Product nameAnti-LRP5 antibody [EPR22477-218] - BSA and Azide free
See all LRP5 primary antibodies
DescriptionRabbit monoclonal [EPR22477-218] to LRP5 - BSA and Azide free
Tested applicationsSuitable for: WB, IPmore details
Unsuitable for: Flow Cyt,ICC/IF or IHC-P
Species reactivityReacts with: Mouse, Rat, Human
Recombinant fragment within Mouse LRP5 aa 1400 to the C-terminus. The exact sequence is proprietary.
Database link: Q91VN0
- IP: 3T3-L1 whole cell lysate.
ab256528 is the carrier-free version of ab223203 This format is designed for use in antibody labeling, including fluorochromes, metal isotopes, oligonucleotides, enzymes.
Our carrier-free formats are supplied in a buffer free of BSA, sodium azide and glycerol for higher conjugation efficiency.
Use our conjugation kits for antibody conjugates that are ready-to-use in as little as 20 minutes with <1 minute hands-on-time and 100% antibody recovery: available for fluorescent dyes, HRP, biotin and gold.
Ab256528 is compatible with the Maxpar® Antibody Labeling Kit from Fluidigm.
Maxpar® is a trademark of Fluidigm Canada Inc.
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents.
This product is a recombinant rabbit monoclonal antibody.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferConstituent: PBS
Concentration information loading...
PurityProtein A purified
Our Abpromise guarantee covers the use of ab256528 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||Use at an assay dependent concentration. Detects a band of approximately 180-200 kDa (predicted molecular weight: 179 kDa).|
|IP||Use at an assay dependent concentration.|
FunctionComponent 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.
Tissue specificityWidely expressed, with the highest level of expression in the liver.
Involvement in diseaseDefects 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.
Sequence similaritiesBelongs to the LDLR family.
Contains 4 EGF-like domains.
Contains 3 LDL-receptor class A domains.
Contains 20 LDL-receptor class B repeats.
modificationsPhosphorylation of cytoplasmic PPPSP motifs regulates the signal transduction of the Wnt signaling pathway through acting as a docking site for AXIN1.
Cellular localizationMembrane. Endoplasmic reticulum. Chaperoned to the plasma membrane by MESD.
- Information by UniProt
- BMND1 antibody
- EVR1 antibody
- EVR4 antibody
LRP5 was immunoprecipitated from 0.35 mg 3T3-L1 (mouse embryonic fibroblast) differentiated adipocytes whole cell lysate 10µg with ab223203 at 1/30 dilution (2µg in 0.35mg lysates). Western blot was performed on the immunoprecipitate using ab223203. VeriBlot for IP Detection Reagent (HRP) (ab131366) was used at 1/1000 dilution.
Lane 1: 3T3-L1 (mouse embryonic fibroblast) differentiated adipocytes whole cell lysate 10µg.
Lane 2: ab223203 IP in 3T3-L1 differentiated adipocytes whole cell lysate.
Blocking/Dilution buffer: 5% NFDM/TBST.
Exposure time: 3 mins.
Differentiation procedure: https://www.abcam.com/protocols/differentiation-of-3t3-l1-cells-into-adipocyte-like-cells-protocol.
This data was developed using the same antibody clone in a different buffer formulation containing PBS, BSA, glycerol, and sodium azide (ab223203).
ab256528 has not yet been referenced specifically in any publications.