Surfing the p53 network

By Bert Vogelstein, David P. Lane, Arnold J. Levine. Nature, 2000

6,700 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/c6de495db611cd13abe12b41faf70e49e7bf1d95

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Citations in the corpus

Prediction of Protein Binding Regions in Disordered Proteins (2009, unknown): “. For example, the primary importance of p53 originates from its involvement of 50% of cancers”
Impact of mutant p53 functional properties on TP53 mutation patterns and tumor phenotype: lessons from recent developments in the IARC TP53 database (2007, background): “The tumor suppressor gene TP53 (OMIM ]191117) encodes a transcription factor that responds to several forms of cellular stress and exerts multiple, antiproliferative functions [Vogelstein et al., 2000].”
Tumor suppressors and cell metabolism: a recipe for cancer growth. (2009, background): “In response to diverse cellular insults including DNA damage, hypoxia, and oxidative stress, p53 becomes post-translationally modified, which promotes both its stabilization and activation, and activates the expression of genes that induce cell cycle arrest, senescence, and apoptosis (Vogelstein et ”
The Tumor Suppressor p53 Down-Regulates Glucose Transporters GLUT1 and GLUT4 Gene Expression (2004, background): “Over the past several years, the p53 tumor suppressor protein has emerged as one of the most important cellular factors for preserving the integrity of the genome (4, 5 ). The p53 protein is a tetrameric phosphoprotein that mediates signal transduction from damaged DNA to genes involved in regulati”
Selection, Tinkering, and Emergence in Complex Networks - Crossing the Land of Tinkering (2002, background): “This is the case, in particular, of the p53 tumor suppressor gene (Figure 3; redrawn from [47]) which is known to play a critical role in genome stability and integrates many different signals related to cell-cycle or apoptosis (programmed cell death) [ 48 ].”
Apoptosis - the p53 network (2003, background): “Indeed, approximately 50% of human cancers bear p53 gene mutations; in the majority of the remaining cancer cases, p53 activity is compromised by alternative mechanisms (Vogelstein et al., 2000).”
p53 regulates biosynthesis through direct inactivation of glucose-6-phosphate dehydrogenase (2011, background): “The tumour suppressor p53 invokes anti-proliferative processes, of which the best understood include cell cycle arrest, DNA repair and apoptosi”
Zinc and human health: an update (2011, unknown): “Hdm2 is a direct downstream target of p53, a classic tumor suppressor that is mutated in more than 50% human cancers and that induces growth arrest and apoptosis upon activation by various stimuli, particularly DNA damage (Giaccia and Kastan 1998; Vogelstein et al. 2000).”
TP53 mutations in human cancers: functional selection and impact on cancer prognosis and outcomes (2007, background): “191117) encodes a transcription factor which is activated in response to several forms of cellular stress and exerts multiple, antiproliferative functions (Vogelstein et al., 2000).”
DNA methylation, methyltransferases, and cancer (2001, background): “Loss of p21, either by mutation of the p21 gene itself or loss of p53, which activates p21 expression in response to DNA damage, is a common event in cancer (Vogelstein et al., 2000).”
Apoptosis and Molecular Targeting Therapy in Cancer (2014, background): “An important cell cycle regulator plays a central role in the regulation of cell cycle arrest and cell death is the tumor suppressor, p53 [116].”
Organelle-specific initiation of cell death pathways (2001, background): “DNA-PK, ATM and ATR, as well as the downstream DNA-damage-induced kinases Chk1 (activated by ultraviolet) and Chk2 (activated by ionizing radiation), phosphorylate serine residues within the amino terminus of p53, a modification that by itself might increase its transactivating function and/or inhib”
Phosphorylation by aurora kinase A induces Mdm2-mediated destabilization and inhibition of p53 (2004, background): “Because p53-mediated regulation of checkpoint response is activated when p53 is stabilized at both G1-S and G2-M transitions of the cell cycl”
Deubiquitination of p53 by HAUSP is an important pathway for p53 stabilization (2002, background): “Stabilization of p53 is crucial for its tumour suppressor functio”
Acetylation of the p53 DNA-binding domain regulates apoptosis induction. (2006, background): “Alternatively, genes encoding other components of the p53 pathway can exhibit mutations (Vogelstein et al., 2000; Vousden and Lu, 2002).”
Intrinsic tumour suppression (2004, background): “p53 is a master regulator p53 is a transcription factor that establishes programmes for apoptosis, senescence, and repair in response to a variety of cellular stresses, including DNA damage, hypoxia, and nutrient deprivatio”