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Journal ArticleDOI

Keeping p53 in check: essential and synergistic functions of Mdm2 and Mdm4.

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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.be

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Journal ArticleDOI

MDMX Regulates Transcriptional Activity of p53 and FOXO Proteins to Stimulate Proliferation of Melanoma Cells

TL;DR: The p53-independent oncogenic functions of MDMX could be partially explained by its regulation of FOXO activity, and a role for Forkhead box (FOX) transcription factors is indicated.
Journal ArticleDOI

MDM2- an indispensable player in tumorigenesis.

TL;DR: In this paper , the precise role of deregulated Murine double minute 2 (MDM2) levels in modulating cellular functions to promote cancer growth is discussed, and the role of MDM2 in inducing resistance against anti-cancerous therapies thus limiting the benefits of cancerous treatment.
Dissertation

Improving Stability of Tumor Suppressor Protein, p53

TL;DR: This study intends to test two p53 mutants for relative stability based on prior computational predictions that involved a previously engineered ‘super-stable’ mutant and a simulated loop deletion mutant, which is predicted to be more stable.
Journal ArticleDOI

ATM induces radioresistance of non-small cell lung cancer A549 cells by downregulation of MDMX

TL;DR: This study indicated that ATM induced radioresistance through downregulating the expression of MDMX, which was at least partly associated with the activation of autophagy and the decrease of DNA damage in A549 cells.
References
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Journal ArticleDOI

WAF1, a potential mediator of p53 tumor suppression

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.

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.
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