Product nameAnti-LRP5 antibody
See all LRP5 primary antibodies
DescriptionRabbit polyclonal to LRP5
SpecificityThis antibody is specific for LRP5 (C term). It has not yet been tested against endogenous LRP5, but on recombinant human LRP5 and mouse LRP5 proteins in transfected 293 cell lysates.
Tested applicationsSuitable for: ICC/IF, IHC-P, WBmore details
Species reactivityReacts with: Mouse, Human
Synthetic peptide corresponding to Human LRP5 aa 1538-1567 (C terminal) conjugated to Keyhole Limpet Haemocyanin (KLH).
Database link: O75197
- IHC-P: Human hepatocarcinoma tissue. ICC/IF: HepG2 cells.
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 bufferPreservative: 0.09% Sodium azide
Concentration information loading...
PurityAmmonium Sulphate Precipitation
Purification notesThis antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.
- Pathways and Processes
- Metabolic signaling pathways
- Lipid and lipoprotein metabolism
- Cholesterol Metabolism
Our Abpromise guarantee covers the use of ab38311 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|ICC/IF||Use a concentration of 1 - 5 µg/ml.|
|IHC-P||1/50 - 1/100.|
|WB||1/1000. Detects a band of approximately 179 kDa (predicted molecular weight: 179 kDa).|
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
All lanes : Anti-LRP5 antibody (ab38311) at 1/1000 dilution
Lane 1 : recombinant human LRP5 transfected 293 cell lysates
Lane 2 : mouse LRP5 transfected 293 cell lysates
Lysates/proteins at 35 µg per lane.
All lanes : Peroxidase-conjugated goat anti-rabbit IgG (H+L) at 1/5000 dilution
Predicted band size: 179 kDa
Observed band size: 179 kDa
Incubation time was overnight at 4°C. Blocking/Dilution buffer: 5% NFDM/TBST.
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) analysis of human hepatocarcinoma tissue labelling LRP5 with ab38311. Tissue was fixed with formaldehyde and blocked with 3% BSA for 0.5 hour at 38°C; antigen retrieval was by heat mediation with a citrate buffer (pH6). Samples were incubated with primary antibody (1/25) for 1 hour at 37°C. A peroxidase-conjugated goat anti-rabbit polyclonal (ready to use) was used as the secondary antibody.
ICC/IF image of ab38311 stained HepG2 cells. The cells were 100% methanol fixed (5 min) and then incubated in 1%BSA / 10% normal goat serum / 0.3M glycine in 0.1% PBS-Tween for 1h to permeabilise the cells and block non-specific protein-protein interactions. The cells were then incubated with the antibody (ab38311, 1µg/ml) overnight at +4°C. The secondary antibody (green) was Alexa Fluor® 488 goat anti-rabbit IgG (H+L) used at a 1/1000 dilution for 1h. Alexa Fluor® 594 WGA was used to label plasma membranes (red) at a 1/200 dilution for 1h. DAPI was used to stain the cell nuclei (blue) at a concentration of 1.43µM.
This product has been referenced in:
- Ma ZP et al. Sesamin Promotes Osteoblastic Differentiation and Protects Rats from Osteoporosis. Med Sci Monit 25:5312-5320 (2019). Read more (PubMed: 31314750) »
- Liu W et al. Alkaline Phosphatase Controls Lineage Switching of Mesenchymal Stem Cells by Regulating the LRP6/GSK3ß Complex in Hypophosphatasia. Theranostics 8:5575-5592 (2018). Read more (PubMed: 30555565) »