Journal ArticleDOI
Keeping p53 in check: essential and synergistic functions of Mdm2 and Mdm4.
Jean-Christophe Marine,Sarah Francoz,Marion M. Maetens,Geoffrey M. Wahl,Franck Toledo,Franck Toledo,Guillermina Lozano +6 more
TLDR
This work presents a novel and scalable approach to gene expression engineering that allows for real-time annotation of gene expression changes in response to cancerigenicity and shows promise in finding novel and efficient treatments for cancer.Abstract:
1 Laboratory For Molecular Cancer Biology, Flanders Interuniversity Institute for Biotechnology (VIB), University of Ghent, Technologiepark, 927, Ghent B9052, Belgium 2 Salk Institute for Biological Studies, Gene Expression Laboratory, La Jolla, CA 92037, USA 3 Gene Expression and Diseases Unit, Institut Pasteur, Paris, France 4 The University of Texas Graduate School of Biomedical Sciences and department of Molecular Genetics, Section of Cancer Genetics, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA * Corresponding author: J-C Marine, Laboratory For Molecular Cancer Biology, VIB, Technologiepark, 927, Ghent B-9052, Belgium. Tel: þ 32-93-313-640; Fax: þ 32-93-313-516; E-mail: chris.marine@dmbr.ugent.beread more
Citations
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Sophoridine inhibits lung cancer cell growth and enhances cisplatin sensitivity through activation of the p53 and Hippo signaling pathways.
Lingling Zhu,Shanshan Huang,Junhe Li,Jun Chen,Yangyang Yao,Li Li,Hui Guo,Xiaojun Xiang,Jun Deng,Jianping Xiong +9 more
TL;DR: It is suggested that sophoridine can inhibit lung cancer progression and enhance the effects of the anticancer drug cisplatin against lung cancer cells.
Journal ArticleDOI
Modifications of p53 and the DNA Damage Response in Cells Expressing Mutant Form of the Protein Huntingtin
TL;DR: Data suggest a possible relationship between p53 and the slow accumulation of DNA damage resulting from the expression of mHtt, and the lack of a proper p53-mediated signaling cascade or its alteration in the presence of DNADamage may contribute to the slow progression of cellular dysfunction which is a hallmark of HD pathology.
Journal ArticleDOI
Cancer Cells Cue the p53 Response of Cancer-Associated Fibroblasts to Cisplatin
Jens O Schmid,Meng Dong,Silke Haubeiss,Godehard Friedel,Sabine Bode,Andreas Grabner,German Ott,Thomas E. Mürdter,Moshe Oren,Walter E. Aulitzky,Heiko van der Kuip +10 more
TL;DR: The findings reveal an interdependence of the p53 response in cancer cells and adjacent CAFs within tumor tissues, arguing that cancer cells control the response of their microenvironment to DNA damage.
Journal ArticleDOI
Apoptosis gene profiling reveals spatio-temporal regulated expression of the p53/Mdm2 pathway during lens development
Jenny Geatrell,Peng Mui Iryn Gan,Fiona C. Mansergh,Fiona C. Mansergh,Lilian Kisiswa,Miguel Jarrin,Miguel Jarrin,Llinos A Williams,Martin J. Evans,Michael E. Boulton,Michael E. Boulton,Michael A. Wride,Michael A. Wride +12 more
TL;DR: First spatio-temporal analysis of expression of p53 pathway molecules (p53, Mdm2 and Mdm4/X) in both developing mouse and chick lenses, suggesting a potential role for the p53/Mdm2 pathway in lens development, which merits further functional analysis.
Journal ArticleDOI
Zinc Metallochaperones as Mutant p53 Reactivators: A New Paradigm in Cancer Therapeutics
Samuel Kogan,Darren R. Carpizo +1 more
TL;DR: ZMCs reactivate mutant p53 using a novel two-part mechanism that involves restoring the wild-type structure by reestablishing zinc binding and activating p53 through post-translational modifications induced by cellular reactive oxygen species (ROS).
References
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Journal ArticleDOI
WAF1, a potential mediator of p53 tumor suppression
Wafik S. El-Deiry,Takashi Tokino,Victor E. Velculescu,Daniel B. Levy,Ramon Parsons,Jeffrey M. Trent,D Lin,W. Edward Mercer,Kenneth W. Kinzler,Bert Vogelstein +9 more
TL;DR: A gene is identified, named WAF1, whose induction was associated with wild-type but not mutant p53 gene expression in a human brain tumor cell line and that could be an important mediator of p53-dependent tumor growth suppression.
Journal ArticleDOI
In vivo activation of the p53 pathway by small-molecule antagonists of MDM2.
Lyubomir T. Vassilev,Binh Thanh Vu,Bradford Graves,Daisy Carvajal,Frank John Podlaski,Zoran Filipovic,Norman Kong,Ursula Kammlott,Christine Lukacs,Christian Klein,Nader Fotouhi,Liu Emily Aijun +11 more
TL;DR: In this article, the authors identify potent and selective small-molecule antagonists of MDM2 and confirm their mode of action through the crystal structures of complexes, leading to cell cycle arrest, apoptosis, and growth inhibition of human tumor xenografts.
Journal ArticleDOI
Mdm2 promotes the rapid degradation of p53
TL;DR: It is proposed that the Mdm2-promoted degradation of p53 provides a new mechanism to ensure effective termination of the p53 signal.
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Regulation of p53 stability by Mdm2
TL;DR: It is shown that interaction with Mdm2 can also result in a large reduction in p53 protein levels through enhanced proteasome-dependent degradation, which may contribute to the maintenance of low p53 concentrations in normal cells.
Journal ArticleDOI
Oncoprotein MDM2 is a ubiquitin ligase E3 for tumor suppressor p53
TL;DR: The data suggest that the MDM2 protein, which is induced by p53, functions as a ubiquitin ligase, E3, in human papillomavirus‐uninfected cells which do not have E6 protein.