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
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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
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Mechanisms Underlying Cancer Growth and Apoptosis by DEK Overexpression in Colorectal Cancer
TL;DR: The results showed that DEK was overexpressed in human CRC tissues, and was correlated with the Ki-67 index and the apoptotic index, and could be a therapeutic target in CRC.
Journal ArticleDOI
Synergistic regulation of p53 by Mdm2 and Mdm4 is critical in cardiac endocardial cushion morphogenesis during heart development
TL;DR: Maternal exposure to low‐dose X‐rays in C57BL/6 mice mimicked the congenital heart malformations seen in the Tie2Cre;Mdm2FM/+; Mdm4+/− model, establishing a link between maternal exposures and CHD susceptibility through the p53 pathway and suggested a possible cause of CHDs due to environmental stress.
Journal ArticleDOI
Puzzling over MDM4-p53 network.
Francesca Mancini,G Di Conza,O Monti,Antonio Macchiarulo,Roberto Pellicciari,Alfredo Pontecorvi,Fabiola Moretti +6 more
TL;DR: A review summarizes the different facets ofMDM4-mediated regulation of p53 and the modifications able to modulate MDM4 localization and function.
Journal ArticleDOI
Relationship between VEGF and p53 expression and tumor cell proliferation in human gastrointestinal carcinomas
TL;DR: It is demonstrated that VEGF and p53 expression are significantly correlated as independent prognostic factors with tumor cell proliferation, and might be associated with relevant events involved in gastrointestinal tumor biology.
Journal ArticleDOI
Conserved sequences in the final intron of MDM2 are essential for the regulation of alternative splicing of MDM2 in response to stress
Ravi K. Singh,Aixa S. Tapia-Santos,Aixa S. Tapia-Santos,Thomas W. Bebee,Thomas W. Bebee,Dawn S. Chandler,Dawn S. Chandler +6 more
TL;DR: Using UV and cisplatin to model alternative splicing of the MDM2 gene, a damage-inducible in vitro splicing system is developed that shows that conserved intronic sequences in intron 11 ofMDM2 are required for normal splicing and that these intronic elements are also required for the regulated damage-induced alternativesplicing of MDM 2.
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.
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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.
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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.
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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.