The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
The Wnt Signaling Inhibitor Dickkopf-1 Is Required for Reentry into the Cell Cycle of Human Adult Stem Cells from Bone Marrow
Open accessAbstract
Adult human mesenchymal stem cells from bone marrow stroma (hMSCs) differentiate into numerous mesenchymal tissue lineages and are attractive candidates for cell and gene therapy. When early passage hMSCs are plated or replated at low density, the cultures display a lag phase of 3-5 days, a phase of rapid exponential growth, and then enter a stationary phase without the cultures reaching confluence. We found that as the cultures leave the lag phase, they secrete high levels of dickkopf-1 (Dkk-1), an inhibitor of the canonical Wnt signaling pathway. The addition of recombinant Dkk-1 toward the end of the lag period increased proliferation and decreased the cellular concentration of beta-catenin. The addition of antibodies to Dkk-1 in the early log phase decreased proliferation. Also, expression of Dkk-1 in hMSCs decreased during cell cycle arrest induced by serum starvation. The results indicated that high levels of Dkk-1 allow the cells to reenter the cell cycle by inhibiting the canonical Wnt/beta-catenin signaling pathway. Since antibodies to Dkk-1 also increased the lag phase of an osteosarcoma line that expressed the gene, Dkk-1 may have a similar role in some other cell systems.
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Cites
High Bone Density Due to a Mutation in LDL-Receptor–Related Protein 5
Boyden, L. M., Mao, J., Belsky, J., Mitzner, L., Farhi, A., Mitnick, M. A., Wu, D., Insogna, K., & Lifton, R. P. (2002) · New England Journal of Medicine · doi:10.1056/nejmoa013444 · Cited by 1,591
Kremen proteins are Dickkopf receptors that regulate Wnt/β-catenin signalling
Mao, B., Wu, W., Davidson, G., Marhold, J., Li, M., Mechler, B. M., Delius, H., Hoppe, D., Stannek, P., Walter, C., et al. (2002) · Nature · doi:10.1038/nature756 · Cited by 1,038
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
Boutros, M., Paricio, N., Strutt, D. I., & Mlodzik, M. (1998) · Cell · doi:10.1016/s0092-8674(00)81226-x · Cited by 801
Sekiya, I., Vuoristo, J. T., Larson, B. L., & Prockop, D. J. (2002) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.052716199 · Cited by 648
Self-citation
Cited by
Wagner, W., Wein, F., Seckinger, A., Frankhauser, M., Wirkner, U., Krause, U., Blake, J., Schwager, C., Eckstein, V., Ansorge, W., et al. (2005) · Experimental Hematology · doi:10.1016/j.exphem.2005.07.003 · Cited by 1,259
Lee, R. H., Kim, B., Choi, I., Kim, H., Choi, H. S., Suh, K., Bae, Y. C., & Jung, J. S. (2004) · Cellular Physiology and Biochemistry · doi:10.1159/000080341 · Cited by 931
Prockop, D. J. (2009) · Molecular Therapy · doi:10.1038/mt.2009.62 · Cited by 577
Self-citationDkk1-mediated inhibition of Wnt signaling in bone results in osteopenia
Li, J., Sarosi, I., Cattley, R. C., Pretorius, J., Asuncion, F., Grisanti, M., Morony, S., Adamu, S., Geng, Z., Qiu, W., et al. (2006) · Bone · doi:10.1016/j.bone.2006.03.017 · Cited by 441
Kumar, B., Garcia, M., Weng, L., Jung, X., Murakami, J. L., Hu, X., McDonald, T., Lin, A., Kumar, A. R., DiGiusto, D. L., et al. (2018) · Leukemia · doi:10.1038/leu.2017.259 · Cited by 441
Metadata
- Authors
- Gregory, C. A., Singh, H., Perry, A. S., & Prockop, D. J.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2003-07
- Volume
- 278
- Issue
- 30
- Pages
- 28067-28078
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2052898286
- Cited by
- 282
- References
- 5
- FWCI
- 7.51
- Type
- journal article
- Language
- en
- Open access
- hybrid
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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.
