Understanding the function–structure and function–mutation relationships of p53 tumor suppressor protein by high-resolution missense mutation analysis

By S. Kato, Shuang-yin Han, Wen Liu, Kazunori Otsuka, H. Shibata, R. Kanamaru, Chikashi Ishioka. 2003

870 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

In Oncology

Citations in the corpus

Quantitative missense variant effect prediction using large-scale mutagenesis data (2017, positive): “To ensure that Envision was not overfitted to deep mutational scanning data, we obtained a TP53 tumor suppressor mutagenesis dataset whereby the effects of 2,312 variants on TP53 transactivation were measured individually using a fluorescent reporter (Kato et al., 2003).”
Computational approaches for predicting the biological effect of p53 missense mutations: a comparison of three sequence analysis based methods (2006, methodology): “(20) measured the transactivation activity of all possible missense mutations (2314) in p53 (codons 2 to 393), resulting from a single nucleotide substitution, on eight different p53-RE derived from the following p53 target-genes BAX , CDKN1 , GADD45A , MDM2 , P53AIP1 , PMAIP1 , RRM2B and SFN .”
Cancer Genome Interpreter annotates the biological and clinical relevance of tumor alterations (2017, result): “…for oncogenic mutations (e.g., they exhibited larger clonal fractions among all mutations in cancer genes), and OncodriveMUT ’ s predictions on a set of recently probed uncommon cancer mutations exhibited a high concordance with experimental evidence [18 – 21] (Additional file 2: Note IVb).”
TP53 mutations in human cancers: functional selection and impact on cancer prognosis and outcomes (2007, methodology): “…(based on intrinsic nucleotide substitution rates calculated by Lunter and Hein, 2004) and functional impact (based on TA assessed in yeast assays on eight different p53-RE by Kato et al., 2003), with new scatter plot graphs that have been implemented in the IARC TP53 database (Figure 1).”
p53 Proteoforms and Intrinsic Disorder: An Illustration of the Protein Structure–Function Continuum Concept (2016, background): “This conclusion is supported by the finding that most mutations affecting PTM-bearing residues only partially compromise p53 transactivation [216], and by the results of the in vitro mutagenesis of each of the p53 residues that can be subjected to PTMs, where no significant reduction of p53 transact”
Systematic exploration of ubiquitin sequence, E1 activation efficiency, and experimental fitness in yeast (2014, background): “While a wealth of studies demonstrate that the fitness effects of mutations are mediated by biochemical changes 19; 20; 21; 22; 23; 24; 25 , most systematic studies of mutants have focused predominantly on either growth effects 14; 26; 27 or biochemical effects 11; 28; 29; 30 .”
TP53 mutations in human cancers: origins, consequences, and clinical use. (2010, methodology): “Kato et al. (2003) have used a yeast-based functional assay to analyze the transactivation of 2314 different missense mutants on eight p53REs.”
Predicting the Functional Effect of Amino Acid Substitutions and Indels (2012, methodology): “Cholesterol efflux was measured in all mutants and wild-type to assess ABCA1 function (Table S2).”
Impact of mutant p53 functional properties on TP53 mutation patterns and tumor phenotype: lessons from recent developments in the IARC TP53 database (2007, background): “…2007 WILEY-LISS, INC. and a single study has performed a systematic analysis of the activity of all possible missense mutations produced by singlenucleotide substitution in the entire sequence of TP53 (2,314 mutations) on eight different p53-RE in yeast cells [Kato et al., 2003].”
Enrich: software for analysis of protein function by enrichment and depletion of variants (2011, background): “These measurements are essential in such applications as protein engineering, drug development, protein design and genome sequence analysis.”
A formal perturbation equation between genotype and phenotype determines the Evolutionary Action of protein-coding variations on fitness (2014, methodology): “…in bacteriophage T4 assayed for plaque formationdue to degradation of the host cell walls by lysozyme (Rennell et al. 1991); 336 HIV-1 protease mutations assayed by the cleavage products (Loeb et al. 1989); and 2314 TP53 mutants assayed for trans- activation (see Methods) (Kato et al. 2003).”
When mutants gain new powers: news from the mutant p53 field (2009, background): “The majority of TP53 mutations observed in human cancers abrogate the sequence-specific DNA-binding activity towards the wild-type p53 responsive elemen”
Integrated Analysis of TP53 Gene and Pathway Alterations in The Cancer Genome Atlas (2019, methodology): “In one study Kato et al. measured the transcriptional activity of TP53 variants in yeast assays using 8 different TP53 response elements (Kato et al., 2003).”
Mutant p53: one name, many proteins. (2012, background): “Indeed, yeast and mammalian cell-based assays have revealed a remarkable complexity in the ability of tumor-derived mutant forms of p53 to activate transcription from known wild-type p53 response elements (Di Como and Prives 1998; Kato et al. 2003; Resnick and Inga 2003; Jordan et al. 2008).”
Variable population prevalence estimates of germline TP53 variants: a gnomAD-based analysis (2018, methodology): “, 2008), its “supertrans” classification in yeast functional assays (Kato et al., 2003), in vitro studies showing apparently normal functional activity (Wang, Niu, Lam, Xiao, & Ren, 2014; Zerdoumi et al.”