The DOI matches its Crossref record; 78 of the 79 references it cites were found in a registry or an index.
Coordination and communication between the p53 and IGF-1–AKT–TOR signal transduction pathways
Open accessAbstract
Over the past 10 years the signal transduction networks for p53, IGF-1-AKT, and TOR pathways have been assembled in worms, flies, and mammals, and their functions elucidated. In the past 1-2 years a number of genes and their proteins have been identified that permit extensive communication and coordination between these pathways. These three pathways are involved in sensing and integrating signals arising from nutrient and growth factor availability, signals from sensory and sexual organs, and intrinsic and extrinsic stress signals. In turn these pathways regulate cell growth, proliferation, and death. These networks are central to our understanding of a variety of physiological and pathological conditions, including cancer, diabetes, and longevity.
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“Furthermore, reports showed that p53 activation is able to inhibit the activity of mTOR through a pathway involving the subsequent activation of TSC gene products TSC1 and TSC2, which are tumour suppressors and negative regulators of mTOR [78, 103–105].”
From PKR, the double stranded RNA‐dependent protein kinase as a critical target in Alzheimer's disease (2009) · cites this paper as [104]
In the citing paper
“There is a growing awareness that, as far as the cell is concerned, sensing nutrient availability and energetic status is an integrated and 'system biology' endeavour 101 .”
From The common biology of cancer and ageing (2007) · cites this paper as [101]
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“Overall lifespan seems to be influenced by many of these sensors and effectors, indicating that there is an intimate connection between energy sensing and longevity 101 .”
From The common biology of cancer and ageing (2007) · cites this paper as [101]
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Cites
p53, the cellular gatekeeper for growth and division
Levine, A. J. (1997) · Cell · doi:10.1016/s0092-8674(00)81871-1 · Cited by 7,693
Self-citationVogelstein, B., Lane, D., & Levine, A. J. (2000) · Nature · doi:10.1038/35042675 · Cited by 6,607 · cited 2×
“These include DNA damage and telomere shortening, hypoxia, low nucleoside triphosphate pool sizes, spindle damage, heat and cold shock, inflammation and nitric oxide production, as well as oncogene activation by mutations (Levine 1997; Vogelstein et al. 2000; Jin and Levine 2001).”
BackgroundSelf-citationPhosphorylation and regulation of Akt/PKB by the rictor-mTOR complex
Sarbassov, D. D., Guertin, D. A., Ali, S. M., & Sabatini, D. M. (2005) · Science · doi:10.1126/science.1106148 · Cited by 6,216
Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery
Datta, S. R., Dudek, H., Tao, X., Masters, S., Fu, H., Gotoh, Y., & Greenberg, M. E. (1997) · Cell · doi:10.1016/s0092-8674(00)80405-5 · Cited by 5,689
Akt Promotes Cell Survival by Phosphorylating and Inhibiting a Forkhead Transcription Factor
Brunet, A., Bonni, A., Zigmond, M. J., Lin, M. Z., Juo, P., Hu, L. S., Anderson, M. J., Arden, K. C., Blenis, J., & Greenberg, M. E. (1999) · Cell · doi:10.1016/s0092-8674(00)80595-4 · Cited by 5,594
In Vivo Activation of the p53 Pathway by Small-Molecule Antagonists of MDM2
Vassilev, L. T., Vu, B. T., Graves, B., Carvajal, D., Podlaski, F., Filipovic, Z., Kong, N., Kammlott, U., Lukacs, C., Klein, C., et al. (2004) · Science · doi:10.1126/science.1092472 · Cited by 4,661
Cancer genes and the pathways they control
Vogelstein, B., & Kinzler, K. W. (2004) · Nature Medicine · doi:10.1038/nm1087 · Cited by 4,346
Upstream and downstream of mTOR
Hay, N., & Sonenberg, N. (2004) · Genes & Development · doi:10.1101/gad.1212704 · Cited by 4,181
TSC2 Mediates Cellular Energy Response to Control Cell Growth and Survival
Inoki, K., Zhu, T., & Guan, K.-L. (2003) · Cell · doi:10.1016/s0092-8674(03)00929-2 · Cited by 3,914
Blume-Jensen, P., & Hunter, T. (2001) · Nature · doi:10.1038/35077225 · Cited by 3,738
Research works printed but not linked: 1
- 10.1172/JCI200320039 · DOI · Paper page
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The LKB1-AMPK pathway: metabolism and growth control in tumour suppression
Shackelford, D. B., & Shaw, R. J. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2676 · Cited by 1,943
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
p53 Target Genes Sestrin1 and Sestrin2 Connect Genotoxic Stress and mTOR Signaling
Budanov, A. V., & Karin, M. (2008) · Cell · doi:10.1016/j.cell.2008.06.028 · Cited by 1,326
Frankel, L. B., Christoffersen, N. R., Jacobsen, A., Lindow, M., Krogh, A., & Lund, A. H. (2008) · Journal of Biological Chemistry · doi:10.1074/jbc.m707224200 · Cited by 1,141
Belfiore, A., Frasca, F., Pandini, G., Sciacca, L., & Vigneri, R. (2009) · Endocrine Reviews · doi:10.1210/er.2008-0047 · Cited by 1,058
Metadata
- Authors
- Levine, A. J., Feng, Z., Mak, T. W., You, H., & Jin, S.
- Affiliations
- University of Toronto (CA)
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2006-02-01
- Volume
- 20
- Issue
- 3
- Pages
- 267-275
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2136212424
- Cited by
- 321
- References
- 79
- Citations by year
- 2025: 3 · 2024: 5 · 2023: 2 · 2022: 9 · 2021: 6 · 2020: 9 · 2019: 14 · 2018: 6 · 2017: 14 · 2016: 11 · 2015: 13 · 2014: 23 · 2013: 18 · 2012: 33
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- p53 pathway, TOR signaling, signaling pathways, pathway integration, nutrient sensing, growth factor signaling, stress signaling, cell growth and proliferation, apoptosis, cancer, diabetes mellitus, longevity
- MeSH terms
- Animals, Enzyme Activation, Humans, Insulin-Like Growth Factor I, Models, Biological, Multienzyme Complexes, Protein Kinases, Signal Transduction, Tumor Suppressor Protein p53, Oncogene Protein v-akt, Forkhead Transcription Factors, TOR Serine-Threonine Kinases
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