Wnt‑16b in HEK293 Human Cell Line. Wnt‑16b was detected in immersion fixed HEK293 human embryonic kidney cell line using Mouse Anti-Human Wnt‑16b Monoclonal Antibody (Catalog # MAB7790) at 25 µg/mL for 3 hours at room temperature. Cells were stained using the NorthernLights™ 557-conjugated Anti-Mouse IgG Secondary Antibody (red; Catalog # NL007) and counterstained with DAPI (blue). Specific staining was localized to cytoplasm. View our protocol for Fluorescent ICC Staining of Cells on Coverslips.
Preparation and Storage
Reconstitute at 0.5 mg/mL in sterile PBS.
The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. *Small pack size (SP) is shipped with polar packs. Upon receipt, store it immediately at -20 to -70 °C
Stability & Storage
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.
6 months, -20 to -70 °C under sterile conditions after reconstitution.
Wnt‑16 is a 40 kDa protein within the Wnt family of secreted, highly conserved, cysteine‑rich, palmitoylated cell signaling glycoproteins that play important roles in vertebrate developmental pattern formation, cell fate decision, axon guidance, and tumor formation (1‑3). Wnt‑16a and Wnt‑16b isoforms in humans differ in the signal sequence and the first two amino acids (aa) of the mature protein (2, 3). Wnt‑16b is the more conserved isoform and is widely expressed, while Wnt‑16a is expressed mainly in the human pancreas (3). Mature human Wnt‑16b shares 92%, 93%, and 95% aa sequence identity with mouse/rat, rabbit/porcine/equine, and bovine Wnt‑16, respectively. Wnt‑16 expression is detected on uterine stroma adjacent to the luminal epithelium during implantation (4). It is up‑regulated during the first embryonic lymphoid progenitor differentiation (5). Congenital heart defects correlate with elevated Wnt‑16 in mouse embryos and human amniotic fluid (6). Low cortical bone thickness and bone mineral density correlate with deletion of Wnt‑16 in mice and a Wnt‑16 missense SNP in humans (7). Wnt‑16 is over‑expressed in cells undergoing replicative senescence, and is up‑regulated in articular cartilage by injury and osteoarthritis (8, 9). Wnt‑16b expression in skin is up‑regulated in human basal cell carcinomas, enhancing cell survival (10). Its expression is also up‑regulated by DNA damage (radiation and chemotherapy) in stroma surrounding prostate tumors, causing enhanced survival and treatment resistance in the tumor cells (11). Pre‑B acute lymphoblastic leukemia with t(1;19) translocation, creating an E2A‑Pbx1 fusion protein, also causes up‑regulation of Wnt‑16 that confers resistance to apoptosis (12, 13). Wnt‑16 signaling through both canonical and JNK‑mediated (non‑canonical) pathways is reported (8‑10).
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Zheng, H.F. et al. (2012) PLoS Genet. 8:31002745.
Dell’accio, F. et al. (2008) Arthritis Rheum. 58:1410.
Binet, R. et al. (2009) Cancer Res. 69:9183.
Teh, M.T. et al. (2006) J. Cell Sci. 120:330.
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Wingless-type MMTV Integration Site Family, Member 16B
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