ELISA/assay

Human Endogenous secretory receptor for Advanced Glycation end Products ELISA Kit

MBS731589

48-Strip-Wells

470 USD

ELISA Kit

Human Endogenous secretory receptor for Advanced Glycation end Products ELISA Kit

Endogenous secretory receptor for Advanced Glycation end Products

endogenous secretory receptor for advanced glycation endproducts; Advanced glycosylation end product-specific receptor; advanced glycosylation end product-specific receptor; advanced glycation end-products receptor; receptor for advanced glycosylation end products; receptor for advanced glycation end-products variant 20; advanced glycosylation end product-specific receptor; Receptor for advanced glycosylation end products

esRAGE

Ager; Ager; RAGE; Rage

RAGE_MOUSE

Human

This assay has high sensitivity and excellent specificity for detection of esRAGE. No significant cross-reactivity or interference between esRAGE and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between esRAGE 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: 0.1 ng/mL.

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

Cancer

Principle of the assay: esRAGE ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-esRAGE antibody and an esRAGE-HRP conjugate. The assay sample and buffer are incubated together with esRAGE-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 esRAGE concentration since esRAGE from samples and esRAGE-HRP conjugate compete for the anti-esRAGE antibody binding site. Since the number of sites is limited, as more sites are occupied by esRAGE from the sample, fewer sites are left to bind esRAGE-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The esRAGE concentration in each sample is interpolated from this standard curve.

84570471

BAE72665.1

42,669 Da

Activated TLR4 Signalling Pathway (970703); Advanced Glycosylation Endproduct Receptor Signaling Pathway (1001253); Cytosolic Sensors Of Pathogen-associated DNA Pathway (1001263); DEx/H-box Helicases Activate Type I IFN And Inflammatory Cytokines Production Pathway (1001271); Immune System Pathway (971216); Innate Immune System Pathway (971212); MyD88 Cascade Initiated On Plasma Membrane Pathway (1001210); MyD88 Dependent Cascade Initiated On Endosome Pathway (1001227); MyD88-independent Cascade Pathway (1001219); MyD88:Mal Cascade Initiated On Plasma Membrane Pathway (970471)

RAGE: Mediates interactions of advanced glycosylation end products (AGE). These are nonenzymatically glycosylated proteins which accumulate in vascular tissue in aging and at an accelerated rate in diabetes. Acts as a mediator of both acute and chronic vascular inflammation in conditions such as atherosclerosis and in particular as a complication of diabetes. AGE/RAGE signaling plays an important role in regulating the production/expression of TNF- alpha, oxidative stress, and endothelial dysfunction in type 2 diabetes. Interaction with S100A12 on endothelium, mononuclear phagocytes, and lymphocytes triggers cellular activation, with generation of key proinflammatory mediators. Interaction with S100B after myocardial infarction may play a role in myocyte apoptosis by activating ERK1/2 and p53/TP53 signaling. Receptor for amyloid beta peptide. Contributes to the translocation of amyloid-beta peptide (ABPP) across the cell membrane from the extracellular to the intracellular space in cortical neurons. ABPP-initiated RAGE signaling, especially stimulation of p38 mitogen-activated protein kinase (MAPK), has the capacity to drive a transport system delivering ABPP as a complex with RAGE to the intraneuronal space. Interacts with S100B, S100A1 and APP. Interacts with S100A12. Endothelial cells. 4 isoforms of the human protein are produced by alternative splicing. Protein type: Cell cycle regulation; Motility/polarity/chemotaxis; Receptor, misc.; Membrane protein, integral. Cellular Component: extracellular space; cell surface; cell soma; membrane; axon; cytoplasm; integral to membrane; plasma membrane; basal plasma membrane; cytosol. Molecular Function: identical protein binding; protein binding; advanced glycation end-product receptor activity. Biological Process: positive regulation of JNK activity; positive regulation of apoptosis; negative regulation of collagen biosynthetic process; positive regulation of smooth muscle cell proliferation; negative regulation of cell adhesion; positive regulation of smooth muscle cell migration; JAK-STAT cascade; activation of NF-kappaB transcription factor; induction of positive chemotaxis; calcium ion homeostasis; positive regulation of fibroblast proliferation; negative regulation of protein amino acid phosphorylation; regulation of DNA binding; positive regulation of neuron apoptosis; negative regulation of endothelial cell proliferation; regulation of inflammatory response; response to hypoxia; positive regulation of protein amino acid phosphorylation; positive regulation of phagocytosis, engulfment; inflammatory response; positive regulation of autophagy; neurite development; positive regulation of inflammatory response; positive regulation of cell migration

48-Strip-Wells

470 USD

96-Strip-Wells

675