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p53 induces differentiation of mouse embryonic stem cells by suppressing Nanog expression
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Citations
Cites
Cell Type- and Promoter-specific Roles of Ser18 Phosphorylation in Regulating p53 Responses
Chao, C., Hergenhahn, M., Kaeser, M. D., Wu, Z., Saito, S., Iggo, R., Hollstein, M., Appella, E., & Xu, Y. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m306938200 · Cited by 141
Self-citation
Research works printed but not linked: 22
- Ko, L. J. & Prives, C. p53: puzzle and paradigm. Genes Dev. 10, 1054–1072 (1996). · DOI · Paper page
- Mitsui, K. et al. The homeoprotein Nanog is required for maintenance of pluripotency in mouse epiblast and ES cells. Cell 113, 631–642 (2003). · DOI · Paper page
- Chambers, I. et al. Functional expression cloning of Nanog, a pluripotency sustaining factor in embryonic stem cells. Cell 113, 643–655 (2003). · DOI · Paper page
- Okamoto, K. et al. A novel octamer binding transcription factor is differentially expressed in mouse embryonic cells. Cell 60, 461–472 (1990). · DOI · Paper page
- Niwa, H., Miyazaki, J. & Smith, A. G. Quantitative expression of Oct-3/4 defines differentiation, dedifferentiation or self-renewal of ES cells. Nature Genet. 24, 372–376 (2000). · DOI · Paper page
- Hoffman, W. H., Biade, S., Zilfou, J. T., Chen, J. & Murphy, M. Transcriptional repression of the anti-apoptotic survivin gene by wild type p53. J. Biol. Chem. 277, 3247–3257 (2002). · DOI · Paper page
- Rohwedel, J., Guan, K. & Wobus, A. M. Induction of cellular differentiation by retinoic acid in vitro. Cells Tissues Organs 165, 190–202 (1999). · DOI · Paper page
- Sabapathy, K., Klemm, M., Jaenisch, R. & Wagner, E. F. Regulation of ES cell differentiation by functional and conformational modulation of p53. EMBO J. 16, 6217–6229 (1997). · DOI · Paper page
- Lutzker, S. G. & Levine, A. J. A functionally inactive p53 protein in teratocarcinoma cells is activated by either DNA damage or cellular differentiation, Nature Med. 2, 804–810 (1996). · DOI · Paper page
- Xu, Y. Regulation of p53 responses by post-translational modifications. Cell Death Differ. 10, 400–403 (2003). · DOI · Paper page
- Luo, J. L., et al. Knock-in mice with a chimeric human/murine p53 gene develop normally and show wild-type p53 responses to DNA damaging agents: a new biomedical research tool. Oncogene 20, 320–328 (2001). · DOI
- Savatier, P., Lapillonne, H., van Grunsven, L. A., Rudkin, B. B. & Samarut, J. Withdrawal of differentiation inhibitory activity/leukemia inhibitory factor up-regulates D-type cyclins and cyclin-dependent kinase inhibitors in mouse embryonic stem cells. Oncogene 12, 309–322 (1996).
- Bischoff, J. R., Friedman, P. N., Marshak, D. R., Prives, C. & Beach, D. Human p53 is phosphorylated by p60–cdc2 and cyclin B–cdc2. Proc. Natl Acad. Sci. USA 87, 4766–4770 (1990). · DOI · Paper page
- Wang, Y. & Prives, C. Increased and altered DNA binding of human p53 by S and G2/M but not G1 cyclin-dependent kinases. Nature 376, 88–91 (1995). · DOI · Paper page
- Wu, Z. et al. Mutation of mouse p53 Ser23 and the response to DNA damage. Mol. Cell. Biol. 22, 2441–2449 (2002). · DOI · Paper page
- Murphy, M. et al. Transcriptional repression by wild-type p53 utilizes histone deacetylases, mediated by interaction with mSin3a. Genes Dev. 13, 2490–2501 (1999). · DOI · Paper page
- Chao, C. et al. p53 transcriptional activity is essential for p53-dependent apoptosis following DNA damage. EMBO J. 19, 4967–4975 (2000). · DOI · Paper page
- Aladjem, M. I. et al. ES cells do not activate p53-dependent stress responses and undergo p53-independent apoptosis in response to DNA damage. Curr. Biol. 8, 145–155 (1998). · DOI · Paper page
- Chao, C., Saito, S., Anderson, C. W., Appella, E. & Xu, Y. Phosphorylation of murine p53 at ser-18 regulates the p53 responses to DNA damage. Proc. Natl Acad. Sci. USA 97, 11936–11941 (2000). · DOI · Paper page
- Yoshida-Koide, U. et al. Involvement of Ras in extraembryonic endoderm differentiation of embryonic stem cells. Biochem. Biophys. Res. Commun. 313, 475–481 (2004). · doi:10.1016/j.bbrc.2003.11.138
- Corbet, S. W., Clarke, A. R., Gledhill, S. & Wyllie, A. H. P53-dependent and -independent links between DNA-damage, apoptosis and mutation frequency in ES cells. Oncogene 18, 1537–1544 (1999). · DOI
- Boley, S. E., Wong, V. A., French, J. E. & Recio, L. p53 heterozygosity alters the mRNA expression of p53 target genes in the bone marrow in response to inhaled benzene. Toxicol. Sci. 66, 209–215 (2002). · DOI
Cited by
Takahashi, K., & Yamanaka, S. (2006) · Cell · doi:10.1016/j.cell.2006.07.024 · Cited by 26,673
Blinded by the Light: The Growing Complexity of p53
Vousden, K. H., & Prives, C. (2009) · Cell · doi:10.1016/j.cell.2009.04.037 · Cited by 3,163
How does p53 induce apoptosis and how does this relate to p53-mediated tumour suppression
Aubrey, B. J., Kelly, G. L., Janic, A., Herold, M. J., & Strasser, A. (2018) · Cell Death & Differentiation · doi:10.1038/cdd.2017.169 · Cited by 1,395
The multiple mechanisms that regulate p53 activity and cell fate
Hafner, A., Bulyk, M. L., Jambhekar, A., & Lahav, G. (2019) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-019-0110-x · Cited by 1,129
Linking the p53 tumour suppressor pathway to somatic cell reprogramming
Kawamura, T., Suzuki, J., Wang, Y. V., Menendez, S., Morera, L. B., Raya, A., Wahl, G. M., & Belmonte, J. C. I. (2009) · Nature · doi:10.1038/nature08311 · Cited by 1,115
Metadata
- Authors
- Lin, T., Chao, C., Saito, S., Mazur, S. J., Murphy, M. E., Appella, E., & Xu, Y.
- Venue
- Nature Cell Biology
- Published
- 2004-12-26
- Volume
- 7
- Issue
- 2
- Pages
- 165-171
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- OpenAlex
- W1976878409
- Cited by
- 859
- References
- 1
- FWCI
- 8.09
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
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- CoChat. (2026). Citation check: p53 induces differentiation of mouse embryonic stem cells by suppressing Nanog expression. https://app.cochat.ai/papers/10.1038/ncb1211
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- Lin, T., Chao, C., Saito, S., Mazur, S. J., Murphy, M. E., Appella, E., & Xu, Y. (2005). p53 induces differentiation of mouse embryonic stem cells by suppressing Nanog expression. Nature Cell Biology. https://doi.org/10.1038/ncb1211
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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.