Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
The extracellular domains of Lrp5/6 behave as physiologically relevant inhibitors of noncanonical Wnt signaling during Xenopus and mouse development in vivo.
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 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).
A novel heterozygous mutation (p.N198Y) in LRP5 was identified in a patient with significantly increased bone mineral density.
The presence of GIIA in the LRP5 complex pinpoints a potential functional connection with PRKCSH. Interestingly, all three PLD-associated protein complexes included filamin A (FLNA), a multifunctional protein described to play a role in ciliogenesis as well as canonical Wnt signalling.
Phenotypic variability was observed in the familial case and molecular analysis identified a novel homozygous c.1145C>T, p.(Pro382Leu) variant in both sibs. Homozygosity for the c.442C>T, p.(Gln148*) variant was also demonstrated in a separate case.
LRP5 (rs556442) had a significant influence on trigylceride (TG) levels in unadjusted analysis and when adjusted for interacting factors. Higher TG levels were observed in AA/AG genotype of rs566442 in comparison to GG genotype (OR = 2.028, 95% CI = 0.997-4.127, p = 0.049).
The detection rate for mutations in the three known genes was 23%. Mutations in LRP5 and TSPAN12 were more frequent, accounting for 10% and 8%
To our knowledge, these are the first two cases of the syndrome described in Italy. Genetic testing proved to be fundamental for definition of the syndrome and confirms the importance of early detection of LRP5 variants for management of systemic features of the disease in patients and carrier relatives.
VAP1 cleaved the extracellular region of LRP5. This cleavage removes four inhibitory beta-propeller structures, resulting in activation of LRP5/6.
Among the detected mutations, LRP5 accounted for the largest proportion with a mean mutation rate of 16.1% (5/31, 16.1%), followed by NDP (3/31, 9.7%), FZD4 (2/31, 6.5%), TSPAN12 (1/31, 3.2%), and KIF11 (1/31, 3.2%). All the novel changes were predicted to be pathogenic by a series of bioinformatics analyses.
wild-type and all five mutant LRP5 proteins were assayed for the ability to activate the Norrin/beta-catenin pathway by established luciferase reporter assays, and all mutants failed to activate the pathway.
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.
Report accelerated lung regeneration by platelet-rich plasma extract through Lrp5/Tie2 pathway.
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