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Marion M. Maetens

Researcher at University of Toronto

Publications -  6
Citations -  919

Marion M. Maetens is an academic researcher from University of Toronto. The author has contributed to research in topics: Transgene & Mdm2. The author has an hindex of 6, co-authored 6 publications receiving 868 citations. Previous affiliations of Marion M. Maetens include Flanders Institute for Biotechnology & Free University of Brussels.

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

TL;DR: 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.
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Mdm4 and Mdm2 cooperate to inhibit p53 activity in proliferating and quiescent cells in vivo

TL;DR: A p53 knock-in allele is combined, in which p53 is silenced by a transcriptional stop element flanked by loxP sites, with the mdm2- and mdm4-null alleles, which allows Cre-mediated conditional p53 expression in tissues in vivo and cells in vitro lacking Mdm2, Mdm4, or both.
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Evolutionarily Conserved Role of Nucleostemin: Controlling Proliferation of Stem/Progenitor Cells during Early Vertebrate Development

TL;DR: The results show that NS has a unique ability, derived from an ancestral function, to control the proliferation rate of stem/progenitor cells in vivo independently of p53.
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Efficient mouse transgenesis using Gateway-compatible ROSA26 locus targeting vectors and F1 hybrid ES cells

TL;DR: The ability to rapidly and efficiently generate reliable Cre/loxP conditional transgenic mice would greatly complement global high-throughput gene targeting initiatives aimed at identifying gene function in the mouse by using Gateway® cloning to build the target vectors.
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Distinct roles of Mdm2 and Mdm4 in red cell production

TL;DR: The data show that Mdm2 is required for rescuing erythroid progenitors from p53-mediated apoptosis during primitive erythropoiesis, and Mdm4 only contributes to p53 regulation at a specific phase of the differentiation program.