ELISA/assay

Human Neutrophil Elastase ELISA Kit

MBS725923

48-Strip-Wells-(Comp

470 USD

ELISA Kit

Human Neutrophil Elastase ELISA Kit

Neutrophil Elastase

neutrophil elastase preproprotein; Neutrophil elastase; neutrophil elastase; elastase-2; medullasin; PMN elastase; leukocyte elastase; elastase 2, neutrophil; human leukocyte elastase; polymorphonuclear elastase; bone marrow serine protease; granulocyte-derived elastase; elastase, neutrophil expressed; Bone marrow serine protease; Elastase-2; Human leukocyte elastase; HLE; Medullasin; PMN elastase

NE

ELANE; ELANE; GE; NE; HLE; HNE; ELA2; SCN1; PMN-E; ELA2; HLE

ELNE_HUMAN

Human

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

Store all reagents at 2-8 degree C.

Assay Type: Competitive or Sandwich. Samples: Serum, plasma, cell culture supernatants, body fluid and tissue homogenate. Sensitivity: 0.1 ng/mL.

Microbiology

Intended Uses: This NE ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Human NE. This ELISA kit for research use only, not for therapeutic or diagnostic applications!. Principle of the Assay NE ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-NE antibody and an NE-HRP conjugate. The assay sample and buffer are incubated together with NE-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 NE concentration since NE from samples and NE-HRP conjugate compete for the anti-NE antibody binding site. Since the number of sites is limited, as more sites are occupied by NE from the sample, fewer sites are left to bind NE-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The NE concentration in each sample is interpolated from this standard curve.

4503549

NP_001963.1

NM_001972.2

28,518 Da

Activation Of Matrix Metalloproteinases Pathway (576264); C-MYB Transcription Factor Network Pathway (138073); Collagen Degradation Pathway (730309); Degradation Of The Extracellular Matrix Pathway (576263); Extracellular Matrix Organization Pathway (576262); Systemic Lupus Erythematosus Pathway (83122); Systemic Lupus Erythematosus Pathway (534); Transcriptional Misregulation In Cancer Pathway (523016); Transcriptional Misregulation In Cancer Pathway (522987); Amb2 Integrin Signaling Pathway (137945)

Elastases form a subfamily of serine proteases that hydrolyze many proteins in addition to elastin. Humans have six elastase genes which encode the structurally similar proteins. The product of this gene hydrolyzes proteins within specialized neutrophil lysosomes, called azurophil granules, as well as proteins of the extracellular matrix following the protein's release from activated neutrophils. The enzyme may play a role in degenerative and inflammatory diseases by its proteolysis of collagen-IV and elastin of the extracellular matrix. This protein degrades the outer membrane protein A (OmpA) of E. coli as well as the virulence factors of such bacteria as Shigella, Salmonella and Yersinia. Mutations in this gene are associated with cyclic neutropenia and severe congenital neutropenia (SCN). This gene is clustered with other serine protease gene family members, azurocidin 1 and proteinase 3 genes, at chromosome 19pter. All 3 genes are expressed coordinately and their protein products are packaged together into azurophil granules during neutrophil differentiation. [provided by RefSeq, May 2009]

ELANE: Modifies the functions of natural killer cells, monocytes and granulocytes. Inhibits C5a-dependent neutrophil enzyme release and chemotaxis. Defects in ELANE are a cause of cyclic haematopoiesis (CH); also known as cyclic neutropenia. CH is an autosomal dominant disease in which blood-cell production from the bone marrow oscillates with 21-day periodicity. Circulating neutrophils vary between almost normal numbers and zero. During intervals of neutropenia, affected individuals are at risk for opportunistic infection. Monocytes, platelets, lymphocytes and reticulocytes also cycle with the same frequency. Defects in ELANE are the cause of neutropenia severe congenital autosomal dominant type 1 (SCN1). SCN1 is a disorder of hematopoiesis characterized by a maturation arrest of granulopoiesis at the level of promyelocytes with peripheral blood absolute neutrophil counts below 0.5 x 10(9)/l and early onset of severe bacterial infections. Belongs to the peptidase S1 family. Elastase subfamily. Protein type: EC 3.4.21.37; Cell cycle regulation; Motility/polarity/chemotaxis; Cell surface; Protease. Chromosomal Location of Human Ortholog: 19p13.3. Cellular Component: cell surface; transcriptional repressor complex; cytoplasm; extracellular region; secretory granule. Molecular Function: heparin binding; peptidase activity; protein binding; protease binding; serine-type endopeptidase activity; cytokine binding; endopeptidase activity. Biological Process: positive regulation of immune response; extracellular matrix organization and biogenesis; positive regulation of smooth muscle cell proliferation; negative regulation of interleukin-8 biosynthetic process; positive regulation of interleukin-8 biosynthetic process; response to lipopolysaccharide; negative regulation of transcription from RNA polymerase II promoter; negative regulation of chemotaxis; proteolysis; phagocytosis; cellular calcium ion homeostasis; collagen catabolic process; extracellular matrix disassembly; positive regulation of MAP kinase activity; negative regulation of inflammatory response; defense response to bacterium; response to yeast; protein catabolic process; leukocyte migration; negative regulation of chemokine biosynthetic process; response to UV; acute inflammatory response to antigenic stimulus. Disease: Cyclic Neutropenia; Neutropenia, Severe Congenital, 1, Autosomal Dominant

48-Strip-Wells-(Competitive)

470 USD

48-Strip-Wells-(Sandwich)

470

96-Strip-Wells-(Competitive)

675

96-Strip-Wells-(Sandwich)

675