Coordination and communication between the p53 and IGF-1–AKT–TOR signal transduction pathways
Open Access
- 1 February 2006
- journal article
- review article
- Published by Cold Spring Harbor Laboratory in Genes & Development
- Vol. 20 (3) , 267-275
- https://doi.org/10.1101/gad.1363206
Abstract
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.Keywords
This publication has 76 references indexed in Scilit:
- Phosphorylation and Regulation of Akt/PKB by the Rictor-mTOR ComplexScience, 2005
- Mammalian TOR complex 2 controls the actin cytoskeleton and is rapamycin insensitiveNature Cell Biology, 2004
- Post-translational modification of p53 in tumorigenesisNature Reviews Cancer, 2004
- Cancer genes and the pathways they controlNature Medicine, 2004
- Stress-Dependent Regulation of FOXO Transcription Factors by the SIRT1 DeacetylaseScience, 2004
- Rheb is a direct target of the tuberous sclerosis tumour suppressor proteinsNature Cell Biology, 2003
- mTOR Interacts with Raptor to Form a Nutrient-Sensitive Complex that Signals to the Cell Growth MachineryCell, 2002
- Cross-talk between Akt, p53 and Mdm2: possible implications for the regulation of apoptosisOncogene, 2002
- Tor, a Phosphatidylinositol Kinase Homologue, Controls Autophagy in YeastJournal of Biological Chemistry, 1998
- High-frequency developmental abnormalities in p53-deficient miceCurrent Biology, 1995