本公司经销DSPP/Dentin phosphophoryn，牙本质磷蛋白抗体，克隆类型为polyclonal，宿主来源是Rabbit，DSPP/Dentin phosphophoryn牙本质磷蛋白抗体可应用于WB、elisa、IP、IF、IHC等实验，欢迎垂询订购！

货号：BY-8557R
英文名称：Anti-DSPP/Dentin phosphophoryn
中文名称：牙本质磷蛋白抗体
其他名称：名Dentin phosphophoryn; Dentin phosphoprotein; dentin phosphoryn; Dentin sialophosphoprotein; Dentin sialophosphoprotein precursor; Dentin sialoprotein; dentinogenesis imperfecta 1; DFNA39; DGI1; DMP3; DPP; DSP; Dspp; DSPP_HUMAN; DTDP2.
抗体来源：Rabbit
克隆类型：polyclonal
蛋白分子量：predicted molecular weight: 47/129kDa
纯化方法：affinity purified by Protein A
交叉反应：hu, mo, rat
产品介绍：DSPP may be an important factor in dentinogenesis. DSPP 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.The dentin sialophosphoprotein （DSPP） gene encodes two major noncollagenous dentin matrix proteins: dentin sialoprotein, known as DSP; ａnd dentin phosphoprotein, known as phosphophoryn or DPP. The DSPP gene maps to human chromosome 4 ａnd yields a 4.6 kb transcript containing 5 exons, with exons 1-4 encoding for DSP ａnd exon 5 encoding for both the C-terminus of DSP ａnd the full length DPP. DPP ａnd DSP are acidic proteins that represent about 50% of the noncollagenous proteins in the dentin extracellular matrix of teeth. The DSPP gene is a likely candidate gene for the genetic diseases associated with abnormal dentin formation such as dentinogenesis imperfecta type II ａnd dentin dysplasia type II. DPP may bind large amounts of calcium ａnd may facilitate initial mineralization of dentin matrix collagen as well as regulate the size ａnd shape of the crystals.Function : 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. Subunit : Interacts with FBLN7 Subcellular Location : Secreted, extracellular space, extracellular matrix. Tissue Specificity : Expressed in teeth. DPP is synthesized by odontoblast ａnd transiently expressed by pre-ameloblasts.Post-translational modifications : DSP is glycosylated. DISEASE : Defects in DSPP are the cause of deafness autosomal dominant type 39 with dentinogenesis imperfecta 1 （DFNA39/DGI1） [MIM:605594]. 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） [MIM:125490]; 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） [MIM:125500]. 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） [MIM:125420]; 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. Database links : UniProtKB/Swiss-Prot: Q9NZW4.2