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anti-Human LRP5 Antibodies:
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Human Polyclonal LRP5 Primary Antibody for WB - ABIN127323
Del Valle-Pérez, Arqués, Vinyoles, de Herreros, Duñach: Coordinated action of CK1 isoforms in canonical Wnt signaling. in Molecular and cellular biology 2011
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Human Polyclonal LRP5 Primary Antibody for IHC (p), ELISA - ABIN542941
Strickland, Ranganathan: Diverse role of LDL receptor-related protein in the clearance of proteases and in signaling. in Journal of thrombosis and haemostasis : JTH 2003
Show all 3 Pubmed References
Polyclonal LRP5 Primary Antibody for IHC (p), IP - ABIN540938
Davidson, Wu, Shen, Bilic, Fenger, Stannek, Glinka, Niehrs: Casein kinase 1 gamma couples Wnt receptor activation to cytoplasmic signal transduction. in Nature 2005
Show all 2 Pubmed References
Human Monoclonal LRP5 Primary Antibody for FACS, ELISA - ABIN969535
Urano, Shiraki, Usui, Sasaki, Ouchi, Inoue: A1330V variant of the low-density lipoprotein receptor-related protein 5 (LRP5) gene decreases Wnt signaling and affects the total body bone mineral density in Japanese women. in Endocrine journal 2009
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Human Monoclonal LRP5 Primary Antibody for ELISA, WB - ABIN517568
Kim, Goel, Alexander: Differentiation generates paracrine cell pairs that maintain basaloid mouse mammary tumors: proof of concept. in PLoS ONE 2011
Polyclonal LRP5 Primary Antibody for IP, ELISA - ABIN541011
Khan, Vijayakumar, de la Torre, Rotolo, Bafico: Analysis of endogenous LRP6 function reveals a novel feedback mechanism by which Wnt negatively regulates its receptor. in Molecular and cellular biology 2007
Human Monoclonal LRP5 Primary Antibody for ELISA, WB - ABIN561692
Badders, Goel, Clark, Klos, Kim, Bafico, Lindvall, Williams, Alexander: The Wnt receptor, Lrp5, is expressed by mouse mammary stem cells and is required to maintain the basal lineage. in PLoS ONE 2009
Human Polyclonal LRP5 Primary Antibody for WB - ABIN549346
Caverzasio, Manen: Essential role of Wnt3a-mediated activation of mitogen-activated protein kinase p38 for the stimulation of alkaline phosphatase activity and matrix mineralization in C3H10T1/2 mesenchymal cells. in Endocrinology 2007
Human Polyclonal LRP5 Primary Antibody for ELISA - ABIN547455
He, Semenov, Tamai, Zeng: LDL receptor-related proteins 5 and 6 in Wnt/beta-catenin signaling: arrows point the way. in Development (Cambridge, England) 2004
Mouse (Murine) Polyclonal LRP5 Primary Antibody for IF, IP - ABIN3020645
Fu, Wang, Wan, Lin, Chang, Han: Wnt5a mediated canonical Wnt signaling pathway activation in orthodontic tooth movement: possible role in the tension force-induced bone formation. in Journal of molecular histology 2017
The extracellular domains of Lrp5/6 behave as physiologically relevant inhibitors of noncanonical Wnt signaling during Xenopus and mouse development in vivo.
The authors found a novel, private, predicted as damaging mutation in LRP5, a gene related to bone density alteration pathologies, and they suggest a link between this mutation and his Chiari malformation as previously shown in humans.
Rescue experiments showed that LRP5 mutation is associated with hearing loss. Knocking down lrp5 in zebrafish results in reduced expression of several genes linked to Wnt signaling pathway and decreased cell proliferation when compared with those in wild-type zebrafish
Data show that in zebrafish, lrp5 also controls cell migration during early morphogenetic processes and contributes to shaping the craniofacial skeleton.
The positive rate for pathogenic mutations in the known FEVR-associated genes was 38.9% (21/54). Among the mutations, LRP5 mutation was the predominant, accounting for 66.7% (14/21) of genetic positive patients. Patients with FEVR-RRD due to LRP5 mutations have less retinal vascular leakage or neovasculization than do patients with FEVR-RRD due to TSPAN12/FZD4 mutations.
loss of Lrp5, the co-receptor thought to transmit extracellular WNT signals during bone mass regulation, did not reduce the bone-anabolic effect of Wnt1, providing direct evidence that Wnt1 function does not require the LRP5 co-receptor.
Mutational analysis uncovers monogenic bone disorders in women with pregnancy-associated osteoporosis: three novel mutations in LRP5, COL1A1, and COL1A2.
LRP5 polymorphism (rs556442) was associated with insulin resistance in Iranian children and adolescents
Our results suggest that the Val667Met LRP5 (rs312009) polymorphism may contribute to an elevated risk for fractures in postmenopausal Polish women.
Our data indicate FEVR status is associated with a significantly smaller FAZ, decreased vascular density in the fovea. In addition, patients with the LRP5 mutation had a milder phenotype than those with the FDZ4 or TSPAN12 mutations.
oligomerizations of FZDs and LRP5/6 can integrate the cytoplasmic protein Dishevelled into the LRP5/6 signalosome, resulting in a robust activation of ligand-independent beta-catenin signaling
The genetic and clinical phenotype of 10 new osteoporosis-pseudoglioma syndrome (OPPG) patients is reported. Mutational screening of LRP5 gene revealed the c.2409_2503+79del deletion in homozygous state, expected to result in a truncated protein. Among 44 members of the pedigree, 10 were identified homozygous and 34 heterozygous. The ten new OPPG patients presented with phenotypical variability in osseous manifestations.
We present two members of a family with a novel LRP5 mutation associated with high bone mass.
the crosstalk between Hsp90ab1 and LRP5 contributed to the upregulation of multiple mesenchymal markers, which are also targets of Wnt/beta-catenin. Collectively, this study uncovers the details of the Hsp90ab1-LRP5 axis, providing novel insights into the role and mechanism of invasion and metastasis in gastric cancer (GC) .
An interaction was found between LRP5 SNP rs648438 and periostin SNP rs9547970 on serum periostin levels and on radial cortical porosity.
Significant associations between LRP5 SNPs (p.A1330V, p.N740N, and p.V667M) and the severity of radiographic damage reinforce the evidence of bone destruction heritability in rheumatoid arthritis.
our results demonstrated an association of the T allele for the LRP5 4037C>T polymorphism with type 1 diabetes mellitus susceptibility in a Brazilian population, moreover the possible relation in the progressive failure of glycemic control.
This is the first study to report a group of patients with digenic familial exudative vitreoretinopathy (FEVR). In most affected eyes, the stage was more severe than stage 3. We speculate that the phenotype of FEVR is more severe in patients with digenic rather than monogenic variants of FEVR-related genes.
These findings expand the mutation spectrums of ABCA4 and LRP5, and will be valuable for genetic counseling and development of therapeutic interventions for patients with Familial exudative vitreoretinopathy.
Data suggest that the risk of type 2 diabetes mellitus (T2DM) may be associated with interactions between the low-density lipoprotein receptor-related protein 5 (LRP5) gene and overweight and obesity.
The data do not support the hypothesis that HBM-causing LRP5 mutations, associated with increased Wnt signaling, improve glucose metabolism in humans. However, it does appear that LRP5 variants may affect LDL metabolism, a major risk factor for coronary artery disease.
In conclusion, the LRP5 mutation influences cell proliferation through the Wnt signaling pathway, thereby reducing the number of supporting cells and hair cells and leading to nonsyndromic hearing loss in this Chinese family.
LRP5 might be an important genetic marker contributing to bone mass accrual early in life.
We identified two novel heterozygous deletion mutations [LRP5, c.4053 DelC (p.Ile1351IlefsX88); TSPAN12, EX8Del] using targeted NGS as a causative mutation for Familial exudative vitreoretinopathy (FEVR).
Anti-LRP5/LRP6 single-domain antibody fragments promote differentiation of Wnt3a-hypersensitive intestinal stem cells.
Heterozygous deletion of the LRP5 gene in mice could alter the profile of the immune cells, influence the balance of immune environment, and modulate bone homeostasis.
Megakaryocytes are increased in the bone marrow of Lrp5G170V/G170V mice. Depletion of megakaryocytes does not affect the Lrp5-induced high bone mass.
The phenotype of the Lrp5(tvrm111B) mutant includes abnormalities of the retinal vasculature and of bone mineral density.
the LRP5 mutation in high bone mass transgenic mice shows altered bone matrix composition
Lrp6 is the key mediator of Wnt3a signaling in osteoblasts and Lrp5 played a less significant role in mediating Wnt3a signaling.
Identification of a link between Wnt-Lrp5 signaling and insulin signaling in the osteoblast that has the potential to influence energy balance and compound the detrimental effects of a HFD on whole-body metabolism.
Lrp5(-/-) mice displayed significantly delayed retinal vascular development, absence of deep layer retinal vessels, leading to increased levels of vascular endothelial growth factor and subsequent pathologic glomeruloid vessels, as well as decreased inner retinal visual function.
A mouse LRP5 ectodomain recombinant was cleaved by VAP1, creating a peptide, VAHLTGIHAVEE, detected by mass spectrometric analysis of the 140-kDa fragment, suggesting that the sessile bond by VAP1 is Glu1206-Val1207.
we revealed miR-375-3p negatively regulated osteogenesis by targeting LRP5 and beta-catenin
lung myeloid cells are responsive to Lrp5/beta-catenin signaling, leading to differentiation of an alveolar macrophage subtype that antagonizes the resolution of lung fibrosis.
LRP5 is a novel anti-inflammatory macrophage marker that positively regulates migration, phagocytosis, lipid uptake and metabolism.
These results revealed a new role of the canonical Lrp5/6-beta-catenin pathway in regulating the morphogenesis of the cerebellum during postnatal development.
LRP5 function in mice causes retinal hypovascularization during development as well as retinal neovascularization in adulthood with disorganized and leaky vessels.
Lrp5 is required for glucose uptake, and glucose uptake regulates the growth rate of mammary epithelial cells in culture.
Data show that LDL receptor-related protein 5 (LRP5) gain-of-function mutations do not activate beta-catenin signaling in osteoblasts.
These in vivo data support in vitro studies regarding the mechanism of HBM-causing mutations, and imply that HBM LRP5 receptors differ in their relative sensitivity to inhibition by SOST and DKK1.
Lrp5 A214V and G171V were partially or fully protected from the bone loss that normally results frommechanical disuse using two models, tail suspension and Botulinum toxin-induced muscle paralysis, in two different Lrp5 HBM knock-in mouse models.
In hypercholesterolemia LRP5(-/-) mice Wnt/beta-catenin pathway was shut down. An antiatherogenic role for LRP5 was demonstrated as HC LRP5(-/-) mice developed larger aortic atherosclerotic lesions than WT mice.
This 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.
Lipoprotein Receptor Related Protein 5
, low density lipoprotein receptor-related protein 5
, low-density lipoprotein receptor-related protein 5
, low-density lipoprotein receptor-related protein 5-like
, low density lipoprotein receptor-related protein 7
, low-density lipoprotein receptor-related protein 7