Reactivity | MuSpecies Glossary |
Applications | Bioactivity |
Format | Carrier-Free |
Details of Functionality | Measured in a cell proliferation/survival assay using IEC‑18 rat small intestinal epithelial cells. The ED50 for this effect is 0.3-1.2 μg/mL. |
Source | Chinese Hamster Ovary cell line, CHO-derived mouse Wnt-10b protein Met1-Lys389 |
Accession # | |
N-terminal Sequence | Asn29 |
Protein/Peptide Type | Recombinant Proteins |
Gene | Wnt10b |
Purity | >85%, by SDS-PAGE under reducing conditions and visualized by silver stain. |
Endotoxin Note | <0.10 EU per 1 μg of the protein by the LAL method. |
Dilutions |
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Theoretical MW | 40.1 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. |
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SDS-PAGE | 42 kDa, reducing conditions |
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Publications |
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Storage | Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
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Buffer | Lyophilized from a 0.2 μm filtered solution in PBS, NaCl, EDTA and CHAPS. |
Purity | >85%, by SDS-PAGE under reducing conditions and visualized by silver stain. |
Reconstitution Instructions | Reconstitute at 100 μg/mL in PBS. |
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). Mouse Wnt-10b cDNA encodes a 361 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). A short isoform is reported that lacks aa 143‑238 of the precursor (1, 4). Mouse Wnt-10b shares 97‑98% aa identity with human, 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 mis‑sense 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-10 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). As a key regulator, Wnt signaling plays a major role in the process of colon carcinogenesis (15).
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