Recombinant Mouse Wnt-10b Protein

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).