The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.
Deciphering the function of canonical Wnt signals in development and disease: conditional loss- and gain-of-function mutations of β-catenin in mice
Open accessAbstract
Wnt signaling is one of a handful of powerful signaling pathways that play crucial roles in the animal life by controlling the genetic programs of embryonic development and adult homeostasis. When disrupted, these signaling pathways cause developmental defects, or diseases, among them cancer. The gateway of the canonical Wnt pathway, which contains >100 genes, is an essential molecule called β-catenin (Armadillo in Drosophila). Conditional loss- and gain-of-function mutations of β-catenin in mice provided powerful tools for the functional analysis of canonical Wnt signaling in many tissues and organs. Such studies revealed roles of Wnt signaling that were previously not accessible to genetic analysis due to the early embryonic lethality of conventional β-catenin knockout mice, as well as the redundancy of Wnt ligands, receptors, and transcription factors. Analysis of conditional β-catenin loss- and gain-of-function mutant mice demonstrated that canonical Wnt signals control progenitor cell expansion and lineage decisions both in the early embryo and in many organs. Canonical Wnt signaling also plays important roles in the maintenance of various embryonic or adult stem cells, and as recent findings demonstrated, in cancer stem cell types. This has opened new opportunities to model numerous human diseases, which have been associated with deregulated Wnt signaling. Our review summarizes what has been learned from genetic studies of the Wnt pathway by the analysis of conditional β-catenin loss- and gain-of-function mice.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Lessons from hereditary colorectal cancer
Kinzler, K. W., & Vogelstein, B. (1996) · Cell · doi:10.1016/s0092-8674(00)81333-1 · Cited by 4,919
Polakis, P. (2000) · Genes & Development · doi:10.1101/gad.14.15.1837 · Cited by 3,183
Functional interaction of β-catenin with the transcription factor LEF-1
Behrens, J., von Kries, J. P., Kühl, M., Bruhn, L., Wedlich, D., Grosschedl, R., & Birchmeier, W. (1996) · Nature · doi:10.1038/382638a0 · Cited by 2,912
Self-citationWnt proteins are lipid-modified and can act as stem cell growth factors
Willert, K., Brown, J. D., Danenberg, E., Duncan, A. W., Weissman, I. L., Reya, T., Yates, J. R., & Nusse, R. (2003) · Nature · doi:10.1038/nature01611 · Cited by 2,257
A role for Wnt signalling in self-renewal of haematopoietic stem cells
Reya, T., Duncan, A. W., Ailles, L., Domen, J., Scherer, D. C., Willert, K., Hintz, L., Nusse, R., & Weissman, I. L. (2003) · Nature · doi:10.1038/nature01593 · Cited by 2,159
Generation of a functional mammary gland from a single stem cell
Shackleton, M., Vaillant, F., Simpson, K. J., Stingl, J., Smyth, G. K., Asselin-Labat, M.-L., Wu, L., Lindeman, G. J., & Visvader, J. E. (2006) · Nature · doi:10.1038/nature04372 · Cited by 2,005
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
Self-citationA Dominant Mutation That Predisposes to Multiple Intestinal Neoplasia in the Mouse
Moser, A. R., Pitot, H. C., & Dove, W. F. (1990) · Science · doi:10.1126/science.2296722 · Cited by 1,591
WNT Signals Are Required for the Initiation of Hair Follicle Development
Andl, T., Reddy, S. T., Gaddapara, T., & Millar, S. E. (2002) · Developmental Cell · doi:10.1016/s1534-5807(02)00167-3 · Cited by 1,088
Stem and progenitor cells: origins, phenotypes, lineage commitments, and transdifferentiations
Weissman, I. L., Anderson, D. J., & Gage, F. (2001) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev.cellbio.17.1.387 · Cited by 948
Thomas, K. R., & Capecchi, M. R. (1990) · Nature · doi:10.1038/346847a0 · Cited by 896
Mao, J., Wang, J., Liu, B., Pan, W., Farr, G. H., Flynn, C., Yuan, H., Takada, S., Kimelman, D., Li, L., et al. (2001) · Molecular Cell · doi:10.1016/s1097-2765(01)00224-6 · Cited by 839 · cited 1×
“In contrast, in the presence of the Wnt ligands, the destruction complex is disassembled through phosphorylation of LRP5/6 and binding of Axin to LRP, which prevents -catenin degradation (Mao et al. 2001; Bilic et al. 2007; Schwarz-Romond et al. 2007).”
BackgroundA common human skin tumour is caused by activating mutations in β-catenin
Chan, E., Gat, U., McNiff, J. M., & Fuchs, E. (1999) · Nature Genetics · doi:10.1038/7747 · Cited by 612
Role that phosphorylation of GSK3 plays in insulin and Wnt signalling defined by knockin analysis
McManus, E. J., Sakamoto, K., Armit, L. J., Ronaldson, L., Shpiro, N., Marquez, R., & Alessi, D. R. (2005) · The EMBO Journal · doi:10.1038/sj.emboj.7600633 · Cited by 594
Essential role of β-catenin in postnatal bone acquisition.
Holmen, S. L., Zylstra, C. R., Mukherjee, A., Sigler, R. E., Faugere, M.-C., Bouxsein, M. L., Deng, L., Clemens, T. L., & Williams, B. O. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m501900200 · Cited by 584
Frizzled/PCP signalling: a conserved mechanism regulating cell polarity and directed motility
Seifert, J. R. K., & Mlodzik, M. (2007) · Nature Reviews Genetics · doi:10.1038/nrg2042 · Cited by 513
β-catenin activation is necessary and sufficient to specify the dorsal dermal fate in the mouse
Atit, R., Sgaier, S. K., Mohamed, O. A., Taketo, M. M., Dufort, D., Joyner, A. L., Niswander, L., & Conlon, R. A. (2006) · Developmental Biology · doi:10.1016/j.ydbio.2006.04.449 · Cited by 400 · cited 1×
“Finally, the function of Wnt/ - catenin signaling has also been studied in the skin mesenchyme by conditional loss- and gain-of-function mutations of -catenin, using an engrailed-1 cre or HoxB6 cre allele (Atit et al. 2006; Ohtola et al. 2008).”
Wnt signaling promotes regeneration in the retina of adult mammals
Osakada, F., Ooto, S., Akagi, T., Mandai, M., Akaike, A., & Takahashi, M. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.4193-06.2007 · Cited by 322
Heads or tails: Wnts and anterior–posterior patterning
Yamaguchi, T. P. (2001) · Current Biology · doi:10.1016/s0960-9822(01)00417-1 · Cited by 276
Heart induction by Wnt antagonists depends on the homeodomain transcription factor Hex
Foley, A. C., & Mercola, M. (2005) · Genes & Development · doi:10.1101/gad.1279405 · Cited by 195
The bHLH factor Olig3 coordinates the specification of dorsal neurons in the spinal cord
Müller, T., Anlag, K., Wildner, H., Britsch, S., Treier, M., & Birchmeier, C. (2005) · Genes & Development · doi:10.1101/gad.326105 · Cited by 150
Helping Wingless take flight: how WNT proteins are secreted
Hausmann, G., Bänziger, C., & Basler, K. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2141 · Cited by 147
β-Catenin is critical for early postnatal liver growth
Apte, U., Zeng, G., Thompson, M. D., Muller, P., Micsenyi, A., Cieply, B., Kaestner, K. H., & Monga, S. P. S. (2007) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.00359.2006 · Cited by 119
Cited by
The many faces and functions of β‐catenin
Valenta, T., Hausmann, G., & Basler, K. (2012) · The EMBO Journal · doi:10.1038/emboj.2012.150 · Cited by 1,598
HDAC1 and HDAC2 regulate oligodendrocyte differentiation by disrupting the β-catenin–TCF interaction
Ye, F., Chen, Y., Hoang, T., Montgomery, R. L., Zhao, X.-H., Bu, H., Hu, T., Taketo, M. M., van Es, J. H., Clevers, H., et al. (2009) · Nature Neuroscience · doi:10.1038/nn.2333 · Cited by 559
The Role of Wnt Signaling in Physiological and Pathological Angiogenesis
Dejana, E. (2010) · Circulation Research · doi:10.1161/circresaha.110.223750 · Cited by 347
Chen, D., Jarrell, A., Guo, C., Lang, R., & Atit, R. (2012) · Development · doi:10.1242/dev.076463 · Cited by 260
Beta-catenin signaling, liver regeneration and hepatocellular cancer: sorting the good from the bad
Nejak-Bowen, K. N., & Monga, S. P. S. (2011) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2010.12.010 · Cited by 260
Metadata
- Authors
- Grigoryan, T., Wend, P., Klaus, A., & Birchmeier, W.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2008-09-01
- Volume
- 22
- Issue
- 17
- Pages
- 2308-2341
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2110838173
- Cited by
- 560
- References
- 23
- Type
- posted content
- Language
- en
- Open access
- diamond
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
