ELISA/assay

Rat Alkaline Phosphatase, Liver/Bone/Kidney ELISA Kit

MBS733777

48-Strip-Wells

470 USD

ELISA Kit

Rat Alkaline Phosphatase, Liver/Bone/Kidney ELISA Kit

Alkaline Phosphatase, Liver/Bone/Kidney

Alkaline phosphatase, liver/bone/kidney; Alkaline phosphatase, tissue-nonspecific isozyme; alkaline phosphatase, tissue-nonspecific isozyme; glycerophosphatase; tissue-nonspecific ALP; alkaline phosphomonoesterase; liver/bone/kidney-type alkaline phosphatase; alkaline phosphatase liver/bone/kidney isozyme; alkaline phosphatase, liver/bone/kidney; Alkaline phosphatase liver/bone/kidney isozyme

ALPL

ALPL; ALPL; HOPS; TNAP; APTNAP; TNSALP; AP-TNAP; AP-TNAP; TNSALP

PPBT_HUMAN

Rat

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

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

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

187954299

AAI36326.1

51,045 Da

AGE/RAGE Pathway (698754); BDNF Signaling Pathway (712093); Endochondral Ossification Pathway (198812); Folate Biosynthesis Pathway (83018); Folate Biosynthesis Pathway (404); Metabolic Pathways (132956); TNF-alpha/NF-kB Signaling Pathway (198884)

There are at least four distinct but related alkaline phosphatases: intestinal, placental, placental-like, and liver/bone/kidney (tissue non-specific). The first three are located together on chromosome 2, while the tissue non-specific form is located on chromosome 1. The product of this gene is a membrane bound glycosylated enzyme that is not expressed in any particular tissue and is, therefore, referred to as the tissue-nonspecific form of the enzyme. The exact physiological function of the alkaline phosphatases is not known. A proposed function of this form of the enzyme is matrix mineralization; however, mice that lack a functional form of this enzyme show normal skeletal development. This enzyme has been linked directly to hypophosphatasia, a disorder that is characterized by hypercalcemia and includes skeletal defects. The character of this disorder can vary, however, depending on the specific mutation since this determines age of onset and severity of symptoms. Alternatively spliced transcript variants have been described. [provided by RefSeq, Apr 2010]

ALPL: This isozyme may play a role in skeletal mineralization. Defects in ALPL are a cause of hypophosphatasia (HOPS). HOPS is an inherited metabolic bone disease characterized by defective skeletal mineralization. Four hypophosphatasia forms are distinguished, depending on the age of onset: perinatal, infantile, childhood and adult type. The perinatal form is the most severe and is almost always fatal. Patients with only premature loss of deciduous teeth, but with no bone disease are regarded as having odontohypophosphatasia (odonto). Defects in ALPL are a cause of hypophosphatasia childhood type (HOPSC). Defects in ALPL are a cause of hypophosphatasia infantile type (HOPSI). Belongs to the alkaline phosphatase family. 3 isoforms of the human protein are produced by alternative splicing. Protein type: EC 3.1.3.1; Motility/polarity/chemotaxis; Membrane protein, GPI anchor; Phosphatase (non-protein); Cofactor and Vitamin Metabolism - folate biosynthesis. Chromosomal Location of Human Ortholog: 1p36.12. Cellular Component: extracellular matrix; extracellular space; membrane; integral to membrane; plasma membrane. Molecular Function: protein binding; pyrophosphatase activity; alkaline phosphatase activity; metal ion binding. Biological Process: osteoblast differentiation; response to antibiotic; response to vitamin D; dephosphorylation; response to glucocorticoid stimulus; reproductive developmental process; response to lipopolysaccharide; skeletal development; endochondral ossification. Disease: Hypophosphatasia, Infantile; Hypophosphatasia, Adult; Hypophosphatasia, Childhood

48-Strip-Wells

470 USD

96-Strip-Wells

675