Mouse Wnt‑5b Antibody

Wnt proteins are secreted glycoproteins with a conserved pattern of 23-24 cysteine residues that play critical roles in both carcinogenesis and embryonic development. Wnts bind to receptors of the Frizzled family, sometimes in conjunction with other membrane-associated proteins such as LRPs or proteoglycans. Downstream effects of Wnt signaling occur through different intracellular components, depending on which pathway is activated. Three pathways have been characterized: the canonical Wnt/ beta -catenin pathway, the Wnt/Ca²⁺ pathway, and the planar cell polarity (1-3). Wnt-5b is a 49 kDa glycoprotein of the subgroup of Wnts that is implicated in the Wnt/Ca²⁺ pathway (3-6). It is not axis-inducing in Xenopus embryos and only weakly transforms C57MG mammary epithelial cells. The non-canonical Wnt pathway can inhibit canonical Wnt/ beta -catenin signaling (3). Mouse Wnt-5b is synthesized as a 359 amino acid (aa) precursor that contains a 17 aa signal sequence and a 342 aa mature region. It is ubiquitously expressed at low but increasing levels throughout embryonic development (4, 5, 7). In adult mice, Wnt-5b is expressed in heart, liver, brain, lung, testes, kidney, and pancreas (4, 8). Wnt-5b appears to promote adipogenesis. It is upregulated in early adipogenesis. Also, Wnt-5b overexpression in 3T3-L1 cells partially inhibits canonical Wnt suppression of adipogenesis (9, 10). Human Wnt-5b polymorphisms have been associated with Type II diabetes (9). Although Wnt-5a and Wnt-5b share 83% aa identity, they show differential expression and regulation of cyclin D1 and p130 during endochondral bone development. Together, they appear to coordinate chondrocyte proliferation and differentiation (11). Mature mouse Wnt-5b shows 94%, 98%, 90%, and 88% aa sequence identity with mature human, rat, chick, and Xenopus Wnt-5b, respectively.