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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
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
Show all 2 Pubmed References
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 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
The extracellular domains of Lrp5/6 behave as physiologically relevant inhibitors of noncanonical Wnt (show WNT2 Antibodies) 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.
The detection rate for mutations in the three known genes was 23%. Mutations in LRP5 and TSPAN12 (show TSPAN12 Antibodies) 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 cle (show AOC3 Antibodies)avage 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 (show NDP Antibodies) (3/31, 9.7%), FZD4 (show FZD4 Antibodies) (2/31, 6.5%), TSPAN12 (show TSPAN12 Antibodies) (1/31, 3.2%), and KIF11 (show KIF11 Antibodies) (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 (show NDP Antibodies)/beta-catenin (show CTNNB1 Antibodies) pathway by established luciferase reporter assays, and all mutants failed to activate the pathway.
findings revealed an unrecognized role of Caprin-2 (show CAPRIN2 Antibodies) in facilitating LRP5/6 constitutive phosphorylation at G2/M through forming a quaternary complex with CDK14 (show CDK14 Antibodies), Cyclin Y (show CCNY Antibodies), and LRP5/6.
This study did not identify LRP5 polymorphisms as a risk factor for osteoporosis in Thai menopausal women.
We identified four novel LRP5 missense mutations in these FEVR (show NDP Antibodies) families: c.C1042T (p.R348W), c.G1141A (p.D381N), c.C1870T (p.R624W), and c.A4550G (p.Y1517C). All four of these LRP5 mutations led to significant reduction of enzymatic activity with response to NORRIN (show NDP Antibodies). Our findings expand the mutational spectrum of FEVR (show NDP Antibodies) in the Indian population and provide some guidelines in clinical diagnosis.
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 Antibodies)) revealed a novel variant in the LRP5 gene that co-segregated with the phenotype in the family.
Lrp6 (show LRP6 Antibodies) is the key mediator of Wnt3a (show WNT3A Antibodies) signaling in osteoblasts and Lrp5 played a less significant role in mediating Wnt3a (show WNT3A Antibodies) signaling.
Identification of a link between Wnt (show WNT2 Antibodies)-Lrp5 signaling and insulin (show INS Antibodies) 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 (show AOC3 Antibodies), creating a peptide, VAHLTGIHAVEE, detected by mass spectrometric analysis of the 140-kDa fragment, suggesting that the sessile bond by VAP1 (show AOC3 Antibodies) is Glu1206-Val1207.
we revealed miR (show MLXIP Antibodies)-375-3p negatively regulated osteogenesis by targeting LRP5 and beta-catenin (show CTNNB1 Antibodies)
lung myeloid cells are responsive to Lrp5/beta-catenin (show CTNNB1 Antibodies) 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 (show CTNNB1 Antibodies) 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.
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