The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
An ARF-Independent c-MYC-Activated Tumor Suppression Pathway Mediated by Ribosomal Protein-Mdm2 Interaction
Open accessAbstract
Summary In vitro studies have shown that inhibition of ribosomal biogenesis can activate p53 through ribosomal protein (RP)-mediated suppression of Mdm2 E3 ligase activity. To study the physiological significance of the RP-Mdm2 interaction, we generated mice carrying a cancer-associated cysteine-to-phenylalanine substitution in the zinc finger of Mdm2 that disrupted its binding to RPL5 and RPL11. Mice harboring this mutation, although retain normal p53 response to DNA damage, lack p53 response to perturbations in ribosome biogenesis. Loss of RP-Mdm2 interaction significantly accelerates Eμ-Myc induced lymphomagenesis. Furthermore, ribosomal perturbation induced p53 response does not require tumor suppressor p19Arf. Collectively, our findings establish RP-Mdm2 interaction as a genuine p53 stress-signaling pathway activated by aberrant ribosomal biogenesis and essential for safeguarding against oncogenic c-Myc-induced tumorigenesis.
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Vogelstein, B., Lane, D., & Levine, A. J. (2000) · Nature · doi:10.1038/35042675 · Cited by 6,607 · cited 2×
“The p53 transcription factor interacts with a large number of proteins and plays a central role in regulating cell growth, proliferation, and apoptosis (Vogelstein et al., 2000).”
5-Fluorouracil: mechanisms of action and clinical strategies
Longley, D. B., Harkin, D. P., & Johnston, P. G. (2003) · Nature Reviews Cancer · doi:10.1038/nrc1074 · Cited by 5,332
Amplification of a gene encoding a p53-associated protein in human sarcomas
Oliner, J. D., Kinzler, K. W., Meltzer, P. S., George, D. L., & Vogelstein, B. (1992) · Nature · doi:10.1038/358080a0 · Cited by 1,949
Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization
Zindy, F., Eischen, C. M., Randle, D. H., Kamijo, T., Cleveland, J. L., Sherr, C. J., & Roussel, M. F. (1998) · Genes & Development · doi:10.1101/gad.12.15.2424 · Cited by 1,245
Disruption of the ARF-Mdm2-p53 tumor suppressor pathway in Myc-induced lymphomagenesis
Eischen, C. M., Weber, J. D., Roussel, M. F., Sherr, C. J., & Cleveland, J. L. (1999) · Genes & Development · doi:10.1101/gad.13.20.2658 · Cited by 819
Mechanisms of action of mycophenolate mofetil
Allison, A. (2005) · Lupus · doi:10.1177/096120330501400102 · Cited by 480
MDMX regulation of p53 response to ribosomal stress
Gilkes, D. M., Chen, L., & Chen, J. (2006) · The EMBO Journal · doi:10.1038/sj.emboj.7601424 · Cited by 142
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MDM2, MDMX and p53 in oncogenesis and cancer therapy
Wade, M., Li, Y.-C., & Wahl, G. M. (2013) · Nature Reviews Cancer · doi:10.1038/nrc3430 · Cited by 1,279
Translational Control in Cancer Etiology
Ruggero, D. (2013) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a012336 · Cited by 367
The role of ubiquitin modification in the regulation of p53
Hock, A. K., & Vousden, K. H. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2013.05.022 · Cited by 168
Osteosarcoma: Molecular Pathogenesis and iPSC Modeling
Lin, Y.-H., Jewell, B. E., Gingold, J., Lu, L., Zhao, R., Wang, L. L., & Lee, D.-F. (2017) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2017.06.004 · Cited by 150
Abnormal MDMX degradation in tumor cells due to ARF deficiency
Li, X., Gilkes, D., Li, B., Cheng, Q., Pernazza, D., Lawrence, H., Lawrence, N., & Chen, J. (2012) · Oncogene · doi:10.1038/onc.2011.534 · Cited by 32
Metadata
- Authors
- Macias, E., Jin, A., Deisenroth, C., Bhat, K., Mao, H., Lindström, M. S., & Zhang, Y.
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2010-09
- Volume
- 18
- Issue
- 3
- Pages
- 231-243
- ISSN
- 1535-6108 (ISSN-L)
- OpenAlex
- W2021709122
- Cited by
- 216
- References
- 7
- FWCI
- 9.40
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Macias, E., Jin, A., Deisenroth, C., Bhat, K., Mao, H., Lindström, M. S., & Zhang, Y. (2010). An ARF-Independent c-MYC-Activated Tumor Suppression Pathway Mediated by Ribosomal Protein-Mdm2 Interaction. Cancer Cell. https://doi.org/10.1016/j.ccr.2010.08.007
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