M
Marc Castellazzi
Researcher at French Institute of Health and Medical Research
Publications - 13
Citations - 1123
Marc Castellazzi is an academic researcher from French Institute of Health and Medical Research. The author has contributed to research in topics: Transcription factor & Activating transcription factor 2. The author has an hindex of 12, co-authored 13 publications receiving 1063 citations. Previous affiliations of Marc Castellazzi include École normale supérieure de Lyon.
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Journal ArticleDOI
Distinct roles of Jun : Fos and Jun : ATF dimers in oncogenesis.
Hans van Dam,Marc Castellazzi +1 more
TL;DR: Avian primary cells transformed by either Jun : Fra2 or Jun:ATF2 thus provide powerful tools for the investigation of the downstream pathways involved in oncogenesis, and further genetic studies with Jun dimerization mutants will be required to be precise and extend the specific roles of the Jun’s:”Fos and Jun”:’ATF dimers during cancer progression in avian and mammalian systems.
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HTLV-1 HBZ cooperates with JunD to enhance transcription of the human telomerase reverse transcriptase gene (hTERT)
Anne-Sophie Kuhlmann,Anne-Sophie Kuhlmann,Julien Villaudy,Julien Villaudy,Louis Gazzolo,Louis Gazzolo,Marc Castellazzi,Marc Castellazzi,Jean-Michel Mesnard,Madeleine Duc Dodon,Madeleine Duc Dodon +10 more
TL;DR: Observations establish for the first time that HBZ by intervening in the re-activation of telomerase, may contribute to the development and maintenance of the leukemic process.
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Autocrine growth and anchorage independence: two complementing Jun-controlled genetic programs of cellular transformation
Hans van Dam,Hans van Dam,Stéphanie Huguier,Klaas Kooistra,Joël Baguet,Emmanuel Vial,Alex J. van der Eb,Peter Herrlich,Peter Angel,Marc Castellazzi +9 more
TL;DR: Data show that Jun-dependent cell transformation can be resolved into at least two distinct and independent processes, anchorage and growth factor independence, obviously triggered by two classes of Jun heterodimers likely regulating different sets of target genes.
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Overexpression of Transcription Factor Sp1 Leads to Gene Expression Perturbations and Cell Cycle Inhibition
Emmanuelle Deniaud,Joël Baguet,Roxane Chalard,Roxane Chalard,Bariza Blanquier,Lilia Brinza,Julien Meunier,Julien Meunier,Marie-Cécile Michallet,Aurélie Laugraud,Claudette Ah-Soon,Anne Wierinckx,Marc Castellazzi,Joël Lachuer,Christian Gautier,Jacqueline Marvel,Yann Leverrier +16 more
TL;DR: It is shown that the binding to DNA of overexpressed Sp1 induces an inhibition of cell cycle progression that precedes apoptosis and a transcriptional response targeting genes containing Sp1 binding sites in their promoter or not suggesting both direct Sp1-driven transcription and indirect mechanisms.
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Transcription factor ATF3 partially transforms chick embryo fibroblasts by promoting growth factor-independent proliferation.
TL;DR: The results suggest that ATF3 might induce growth factor independence by down-regulating a subset of the genes repressed by v-Jun, including those coding for the extracellular components fibronectin, decorin, thrombospondin 2, and the pro-apoptotic protein Par-4.