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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Journal ArticleDOI
Guilty as CHARGED: p53's expanding role in disease.
TL;DR: Molecular analyses revealed that wild-type p53 is inappropriately activated in p535,26,53,54/+ embryos, triggering cell-cycle arrest or apoptosis during development to cause CHARGE phenotypes, and it is shown that activated p53 contributes to phenotypes caused by CHD7-deficiency.
Book ChapterDOI
Notch and the p53 Clan of Transcription Factors
TL;DR: It seems that Notch acts as a tumour suppressor in cellular contexts where Notch signalling supports p53 activation and both together can bring on its way an anti-proliferative programme of differentiation, senescence or apoptosis.
Journal ArticleDOI
Screening of Pleural Mesotheliomas for DNA-damage Repair Players by Digital Gene Expression Analysis Can Enhance Clinical Management of Patients Receiving Platin-Based Chemotherapy
Robert Fred Henry Walter,Claudia Vollbrecht,Robert Werner,Thomas Mairinger,Jan Schmeller,Elena Flom,Jeremias Wohlschlaeger,Nikolaos Barbetakis,Dimitrios Paliouras,Fotios Chatzinikolaou,Vasilis Adamidis,Kosmas Tsakiridis,Paul Zarogoulidis,Georgia Trakada,Daniel C. Christoph,Kurt Werner Schmid,Fabian Dominik Mairinger +16 more
TL;DR: DNA-damage response plays a crucial role in response to platin-based chemotherapeutic regimes, in particular, CHEK1, XRCC2 and TP73 are strongly associated with tumour progression.
Journal ArticleDOI
miRNA regulation is important for DNA damage repair and recognition in malignant pleural mesothelioma
Fabian Dominik Mairinger,Robert Werner,Elena Flom,Jan Schmeller,Sabrina Borchert,Michael Wessolly,Jeremias Wohlschlaeger,Thomas Hager,Thomas Mairinger,Jens Kollmeier,Daniel C. Christoph,Kurt Werner Schmid,Robert Fred Henry Walter +12 more
TL;DR: Taking the specific molecular profile of the tumour into account can help to enhance the clinical management prospectively and to smooth the way to better response prediction, which would be a long-needed improvement for MPM patients.
Journal ArticleDOI
Polymorphisms of MDM4 and risk of squamous cell carcinoma of the head and neck.
TL;DR: It is suggested that the joint effect of MDM4 variants may contribute to the risk of oropharyngeal cancer in non-Hispanic whites.
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.
Journal ArticleDOI
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.