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、PCR、Q-PCR、RT-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、WB、ELISA、IP、IF、IHC、FACS、Confocal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
别 名 BEER; Cortical hyperostosis with syndactyly; Sclerosteosis; Sclerostin; SOST; SOST_HUMAN; VBCH.
产品属性:
浓 度 1mg/1ml
规 格 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
性 状 Lyophilized or Liquid
免 疫 原 KLH conjugated synthetic peptide derived from human Sclerostin
亚 型 IgG
纯化方法 affinity purified by Protein A
储 存 液 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
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