Mutant p53: one name, many proteins

Freed-Pastor, William A.; Prives, Carol

doi:10.1101/gad.190678.112

Cited by 1,057 publications

(1,267 citation statements)

References 195 publications

(222 reference statements)

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“…In contrast, elevated doses caused abortive mitosis leading to mitotic catastrophy and apoptosis in p53-deficient cells. 49 In addition, some mutants reveal gain-of-function 50 and some mutants, such as codon 175 mutations, are involved in DNA binding, but induces conformational changes as well. 51 Finally, p53 may induce apoptosis in a non-transcriptional way through direct binding to components of the bcl-2 system, such as bax.…”

Section: Tp53mentioning

confidence: 99%

Mapping genetic alterations causing chemoresistance in cancer: identifying the roads by tracking the drivers

Lønning

Knappskog

2013

Oncogene

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Although new agents are implemented to cancer therapy, we lack fundamental understandings of the mechanisms of chemoresistance, the main obstacle to cure in cancer. Here we review clinical evidence linking molecular defects to drug resistance across different tumour forms and discuss contemporary experimental evidence exploring these mechanisms. Although evidence, in general, is sparse and fragmentary, merging knowledge links drug resistance, and also sensitivity, to defects in functional pathways having a key role in cell growth arrest or death and DNA repair. As these pathways may act in concert, there is a need to explore multiple mechanisms in parallel. Taking advantage of massive parallel sequencing and other novel high-throughput technologies and base research on biological hypotheses, we now have the possibility to characterize functional defects related to these key pathways and to design a new generation of studies identifying the mechanisms controlling resistance to different treatment regimens in different tumour forms.

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Section: Tp53mentioning

confidence: 99%

Mapping genetic alterations causing chemoresistance in cancer: identifying the roads by tracking the drivers

Lønning

Knappskog

2013

Oncogene

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“…olivier.albagli-curiel@inserm.fr D'innombrables données démontrent le rôle du gène p53 1 dans la suppression tumorale. Plusieurs oncoprotéines virales neutralisent p53 [1,2]. In vitro, l'inactivation de p53 promeut l'immortalisation cellulaire rales.…”

Section: Le Triumviratunclassified

“…Un point mal élucidé reste comment p53 « choisit » parmi ces trois programmes. p53 apparaît principalement comme un facteur de transcription régulant, positivement ou négativement, l'expression de nombreux ARN codants ou non codants (Figures 1 et 2) [1,2,4,7]. Les cofacteurs de p53, ses modifications post-traductionnelles et sa quantité, contribuent à déterminer ses gènes cibles et l'intensité de leur modulation, sélec-tionnant ainsi l'un des trois programmes du triumvirat [8].…”

Section: Le Triumviratunclassified

“…Dans les tumeurs des patients ayant hérité d'un allèle nul de p53, l'autre allèle (normal) est invariablement perdu [5]. Chez la souris, l'invalidation homozygote ou même (dans une moindre mesure) hétérozygote de p53 conduit à une impressionnante accélération de la survenue des tumeurs [1,2]. Le développement de ces souris n'est cependant que faiblement affecté, même si la fertilité des femelles est diminuée [2].…”

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Protéger et sévir : p53, métabolisme et suppression tumorale

Albagli

2015

Med Sci (Paris)

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“…Most of these students enroll concurrently in an introductory biology lecture‐based course. The course combines a question of significant biomedical relevance that piques student interest, analysis of mutations in the tumor suppressor gene p53, which is mutated in ∼50% of cancerous tumors 14, with a tractable experimental system, the yeast Saccharomyces cerevisiae . Here we present a detailed curriculum with experimental methods and protocols together with sample student results and analyses.…”

Section: Introductionmentioning

confidence: 99%

Using yeast to determine the functional consequences of mutations in the human p53 tumor suppressor gene: An introductory course‐based undergraduate research experience in molecular and cell biology

Hekmat-Scafe¹,

Brownell²,

Seawell³

et al. 2016

Biochem Molecular Bio Educ

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The opportunity to engage in scientific research is an important, but often neglected, component of undergraduate training in biology. We describe the curriculum for an innovative, course‐based undergraduate research experience (CURE) appropriate for a large, introductory cell and molecular biology laboratory class that leverages students′ high level of interest in cancer. The course is highly collaborative and emphasizes the analysis and interpretation of original scientific data. During the course, students work in teams to characterize a collection of mutations in the human p53 tumor suppressor gene via expression and analysis in yeast. Initially, student pairs use both qualitative and quantitative assays to assess the ability of their p53 mutant to activate expression of reporter genes, and they localize their mutation within the p53 structure. Through facilitated discussion, students suggest possible molecular explanations for the transactivation defects displayed by their p53 mutants and propose experiments to test these hypotheses that they execute during the second part of the course. They use a western blot to determine whether mutant p53 levels are reduced, a DNA‐binding assay to test whether recognition of any of three p53 target sequences is compromised, and fluorescence microscopy to assay nuclear localization. Students studying the same p53 mutant periodically convene to discuss and interpret their combined data. The course culminates in a poster session during which students present their findings to peers, instructors, and the greater biosciences community. Based on our experience, we provide recommendations for the development of similar large introductory lab courses. © 2016 by The International Union of Biochemistry and Molecular Biology, 45(2):161–178, 2017.

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Mutant p53: one name, many proteins

Cited by 1,057 publications

References 195 publications

Mapping genetic alterations causing chemoresistance in cancer: identifying the roads by tracking the drivers

Mapping genetic alterations causing chemoresistance in cancer: identifying the roads by tracking the drivers

Protéger et sévir : p53, métabolisme et suppression tumorale

Using yeast to determine the functional consequences of mutations in the human p53 tumor suppressor gene: An introductory course‐based undergraduate research experience in molecular and cell biology

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