Anti-LRP5抗体[31E7] (ab129118)
Key features and details
- Mouse monoclonal [31E7] to LRP5
- Suitable for: WB
- Reacts with: Human
- Isotype: IgG2b
概述
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产品名称
Anti-LRP5抗体[31E7]
参阅全部 LRP5 一抗 -
描述
小鼠单克隆抗体[31E7] to LRP5 -
宿主
Mouse -
经测试应用
适用于: WBmore details -
种属反应性
与反应: Human -
免疫原
Recombinant fragment corresponding to Human LRP5. (Entire Cytoplasmic domain.)
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阳性对照
- This antibody gave a positive signal when tested against a whole cell lysate of 293T cells overexpressing LRP5 protein.
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常规说明
This antibody clone is manufactured by Abcam. If you require a custom buffer formulation or conjugation for your experiments, please contact orders@abcam.com.
The Life Science industry has been in the grips of a reproducibility crisis for a number of years. Abcam is leading the way in addressing this with our range of recombinant monoclonal antibodies and knockout edited cell lines for gold-standard validation. Please check that this product meets your needs before purchasing.
If you have any questions, special requirements or concerns, please send us an inquiry and/or contact our Support team ahead of purchase. Recommended alternatives for this product can be found below, along with publications, customer reviews and Q&As
性能
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形式
Liquid -
存放说明
Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle. -
存储溶液
pH: 7.40
Preservative: 0.02% Sodium azide
Constituents: PBS, 6.97% L-Arginine -
Concentration information loading...
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纯度
Protein G purified -
克隆
单克隆 -
克隆编号
31E7 -
同种型
IgG2b -
研究领域
相关产品
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Compatible Secondaries
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Isotype control
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Recombinant Protein
应用
The Abpromise guarantee
Abpromise™承诺保证使用ab129118于以下的经测试应用
“应用说明”部分 下显示的仅为推荐的起始稀释度;实际最佳的稀释度/浓度应由使用者检定。
应用 | Ab评论 | 说明 |
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WB |
Use a concentration of 1 µg/ml. Detects a band of approximately 179 kDa (predicted molecular weight: 179 kDa).
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说明 |
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WB
Use a concentration of 1 µg/ml. Detects a band of approximately 179 kDa (predicted molecular weight: 179 kDa). |
靶标
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功能
Component of the Wnt-Fzd-LRP5-LRP6 complex that triggers beta-catenin signaling through inducing aggregation of receptor-ligand complexes into ribosome-sized signalsomes. Cell-surface coreceptor of Wnt/beta-catenin signaling, which plays a pivotal role in bone formation. The Wnt-induced Fzd/LRP6 coreceptor complex recruits DVL1 polymers to the plasma membrane which, in turn, recruits the AXIN1/GSK3B-complex to the cell surface promoting the formation of signalsomes and inhibiting AXIN1/GSK3-mediated phosphorylation and destruction of beta-catenin. Appears be required for postnatal control of vascular regression in the eye. Required for posterior patterning of the epiblast during gastrulation. -
组织特异性
Widely expressed, with the highest level of expression in the liver. -
疾病相关
Defects in LRP5 are the cause of vitreoretinopathy exudative type 4 (EVR4) [MIM:601813]. EVR4 is a disorder of the retinal vasculature characterized by an abrupt cessation of growth of peripheral capillaries, leading to an avascular peripheral retina. This may lead to compensatory retinal neovascularization, which is thought to be induced by hypoxia from the initial avascular insult. New vessels are prone to leakage and rupture causing exudates and bleeding, followed by scarring, retinal detachment and blindness. Clinical features can be highly variable, even within the same family. Patients with mild forms of the disease are asymptomatic, and their only disease related abnormality is an arc of avascular retina in the extreme temporal periphery. EVR4 inheritance can be autosomal dominant or recessive.
Genetic variations in LRP5 are a cause of susceptibility to osteoporosis (OSTEOP) [MIM:166710]; also known as senile osteoporosis or postmenopausal osteoporosis. Osteoporosis is characterized by reduced bone mass, disruption of bone microarchitecture without alteration in the composition of bone. Osteoporotic bones are more at risk of fracture.
Defects in LRP5 are the cause of osteoporosis-pseudoglioma syndrome (OPPG) [MIM:259770]; also known as osteogenesis imperfecta ocular form. OPPG is a recessive disorder characterized by very low bone mass and blindness. Individualy with OPPG are prone to develop bone fractures and deformations and have various eye abnormalities, including phthisis bulbi, retinal detachments, falciform folds or persistent vitreal vasculature.
Defects in LRP5 are a cause of high bone mass trait (HBM) [MIM:601884]. HBM is a rare phenotype characterized by exceptionally dense bones. HBM individuals show otherwise a completely normal skeletal structure and no other unusual clinical findings.
Defects in LRP5 are a cause of endosteal hyperostosis Worth type (WENHY) [MIM:144750]; also known as autosomal dominant osteosclerosis. WENHY is an autosomal dominant sclerosing bone dysplasia clinically characterized by elongation of the mandible, increased gonial angle, flattened forehead, and the presence of a slowly enlarging osseous prominence of the hard palate (torus palatinus). Serum calcium, phosphorus and alkaline phosphatase levels are normal. Radiologically, it is characterized by early thickening of the endosteum of long bones, the skull and of the mandible. With advancing age, the trabeculae of the metaphysis become thickened. WENHY becomes clinically and radiologically evident by adolescence, does not cause deformity except in the skull and mandible, and is not associated with bone pain or fracture. Affected patients have normal height, proportion, intelligence and longevity.
Defects in LRP5 are the cause of osteopetrosis autosomal dominant type 1 (OPTA1) [MIM:607634]. Osteopetrosis is a rare genetic disease characterized by abnormally dense bone, due to defective resorption of immature bone. The disorder occurs in two forms: a severe autosomal recessive form occurring in utero, infancy, or childhood, and a benign autosomal dominant form occurring in adolescence or adulthood. OPTA1 is characterized by generalized osteosclerosis most pronounced in the cranial vault. Patients are often asymptomatic, but some suffer from pain and hearing loss. It appears to be the only type of osteopetrosis not associated with an increased fracture rate.
Defects in LRP5 are the cause of van Buchem disease type 2 (VBCH2)[MIM:607636]. VBCH2 is an autosomal dominant sclerosing bone dysplasia characterized by cranial osteosclerosis, thickened calvaria and cortices of long bones, enlarged mandible and normal serum alkaline phosphatase levels. -
序列相似性
Belongs to the LDLR family.
Contains 4 EGF-like domains.
Contains 3 LDL-receptor class A domains.
Contains 20 LDL-receptor class B repeats. -
翻译后修饰
Phosphorylation of cytoplasmic PPPSP motifs regulates the signal transduction of the Wnt signaling pathway through acting as a docking site for AXIN1. -
细胞定位
Membrane. Endoplasmic reticulum. Chaperoned to the plasma membrane by MESD. - Information by UniProt
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数据库链接
- Entrez Gene: 4041 Human
- Omim: 603506 Human
- SwissProt: O75197 Human
- Unigene: 6347 Human
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别名
- BMND1 antibody
- EVR1 antibody
- EVR4 antibody
see all
图片
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All lanes : Anti-LRP5 antibody [31E7] (ab129118)
Lane 1 : HEK293 (Human embryonic kidney cell line) Whole Cell Lysate
Lane 2 : 293T Overexpressing Human LRP5 - Whole Cell Lysate
Lysates/proteins at 10 µg per lane.
Secondary
All lanes : Goat Anti-Mouse IgG H&L (HRP) preadsorbed (ab97040) at 1/10000 dilution
Developed using the ECL technique.
Performed under reducing conditions.
Predicted band size: 179 kDa
Observed band size: 179 kDa
Exposure time: 4 minutes
数据表及文件
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Datasheet download
文献 (1)
ab129118 被引用在 1 文献中.
- Vijayakumar S et al. Extracellular LDLR repeats modulate Wnt signaling activity by promoting LRP6 receptor endocytosis mediated by the Itch E3 ubiquitin ligase. Genes Cancer 8:613-627 (2017). WB . PubMed: 28966723