LRP5 rabbit pAb

LRP5 rabbit pAb

AO-06-ES15106-100

LRP5 rabbit pAb 100μL

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Antibody Product Overview

ELK.NoES15106
Product nameLRP5 rabbit pAb
ReactivityHuman; Mouse
ApplicationsWB
Other name
Size100μL
Unit price ($)248
Human gene ID4041
Human Swiss-ProtO75197
SourceRabbit
IsotypeIgG
TargetLRP5
Fields>>mTOR signaling pathway;>>Wnt signaling pathway;>>Parathyroid hormone synthesis, secretion and action;>>Alzheimer disease;>>Pathways of neurodegeneration - multiple diseases;>>Pathways in cancer;>>Breast cancer;>>Hepatocellular carcinoma;>>Gastric cancer
Gene nameLRP5 LR3 LRP7
Protein nameLRP5
Human gene linkView Human Gene
Human Swiss linkView Human Swiss-Prot
Mouse gene ID16973
Mouse gene linkView Mouse Gene
Mouse Swiss-ProtQ91VN0
Mouse Swiss linkView Mouse Swiss-Prot
Rat gene ID
Rat gene link
Rat Swiss-Prot
Rat Swiss link
ImmunogenSynthesized peptide derived from human LRP5 AA range: 1047-1097
SpecificityThis antibody detects endogenous levels of LRP5 at Human/Mouse
FormulationLiquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
ClonalityPolyclonal
DilutionWB 1:500-2000
PurificationThe antibody was affinity-purified from rabbit serum by affinity-chromatography using specific immunogen.
Concentration1 mg/ml
Storage stability-20°C/1 year
Molecular Weight (Da)178kD
Observed band (KD)
BackgroundThis gene encodes a transmembrane low-density lipoprotein receptor that binds and internalizes ligands in the process of receptor-mediated endocytosis. This protein also acts as a co-receptor with Frizzled protein family members for transducing signals by Wnt proteins and was originally cloned on the basis of its association with type 1 diabetes mellitus in humans. This protein plays a key role in skeletal homeostasis and many bone density related diseases are caused by mutations in this gene. Mutations in this gene also cause familial exudative vitreoretinopathy. Alternative splicing results in multiple transcript variants. [provided by RefSeq, May 2014],
Functiondisease: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 characterizd 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
Subcellular locationMembrane ; Single-pass type I membrane protein . Endoplasmic reticulum . Chaperoned to the plasma membrane by MESD. .
ExpressionWidely expressed, with the highest level of expression in the liver and in aorta.

Additional Images

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Western blot analysis of lysates from HpeG2 cells, primary antibody was diluted at 1:1000, 4°over night
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: AO-06-ES15106-100
: 10 Items
Hurry! only 10 items left in stock.

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