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A Member of the Frizzled Protein Family Mediating Axis Induction by Wnt-5A
Abstract
In Xenopus laevis embryos, the Wingless/Wnt-1 subclass of Wnt molecules induces axis duplication, whereas the Wnt-5A subclass does not. This difference could be explained by distinct signal transduction pathways or by a lack of one or more Wnt-5A receptors during axis formation. Wnt-5A induced axis duplication and an ectopic Spemann organizer in the presence of hFz5, a member of the Frizzled family of seven-transmembrane receptors. Wnt-5A/hFz5 signaling was antagonized by glycogen synthase kinase-3 and by the amino-terminal ectodomain of hFz5. These results identify hFz5 as a receptor for Wnt-5A.
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Cited by
Wnt/β-Catenin Signaling in Development and Disease
Clevers, H. (2006) · Cell · doi:10.1016/j.cell.2006.10.018 · Cited by 5,568
Polakis, P. (2000) · Genes & Development · doi:10.1101/gad.14.15.1837 · Cited by 3,183
Wnt signaling: a common theme in animal development
Cadigan, K. M., & Nusse, R. (1997) · Genes & Development · doi:10.1101/gad.11.24.3286 · Cited by 2,567
Secreted antagonists of the Wnt signalling pathway
Kawano, Y., & Kypta, R. (2003) · Journal of Cell Science · doi:10.1242/jcs.00623 · Cited by 1,584
Wnt signalling and its impact on development and cancer
Klaus, A., & Birchmeier, W. (2008) · Nature Reviews Cancer · doi:10.1038/nrc2389 · Cited by 1,595
Metadata
- Authors
- He, X., Saint-Jeannet, J.-P., Wang, Y., Nathans, J., Dawid, I., & Varmus, H.
- Venue
- Science
- Published
- 1997-03-14
- Volume
- 275
- Issue
- 5306
- Pages
- 1652-1654
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2071397057
- Cited by
- 492
- References
- 0
- FWCI
- 9.22
- Type
- journal article
- Language
- en
- Open access
- closed
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- He, X., Saint-Jeannet, J.-P., Wang, Y., Nathans, J., Dawid, I., & Varmus, H. (1997). A Member of the Frizzled Protein Family Mediating Axis Induction by Wnt-5A. Science. https://doi.org/10.1126/science.275.5306.1652
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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