• Purity

  >90%, by SDS-PAGE under reducing conditions and visualized by silver stain

• Endotoxin Level

  <0.10 EU per 1 μg of the protein by the LAL method.  

• Activity

  Measured by its binding ability in a functional ELISA. When Recombinant Human R‑Spondin 3 (Catalog # ) is coated at 0.5 μg/mL, Recombinant Human Lgr4/GPR48 Fc Chimera binds with an apparent K    _D <10 nM.  

• Source

  Chinese Hamster Ovary cell line, CHO-derived

  Human Lgr4 (Ala25-Thr544) Accession # Q9BXB1	IEGRMD	Human IgG1 (Pro100-Lys330)
  N-terminus		C-terminus

• Accession #

• N-terminal Sequence    
  Analysis

  Ala25

• Structure / Form

  Disulfide-linked homodimer

• Predicted Molecular Mass

  83.8 kDa (monomer)

• SDS-PAGE

  100-130 kDa, reducing conditions

Background: Lgr4/GPR48

Lgr4 (leucine‑rich repeat GPR 4), also called GPR48 (G‑protein‑coupled receptor 48), is a seven‑transmembrane glycoprotein receptor in the Lgr family of cell surface receptors (1, 2). While this family includes receptors for hormones such as LH, FSH, TSH, and HCG, the subfamily comprising Lgr4, Lgr5, and Lgr6 are G‑protein‑independent mediators of the potentiating effect of R‑Spondins on Wnt signaling (1‑6). Lgr4 binds and forms complexes with R‑Spondins, Frizzled Wnt receptors and LRP Wnt co‑receptors (5). It acts at least in part by enhancing Wnt‑dependent LRP phosphorylation, internalization of LRPs, and accumulation of beta ‑catenin (3, 4). Human Lgr4 cDNA encodes 951 amino acids (aa), including a long N‑terminal extracellular domain (ECD, aa 25‑544) with 16‑17 LRR domains that mediate ligand interaction (1). The LRR‑containing ECD of human Lgr4 shares 93% aa sequence identity with mouse, rat and bovine Lgr4, and 50‑60% aa identity with human Lgr5 and Lgr6. Lgr4 is widely expressed in both embryo and adult. Expression of Lgr4 mRNA in adult humans is highest in pancreas, followed by liver, heart, muscle, brain, and placenta (1). In rodents, embryonic and adult expression includes liver, kidney, adrenals, bone/cartilage, and heart (2, 7‑9). Lgr4 deletion in the mouse affects development in areas of expression, for example, inhibiting fetal liver definitive erythropoiesis (9). Deletion of Lgr4 specifically from stem and progenitor cells in intestinal crypts induces loss of crypts due to insufficient Wnt signaling (5, 6). Lgr4 may be over‑expressed in carcinomas and may promote invasiveness and metastasis by down‑regulating p27^Kip1 expression (10).

• References:

1. Loh, E.D. et al. (2001) Biochem. Biophys. Res. Commun. 282:757.

2. Hsu, S.Y. et al. (1998) Mol. Endocrinol. 12:1830.

3. Carmon, K.S. et al. (2011) Proc. Natl. Acad. Sci. USA 108:11452.

4. Glinka, A. et al. (2011) EMBO Rep. 12:1055.

5. de Lau, W. et al. (2011) Nature 476:293.

6. Ruffner, H. et al. (2012) PLoS ONE 7:e40975.

7. Van Schoore, G. et al. (2005) Histochem. Cell Biol. 124:35.

8. Mazerbourg, S. et al. (2004) Mol. Endocrinol. 18:2241.

9. Song, H. et al. (2008) J. Biol. Chem. 283:36687.

10. Gao, Y. et al. (2006) Cancer Res. 66:11623.

• Long Name:

  Leucine-rich Repeat Containing G Protein-coupled Receptor 4

• Entrez Gene IDs:

  55366 (Human); 107515 (Mouse); 286994 (Rat)

• Alternate Names:

  GPR48; GPR48G protein-coupled receptor 48; G-protein coupled receptor 48; leucine-rich repeat containing G protein-coupled receptor 4; Lgr4