ELISA/assay

Human Bone-specific Alkphase B ELISA Kit

MBS720223

48-Strip-Wells

470 USD

ELISA Kit

Human Bone-specific Alkphase B ELISA Kit

Bone-specific Alkphase B

Human Bone-specific Alkphase B ELISA Kit; Bone-specific Alkphase B; Bone-specific Alkphase B (Human)

alkaline phosphatase; 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

ALP-B

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

PPBT_HUMAN

Human

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

Human ELISA Kit

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

178462

AAB59378

P05186

57,305 Da

AGE/RAGE Pathway (698754); BDNF Signaling Pathway (712093); Endochondral Ossification Pathway (198812); Folate Biosynthesis Pathway (83018); Folate Biosynthesis Pathway (404); 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]

Function: This isozyme may play a role in skeletal mineralization. Catalytic activity: A phosphate monoester + H2O = an alcohol + phosphate. Cofactor: Binds 1 magnesium ion . By similarity.Binds 2 zinc ions . By similarity. Subunit structure: Homodimer. Subcellular location: Cell membrane; Lipid-anchor GPI-anchor. Post-translational modification: Glycosylated. Ref.11. Involvement in disease: Hypophosphatasia (HOPS) [MIM:146300]: A metabolic bone disease characterized by defective skeletal mineralization and biochemically by deficient activity of the tissue non-specific isoenzyme of alkaline phosphatase. Four 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. The adult form is mild and characterized by recurrent fractures, osteomalacia, rickets, and loss of teeth. Some cases are asymptomatic, while some patients manifest dental features without skeletal manifestations (odontohypophosphatasia).Note: The disease is caused by mutations affecting the gene represented in this entry. Ref.4 Ref.16 Ref.17 Ref.18 Ref.19 Ref.20 Ref.21 Ref.22 Ref.23 Ref.24 Ref.25 Ref.26 Ref.27 Ref.28 Ref.29 Ref.30 Ref.31 Ref.32 Ref.33 Ref.34 Ref.35 Ref.36 Ref.37 Ref.38Hypophosphatasia childhood type (HOPSC) [MIM:241510]: A bone disease characterized by defective skeletal mineralization and biochemically by deficient activity of the tissue non-specific isoenzyme of alkaline phosphatase.Note: The disease is caused by mutations affecting the gene represented in this entry.Hypophosphatasia infantile type (HOPSI) [MIM:241500]: A severe bone disease characterized by defective skeletal mineralization and biochemically by deficient activity of the tissue non-specific isoenzyme of alkaline phosphatase. Three more or less distinct types of infantile hypophosphatasia can be identified: (1) type 1 with onset in utero or in early postnatal life, craniostenosis, severe skeletal abnormalities, hypercalcemia, and death in the first year or so of life; (2) type 2 with later, more gradual development of symptoms, moderately severe 'rachitic' skeletal changes and premature loss of teeth; (3) type 3 with no symptoms, the condition being determined on routine studies.Note: The disease is caused by mutations affecting the gene represented in this entry. Sequence similarities: Belongs to the alkaline phosphatase family. Sequence caution: The sequence BAD93051.1 differs from that shown. Reason: Erroneous initiation. Translation N-terminally shortened.

48-Strip-Wells

470 USD

96-Strip-Wells

675