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骨形态发生抑制蛋白SOST抗体说明书
  • 品牌:上海莼试
  • 产地:进口、国产
  • 货号:CS11248
  • 发布日期: 2019-01-10
  • 更新日期: 2024-11-26
产品详请
产地 进口、国产
品牌 上海莼试
保存条件 Store at -20 °C
货号 CS11248
应用范围 WB=1:100-500 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 ICC=1:100-500 IF=1:100-500
CAS编号
抗体名 Anti-Sclerostin
克隆性
靶点 详见说明书
适应物种 详见说明书
形态 详见说明书
宿主 详见说明书
亚型 IgG
标识物 详见说明书
浓度 1mg/1ml%
免疫原 KLH conjugated synthetic peptide derived from human Sclerostin

技术外包服务:

骨形态发生抑制蛋白SOST抗体说明书 分子生物学:质粒抽提、PCRQ-PCRRT-PCR、分子生物学:基因合成、引物合成、基因测序、载体构建等

蛋白工程:原核、哺乳动物蛋白表达系统等

病毒包装:腺病毒、慢病毒等

抗体工程:磁珠分选、病理染色、WBELISAIPIFIHCFACSConfocal等等

细胞工程:细胞表型分析(凋亡、增殖、周期、迁移、侵袭、修复、克隆形成)、细胞培养、细胞膜制备、稳定细胞株构建、细胞RNAi技术等等。

实验流程:

骨形态发生抑制蛋白SOST抗体说明书 英文名称  Anti-Sclerostin

中文名称  骨形态发生抑制蛋白SOST抗体说明书 

     BEER; Cortical hyperostosis with syndactyly; Sclerosteosis; Sclerostin; SOST; SOST_HUMAN; VBCH.

产品属性:

      1mg/1ml

  0.2ml/200μg

抗体来源  Rabbit

克隆类型   polyclonal

交叉反应   Human, Mouse, Rat, Dog, Pig, Cow, Horse, Rabbit, Sheep

产品类型   一抗  

研究领域    细胞生物 信号转导 生长因子和激素

蛋白分子量  predicted molecular weight: 21kDa 

       Lyophilized or Liquid

  KLH conjugated synthetic peptide derived from human Sclerostin

      IgG

纯化方法   affinity purified by Protein A

   Preservative: 15mM Sodium Azide, Constituents: 1% BSA, 0.01M PBS, pH 7.4

骨形态发生抑制蛋白SOST抗体说明书 产品应用   WB=1:100-500 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 ICC=1:100-500 IF=1:100-500

(石蜡切片需做抗原修复) 

 not yet tested in other applications.

 optimal dilutions/concentrations should be determined by the end user.  

保存条件  Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. 

Important Note  This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. 

产品介绍 Negative regulator of bone growth.Sclerostin (SOST) is a bone morphogenetic protein (BMP) antagonist, leading to the activation of BMP signaling. It negatively regulates the formation of bone by repressing the differentiation and/or function of osteoblasts induced by BMPs. It has been shown that Sclerostin binds BMP-5, -6, and -7 with high affinity and BMP-2 and -4 with low affinity. The noggin-sclerostin protein complex represents a novel mechanism for the fine-tuning of BMP activity in bone homeostasis. Evidence is accumulating that one of the important mechanisms of bone regulation by sclerostin is the modulation of Wnt/Beta-catenin signaling. Sclerostin also rapidly activated ERK-1/2 MAPK signaling, indicating the involvement of additional signaling pathways

Function : Negative regulator of bone growth that acts through inhibition of Wnt signaling and bone formation.

Subunit : Interacts with LRP4 (via the extracellular domain); the interaction facilitates the inhibition of Wnt signaling. Interacts with LRP5 (via the first two YWTD-EGF repeat domains); the interaction inhibits Wnt-mediated signaling. Interacts with LRP6.

Subcellular Location : Secreted.

Tissue Specificity : Widely expressed at low levels with highest levels in bone, cartilage, kidney, liver, bone marrow and primary osteeoblasts differentiated for 21 days.

DISEASE : Defects in SOST are the cause of sclerosteosis (SOST) [MIM:269500]; also known as cortical hyperostosis with syndactyly. SOST is an autosomal recessive sclerosing bone dysplasia characterized by a generalized hyperostosis and sclerosis leading to a markedly thickened skull, with mandible, ribs, clavicles and all long bones also being affected. Due to narrowing of the foramina of the cranial nerves, facial nerve palsy, hearing loss and atrophy of the optic nerves can occur. Sclerosteosis is clinically and radiologically very similar to van Buchem disease, mainly differentiated by hand malformations and a large stature in sclerosteosis patients.

Note=A 52 kb deletion downstream of SOST results in SOST transcription suppression and is a cause of van Buchem disease (VBCH) [MIM:239100]; also known as hyperostosis corticalis generalisata. VBCH is an autosomal recessive sclerosing bone dysplasia characterized by endosteal hyperostosis of the mandible, skull, ribs, clavicles, and diaphyses of the long bones. Affected patients present a symmetrically increased thickness of bones, most frequently found as an enlarged jawbone, but also an enlargement of the skull, ribs, diaphysis of long bones, as well as tubular bones of hands and feet. The clinical consequence of increased thickness of the skull include facial nerve palsy causing hearing loss, visual problems, neurological pain, and, very rarely, blindness as a consequence of optic atrophy. Serum alkaline phosphatase levels are elevated.

Similarity : Belongs to the sclerostin family. Contains 1 CTCK (C-terminal cystine knot-like) domain.

Database links : UniProtKB/Swiss-Prot: Q9BQB4.1

全、新、优、品、好四大特点:

骨形态发生抑制蛋白SOST抗体说明书 全:公司提供上万种产品,涵盖了生物试剂,elisa试剂盒,标准品,培养基,原装耗材,抗体、培养基、ATCC细胞等,基本上各种科研所需产品在我司都能找到。

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好:我公司具有优质的技术团队,产品一旦售出,实验过程中遇到困难可提供在线技术咨询。使您使用产品时没有任何的后顾之忧。

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