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anti-Human LRP5 Anticorps:
anti-Mouse (Murine) LRP5 Anticorps:
anti-Rat (Rattus) LRP5 Anticorps:
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Human Polyclonal LRP5 Primary Antibody pour EIA, WB - ABIN953209
Abramowitz, Muntner, Coco, Southern, Lotwin, Hostetter, Melamed: Serum alkaline phosphatase and phosphate and risk of mortality and hospitalization. dans Clinical journal of the American Society of Nephrology : CJASN 2010
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Human Monoclonal LRP5 Primary Antibody pour 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. dans Endocrine journal 2009
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Human Polyclonal LRP5 Primary Antibody pour IHC, ELISA - ABIN185410
He, Semenov, Tamai, Zeng: LDL receptor-related proteins 5 and 6 in Wnt/beta-catenin signaling: arrows point the way. dans Development (Cambridge, England) 2004
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Human Polyclonal LRP5 Primary Antibody pour WB - ABIN127323
Del Valle-Pérez, Arqués, Vinyoles, de Herreros, Duñach: Coordinated action of CK1 isoforms in canonical Wnt signaling. dans Molecular and cellular biology 2011
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Human Monoclonal LRP5 Primary Antibody pour ELISA, WB - ABIN517568
Kim, Goel, Alexander: Differentiation generates paracrine cell pairs that maintain basaloid mouse mammary tumors: proof of concept. dans PLoS ONE 2011
The extracellular domains of Lrp5/6 behave as physiologically relevant inhibitors of noncanonical Wnt (Montrer WNT2 Anticorps) 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.
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 (Montrer NDP Anticorps) 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 (Montrer NDP Anticorps). Our findings expand the mutational spectrum of FEVR (Montrer NDP Anticorps) 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 (Montrer NDP Anticorps)) 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 (Montrer APOE Anticorps), 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 (Montrer MLXIP Anticorps)-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 (Montrer TSPAN12 Anticorps) 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.
These results revealed a new role of the canonical Lrp5/6-beta-catenin (Montrer CTNNB1 Anticorps) 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 (Montrer LDLR Anticorps)-related protein 5 (Montrer CAPS Anticorps) (LRP5) gain-of-function mutations do not activate beta-catenin (Montrer CTNNB1 Anticorps) 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 (Montrer SOST Anticorps) and DKK1 (Montrer DKK1 Anticorps).
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 (Montrer WNT2 Anticorps)/beta-catenin (Montrer CTNNB1 Anticorps) 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 (Montrer TEK Anticorps) pathway.
Data show that low density lipoprotein receptor-related protein 5 (LRP5) and the canonical Wnt (Montrer WNT2 Anticorps) 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