external side of plasma membrane; lipid raft. Molecular Function: identical protein binding; signal transducer activity; protein binding; transmembrane receptor activity; receptor activity; kinase binding. Biological Process: spleen development; caspase activation; circadian rhythm; regulation of myeloid cell differentiation; renal system process; transformed cell apoptosis; positive regulation of protein homooligomerization; positive regulation of apoptosis; apoptosis; response to toxin; regulation of lymphocyte differentiation; response to glucocorticoid stimulus; negative regulation of B cell activation; signal transduction; negative thymic T cell selection; regulation of apoptosis; B cell mediated immunity; inflammatory cell apoptosis; induction of apoptosis via death domain receptors; gene expression; protein complex assembly; immunoglobulin production; activated T cell apoptosis; protein homooligomerization; negative regulation of apoptosis. Disease: Autoimmune Lymphoproliferative Syndrome

48-Strip-Wells

470 USD

96-Strip-Wells

675