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p53 regulates glucose metabolism through an IKK-NF-κB pathway and inhibits cell transformation
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“p53 regulates glucose transporters (GLUTs) that promote glucose transport across the cellular plasma membrane to inhibit glucose uptake.84,85”
From p53: from understanding its structure to advances in therapeutic targeting (2026) · cites this paper as [85]
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Vogelstein, B., Lane, D., & Levine, A. J. (2000) · Nature · doi:10.1038/35042675 · Cited by 6,607 · cited 1×
“6 ), which functions as a transcriptional activator and exerts its biological activity by inducing expression of its target gene”
BackgroundOncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218 · cited 1×
“Recently, it was reported that activation of oncogenes such as ras trigger DNA-damage responses, inducing apoptosis or senescence through a p53-dependent pathway in normal cell”
BackgroundWhy Do Cancers Have High Aerobic Glycolysis?
Gatenby, R. A., & Gillies, R. J. (2004) · Nature reviews. Cancer · doi:10.1038/nrc1478 · Cited by 4,784
Activators and target genes of Rel/NF-κB transcription factors
Pahl, H. L. (1999) · Oncogene · doi:10.1038/sj.onc.1203239 · Cited by 3,727
p53 Regulates Mitochondrial Respiration
Matoba, S., Kang, J.-G., Patino, W. D., Wragg, A., Boehm, M., Gavrilova, O., Hurley, P. J., Bunz, F., & Hwang, P. M. (2006) · Science · doi:10.1126/science.1126863 · Cited by 1,650
Glycolytic Enzymes Can Modulate Cellular Life Span
Kondoh, H., Lleonart, M. E., Gil, J., Wang, J., Degan, P., Peters, G., Martinez, D., Carnero, A., & Beach, D. (2005) · Cancer Research · doi:10.1158/0008-5472.177.65.1 · Cited by 647
Transcriptional Cross Talk between NF-κB and p53
Webster, G. A., & Perkins, N. D. (1999) · Molecular and Cellular Biology · doi:10.1128/mcb.19.5.3485 · Cited by 598
Tanaka, N., Ishihara, M., Kitagawa, M., Harada, H., Kimura, T., Matsuyama, T., Lamphier, M. S., Aizawa, S., Mak, T. W., & Taniguchi, T. (1994) · Cell · doi:10.1016/0092-8674(94)90132-5 · Cited by 491 · cited 1×
“Primary cultured cells from p53-deficient ( p53 −/− ) mice are easily transformed by a diverse range of oncogene”
BackgroundSelf-citation
Research works printed but not linked: 22
- Warburg, O. On respiratory impairment in cancer cells. Science 124, 269–270 (1956). · DOI · Paper page
- Kim, J. W. & Dang, C. V. Cancer's molecular sweet tooth and the Warburg effect. Cancer Res. 66, 8927–8930 (2006). · DOI · Paper page
- Dang, C. V. & Semenza, G. L. Oncogenic alterations of metabolism. Trends Biochem. Sci. 24, 68–72 (1999). · DOI · Paper page
- Meller, J., Sahlmann, C. O. & Scheel, A. K. 18F-FDG PET and PET/CT in fever of unknown origin. J. Nucl. Med. 48, 35–45 (2007).
- Hamroun, D. et al. The UMD TP53 database and website: update and revisions. Hum. Mutat. 27, 14–20 (2006). · DOI · Paper page
- Lowe, S. W., Jacks, T., Housman, D. E. & Ruley, H. E. Abrogation of oncogene-associated apoptosis allows transformation of p53-deficient cells. Proc. Natl Acad. Sci. USA 91, 2026–2030 (1994). · DOI · Paper page
- Bartek, J., Lukas, J. & Bartkova, J. DNA damage response as an anti-cancer barrier: damage threshold and the concept of 'conditional haploinsufficiency'. Cell Cycle 6, 2344–2347 (2007). · DOI
- Finco, T. S. et al. Oncogenic Ha-Ras-induced signaling activates NF-κB transcriptional activity, which is required for cellular transformation. J. Biol. Chem. 272, 24113–24116 (1997). · DOI · Paper page
- Rayet, B. & Gelinas, C. Aberrant rel/nfκb genes and activity in human cancer. Oncogene 18, 6938–6947 (1999). · DOI · Paper page
- Ryan, K. M., Ernst, M. K., Rice, N. R. & Vousden, K. H. Role of NF-κB in p53-mediated programmed cell death. Nature 404, 892–897 (2000). · DOI · Paper page
- Huang, W. C., Ju, T. K., Hung, M. C. & Chen, C. C. Phosphorylation of CBP by IKKα promotes cell growth by switching the binding preference of CBP from p53 to NF-κB. Mol. Cell 26, 75–87 (2007). · DOI · Paper page
- Janssens, S. & Tschopp, J. Signals from within: the DNA-damage-induced NF-κB response. Cell Death Differ. 13, 773–784 (2006). · DOI · Paper page
- Schwartzenberg-Bar-Yoseph, F., Armoni, M. & Karnieli, E. The tumor suppressor p53 down-regulates glucose transporters GLUT1 and GLUT4 gene expression. Cancer Res. 64, 2627–2633 (2004). · DOI · Paper page
- Mayo, M. W. & Baldwin, A. S. The transcription factor NF-κB: control of oncogenesis and cancer therapy resistance. Biochim. Biophys. Acta 1470, M55–62 (2000).
- Zhong, H., Voll, R. E. & Ghosh, S. Phosphorylation of NF-κB p65 by PKA stimulates transcriptional activity by promoting a novel bivalent interaction with the co-activator CBP/p300. Mol. Cell 1, 661–671 (1998). · DOI · Paper page
- Macheda, M. L., Rogers, S. & Best, J. D. Molecular and cellular regulation of glucose transporter (GLUT) proteins in cancer. J. Cell Physiol. 202, 654–662 (2005). · DOI · Paper page
- Medina, R. A. & Owen, G. I. Glucose transporters: expression, regulation and cancer. Biol. Res. 35, 9–26 (2002). · DOI · Paper page
- Anest, V. et al. A nucleosomal function for IκB kinase-α in NF-κB-dependent gene expression. Nature 423, 659–663 (2003). · DOI · Paper page
- Yamamoto, Y., Verma, U. N., Prajapati, S., Kwak, Y. T. & Gaynor, R. B. Histone H3 phosphorylation by IKK-α is critical for cytokine-induced gene expression. Nature 423, 655–659 (2003). · DOI · Paper page
- Weisz, L. et al. Mutant p53 enhances nuclear factor κB activation by tumor necrosis factor α in cancer cells. Cancer Res. 67, 2396–2401 (2007). · DOI · Paper page
- Bensaad, K. et al. TIGAR, a p53-inducible regulator of glycolysis and apoptosis. Cell 126, 107–120 (2006). · DOI · Paper page
- Sato, M. et al. Distinct and essential roles of transcription factors IRF-3 and IRF-7 in response to viruses for IFN-α/β gene induction. Immunity 13, 539–548 (2000). · DOI · Paper page
Cited by
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
NF-κB, inflammation, immunity and cancer: coming of age
Taniguchi, K., & Karin, M. (2018) · Nature Reviews Immunology · doi:10.1038/nri.2017.142 · Cited by 2,679
Cancer cell metabolism: warburg and beyond
Hsu, P. P., & Sabatini, D. M. (2008) · Cell · doi:10.1016/j.cell.2008.08.021 · Cited by 2,452
“Other work also suggests that p53-mediated regulation of glucose metabolism may be dependent on the transcription factor NF-κB (Kawauchi et al., 2008).”
BackgroundNF-κB, an Active Player in Human Cancers
Xia, Y., Shen, S., & Verma, I. M. (2014) · Cancer Immunology Research · doi:10.1158/2326-6066.cir-14-0112 · Cited by 1,213
P53 in survival, death and metabolic health: a lifeguard with a licence to kill.
Kruiswijk, F., Labuschagne, C. F., & Vousden, K. H. (2015) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm4007 · Cited by 1,080
Metadata
- Authors
- Kawauchi, K., Araki, K., Tobiume, K., & Tanaka, N.
- Venue
- Nature Cell Biology
- Published
- 2008-04-06
- Volume
- 10
- Issue
- 5
- Pages
- 611-618
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- OpenAlex
- W2029000257
- Cited by
- 637
- References
- 8
- FWCI
- 8.49
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
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- Kawauchi, K., Araki, K., Tobiume, K., & Tanaka, N. (2008). p53 regulates glucose metabolism through an IKK-NF-κB pathway and inhibits cell transformation. Nature Cell Biology. https://doi.org/10.1038/ncb1724
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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.