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The extracellular domains of Lrp5/6 behave as physiologically relevant inhibitors of noncanonical Wnt (show WNT2 Proteins) signaling during Xenopus and mouse development in vivo.
Data show that in zebrafish, lrp5 also controls cell migration during early morphogenetic processes and contributes to shaping the craniofacial skeleton.
In this study, the splice site mutation c.2827thorn1G > A found in LRP5 (603506) gene is thought to cause microphthalmia in this family.
A genetic evaluation of the known genes associated with familial exudative vitreoretinopathy (FEVR (show NDP Proteins)) revealed a novel variant in the LRP5 gene that co-segregated with the phenotype in the family.
Meta-analysis indicates that the LRP5 Ala1330Val polymorphism may not be correlated with fracture susceptibility.
Independently or combined with APOE (show APOE Proteins), LRP5 polymorphisms may lead to dyslipidemia and are associated with generalized aggressive periodontitis. Dyslipidemia may be a risk indicator for generalized aggressive periodontitis in the Chinese population. Furthermore, two LRP5 polymorphisms (rs682429 and rs312016) might be useful for identifying subjects at higher risk of generalized aggressive periodontitis.
miR (show MLXIP Proteins)-23a plays an inhibitory role in osteogenic differentiation of hBMSCs, which may act by targeting LRP5
The authors report a case of familial exudative vitreoretinopathy in the spectrum of osteoporosis pseudoglioma syndrome associated with novel mutations of the LRP5 and TSPAN12 (show TSPAN12 Proteins) genes that resulted in a phenotype similar to bilateral persistent fetal vasculature.
LRP5 is a novel anti-inflammatory macrophage marker that positively regulates migration, phagocytosis, lipid uptake and metabolism.
LRP5 is a signature of the anti-inflammatory defensive phenotype of macrophages.
we identified a total of four different LRP5 variants that were predicted to be pathogenic by in silico tools. One ADPKD patient has a positive family history for ADPKD and variant LRP5 segregated with the disease.
finding corroborates the relationship between LRP5 genotype and bone phenotype in postmenopausal women, however, the complete mechanism of this relationship requires further investigations.
These results revealed a new role of the canonical Lrp5/6-beta-catenin (show CTNNB1 Proteins) 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 (show LDLR Proteins)-related protein 5 (show CAPS Proteins) (LRP5) gain-of-function mutations do not activate beta-catenin (show CTNNB1 Proteins) 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 (show SOST Proteins) and DKK1 (show DKK1 Proteins).
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 (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) 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 (show TEK Proteins) pathway.
Data show that low density lipoprotein receptor-related protein 5 (LRP5) and the canonical Wnt (show WNT2 Proteins) pathway down-regulation regulate the dyslipidaemic profile by promoting lipid and macrophage retention in the vessel wall.
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