ELISA/assay

Human Dentin Sialophosphoprotein ELISA Kit

MBS729804

48-Strip-Wells

470 USD

ELISA Kit

Human Dentin Sialophosphoprotein ELISA Kit

Dentin Sialophosphoprotein

dentin sialophosphoprotein preproprotein; Dentin sialophosphoprotein; dentin sialophosphoprotein; dentin phosphoryn; dentin sialoprotein; dentin phosphophoryn; dentin phosphoprotein; dentin sialophosphoprotein; Dentin phosphophoryn; DPP

DSPP

DSPP; DSPP; DPP; DSP; DGI1; DMP3; DTDP2; DFNA39; DPP; DSP

DSPP_HUMAN

Human

This assay has high sensitivity and excellent specificity for detection of DSPP. No significant cross-reactivity or interference between DSPP and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between DSPP 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 DSPP ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Human DSPP. This ELISA kit for research use only, not for therapeutic or diagnostic applications

Signal Transduction

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

89001107

NP_055023.2

NM_014208.3

131,151 Da

ECM Proteoglycans Pathway (833812); Extracellular Matrix Organization Pathway (576262)

This gene encodes two principal proteins of the dentin extracellular matrix of the tooth. The preproprotein is secreted by odontoblasts and cleaved into dentin sialoprotein and dentin phosphoprotein. Dentin phosphoprotein is thought to be involved in the biomineralization process of dentin. Mutations in this gene have been associated with dentinogenesis imperfecta-1; in some individuals, dentinogenesis imperfecta occurs in combination with an autosomal dominant form of deafness. Allelic differences due to repeat polymorphisms have been found for this gene. [provided by RefSeq, Jul 2008]

DSPP: DSP may be an important factor in dentinogenesis. DPP may bind high amount of calcium and facilitate initial mineralization of dentin matrix collagen as well as regulate the size and shape of the crystals. Defects in DSPP are the cause of deafness autosomal dominant type 39 with dentinogenesis imperfecta 1 (DFNA39/DGI1). Affected individuals present DGI1 associated with early onset progressive sensorineural high-frequency hearing loss. Defects in DSPP are the cause of dentinogenesis imperfecta type 1 (DGI1); also known as dentinogenesis imperfecta Shields type 2 (DGI2). DGI1 is an autosomal dominant disorder in which both the primary and the permanent teeth are affected. It occurs with an incidence of 1:8000 live births. The teeth are amber and opalescent, the pulp chamber being obliterated by abnormal dentin. The enamel, although unaffected, tends to fracture, which makes dentin undergo rapid attrition, leading to shortening of the teeth. Defects in DSPP are a cause of dentinogenesis imperfecta Shields type 3 (DGI3). Patients with DGI3 do not have stigmata of osteogenesis imperfecta. The finding that a single defects in the DSPP gene causes both phenotypic patterns of DGI2 and DGI3 strongly supports the conclusion that these two disorders are not separate diseases but rather the phenotypic variation of a single genetic defect. Defects in DSPP are the cause of dentin dysplasia type 2 (DTDP2); also known as dentin dysplasia Shields type 2. DTDP2 is an autosomal dominant disorder in which mineralization of the dentine of the primary teeth is abnormal. On the basis of the phenotypic overlap between, and shared chromosomal location with DGI2 it has been proposed that DTDP2 and DGI2 are allelic. From the results of recent studies, it is clear that different types of mutations in DSPP lead to the two different phenotypes. Protein type: Secreted; Secreted, signal peptide; Extracellular matrix. Chromosomal Location of Human Ortholog: 4q21.3. Cellular Component: proteinaceous extracellular matrix; cytoplasm; extracellular region. Molecular Function: collagen binding; extracellular matrix structural constituent; calcium ion binding. Biological Process: ossification; extracellular matrix organization and biogenesis; biomineral formation; multicellular organismal development; skeletal development. Disease: Deafness, Autosomal Dominant 39, With Dentinogenesis Imperfecta 1; Dentinogenesis Imperfecta, Shields Type Iii; Dentin Dysplasia, Type Ii; Dentinogenesis Imperfecta 1

48-Strip-Wells

470 USD

96-Strip-Wells

675