R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
LRP5 (D5G4) Rabbit mAb #5440
Filter:
- WB
Supporting Data
| REACTIVITY | H M R Mk |
| SENSITIVITY | Endogenous |
| MW (kDa) | 200 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
- Mk-Monkey
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
LRP5 (D5G4) Rabbit mAb detects endogenous levels of total LRP5 protein.
Species Reactivity:
Human, Mouse, Rat, Monkey
Source / Purification
Monoclonal antibody is produced by immunizing animals with a recombinant human LRP5 protein (extracellular region).
Background
LRP5 and LRP6 are single-pass transmembrane proteins belonging to the low-density lipoprotein receptor (LDLR)-related protein family. Unlike other members of the LDLR family, LRP5 and LRP6 have four EGF and three LDLR repeats in the extracellular domain, and proline-rich motifs in the cytoplasmic domain (1). They function as co-receptors for Wnt and are required for the canonical Wnt/β-catenin signaling pathway (2,3). LRP5 and LRP6 are highly homologous and have redundant roles during development (4,5). The activity of LRP5 and LRP6 can be inhibited by the binding of some members of the Dickkopf (DKK) family of proteins (6,7). Upon stimulation with Wnt, LRP6 is phosphorylated at multiple sites including Thr1479, Ser1490, and Thr1493 by kinases such as GSK-3 and CK1 (8-10). Phosphorylated LRP6 recruits axin to the membrane and presumably activates β-catenin signaling (8-10).
LRP5 is involved in the regulation of bone homeostasis. Mutations and polymorphisms in LPR5 are associated with bone diseases like osteoporosis-pseudoglioma syndrome and high-bone-mass disorders (11-13). In addition, mutations in LRP5 are found in patients with hyperparathyroid tumor and breast cancer (14,15).
LRP5 is involved in the regulation of bone homeostasis. Mutations and polymorphisms in LPR5 are associated with bone diseases like osteoporosis-pseudoglioma syndrome and high-bone-mass disorders (11-13). In addition, mutations in LRP5 are found in patients with hyperparathyroid tumor and breast cancer (14,15).
- Brown, S.D. et al. (1998) Biochem. Biophys. Res. Commun. 248, 879-888.
- Pinson, K.I. et al. (2000) Nature 407, 535-538.
- Tamai, K. et al. (2000) Nature 407, 530-535.
- Kelly, O.G. et al. (2004) Development 131, 2803-2815.
- He, X. et al. (2004) Development 131, 1663-1677.
- Semënov, M.V. et al. (2001) Curr Biol 11, 951-61.
- Bafico, A. et al. (2001) Nat. Cell Biol. 3, 683-668.
- Tamai, K. et al. (2004) Mol. Cell 13, 149-156.
- Zeng, X. et al. (2005) Nature 438, 873-877.
- Davidson, G. et al. (2005) Nature 438, 867-872.
- Levasseur, R. et al. (2005) Joint Bone Spine 72, 207-14.
- Ferrari, S.L. et al. (2005) Curr Opin Lipidol 16, 207-14.
- Balemans, W. and Van Hul, W. (2007) Endocrinology 148, 2622-9.
- Björklund, P. et al. (2007) PLoS Med 4, e328.
- Björklund, P. et al. (2009) PLoS One 4, e4243.
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