>85%, by SDS-PAGE under reducing conditions and visualized by silver stain
Endotoxin Note
<0.01 EU per 1 μg of the protein by the LAL method.
Applications/Dilutions
Dilutions
Bioactivity
Theoretical MW
40 kDa. Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
SDS-PAGE
41 kDa, reducing conditions
Publications
Read Publications using 7196-WN in the following applications:
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
12 months from date of receipt, -20 to -70 °C as supplied.
1 month, 2 to 8 °C under sterile conditions after reconstitution.
3 months, -20 to -70 °C under sterile conditions after reconstitution.
Buffer
Lyophilized from a 0.2 μm filtered solution in PBS, EDTA and CHAPS with BSA as a carrier protein.
Purity
>85%, by SDS-PAGE under reducing conditions and visualized by silver stain
Reconstitution Instructions
Reconstitute at 100 μg/mL in PBS containing at least 0.1% human or bovine serum albumin.
Notes
This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.
Alternate Names for Recombinant Human Wnt-10b Protein
protein Wnt-10b
Protein Wnt-12
SHFM6WNT-10B protein
wingless-type MMTV integration site family, member 10B
Wnt10b
Wnt-10b
WNT12
Wnt-12
Background
Wnt-10b (also known as Wnt-12) is a 42 ‑ 44 kDa member of the Wnt family of secreted, highly conserved, cysteine-rich glycoproteins that play important roles in vertebrate pattern formation, cell fate decision, axon guidance, and tumor formation (1 ‑ 3). Human Wnt-10b cDNA encodes a 389 amino acid (aa) precursor that contains a 28 aa signal sequence plus a 361 aa mature protein that contains two glycosylation sites, three potential phosphorylation sites, and a potential palmitoylation site (3, 4). Human Wnt-10b shares 97 ‑ 99% aa identity with mouse, rat, equine, porcine, and canine Wnt-10b. Wnt-10b plays a critical role in maintaining mesenchymal stem cells and determining whether they differentiate to adipocytes or osteoblasts (5 ‑ 7). Mouse Wnt-10b deletion produces age‑dependent loss of bone mass due to defective production of osteoblasts, while transgenic over‑expression increases postnatal osteoblast differentiation and inhibits adipocyte differentiation (5 ‑ 7). Ectopic expression of Wnt-10b in an obesity and diabetes‑prone background, such as the ob/ob mouse, inhibits obesity (8). In mouse skeletal muscle, Wnt-10b is expressed inversely with SREBP1c and increases insulin sensitivity (9). In humans, a missense polymorphism is responsible for a malformation of hands and feet, while a C256Y inactivating mutation is associated with severe early-onset obesity (10, 11). Wnt-10b is mainly produced by stem cells and pre-osteoblasts, but also by adult bone marrow CD8+ T lymphocytes stimulated with parathyroid hormone (12). In some hepatocellular carcinomas, Wnt-10b can inhibit cancer cell growth, but in others, it can act synergistically with FGFs to stimulate cell growth (13). Several Wnts, including Wnt-10b, are expressed in both normal and/or malignant colon tissues (14).
Hardiman, G. et al. (1997) Cytogenet. Cell Genet. 77:278.
Katoh, M. (2008) Curr. Drug Targets 9:565.
Hausmann, G. et al. (2007) Nat. Rev. Mol. Cell Biol. 8:331.
Swiss Prot Accession # O00744.
Stevens, J.R. et al. (2010) J. Bone Miner. Res. 25:2138.
Bennett, C.N. et al. (2007) J. Bone Miner. Res. 22:1924.
Bennett, C.N. et al. (2005) Proc. Natl. Acad. Sci. USA 102:3324.
Wright, W.S. et al. (2007) Diabetes 56:295.
Abiola, M. et al. (2009) PLoS ONE 4:e8509.
Ugur, S.A. and A. Tolun (2008) Hum. Mol. Genet. 17:2644.
Christodoulides, C. et al. (2006) Diabetologia 49:678.
Terauchi, M. et al. (2009) Cell Metab. 10:229.
Yoshikawa, H. et al. (2007) Mol. Biol. Cell 18:4292.
Holcombe, R.F. et al. (2002) J. Clin. Pathol: Mol. Pathol. 55:220.
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