Vice Mandic
University of Erlangen-Nuremberg
4 Papers
Vice Mandic is an academic researcher from University of Erlangen-Nuremberg. The author has contributed to research in topics: Osteoblast & Cellular differentiation. The author has an hindex of 4, co-authored 4 publications.
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Papers
Glucocorticoids Suppress Bone Formation by Attenuating Osteoblast Differentiation via the Monomeric Glucocorticoid Receptor
Alexander Rauch,Sebastian Seitz,Ulrike Baschant,Arndt F. Schilling,Anett Illing,Brenda D. Stride,Milen Kirilov,Vice Mandic,Andrea Takacz,Ruth Schmidt-Ullrich,Susanne Ostermay,Thorsten Schinke,Rainer Spanbroek,Mario M. Zaiss,Peter Angel,Ulf H. Lerner,Ulf H. Lerner,Jean-Pierre David,Holger M. Reichardt,Michael Amling,Günther Schütz,Jan Tuckermann +21 more
TL;DR: It is demonstrated that GCs are unable to repress bone formation in the absence of glucocorticoid receptor (GR) expression in osteoblasts as they become refractory to hormone-induced apoptosis, inhibition of proliferation, and differentiation.
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Increased skeletal VEGF enhances β‐catenin activity and results in excessively ossified bones
Christa Maes,Steven Goossens,Sonia Bartunkova,Benjamin Drogat,Lieve Coenegrachts,Ingrid Stockmans,Karen Moermans,Omar Nyabi,Katharina Haigh,Michael Naessens,Lieven Haenebalcke,Jan Tuckermann,Marc Tjwa,Peter Carmeliet,Vice Mandic,Jean-Pierre David,Axel Behrens,Andras Nagy,Andras Nagy,Geert Carmeliet,Jody J. Haigh +20 more
TL;DR: New insights into the actions of VEGF in the bone and marrow environment underscore its power as pleiotropic bone anabolic agent but also warn for caution in its therapeutic use.
Essential role of RSK2 in c-Fos-dependent osteosarcoma development
Jean-Pierre David,Denis Mehic,Latifa Bakiri,Arndt F. Schilling,Vice Mandic,Matthias Priemel,Maria Helena Idarraga,Markus Reschke,Oskar Hoffmann,Michael Amling,Erwin F. Wagner +10 more
TL;DR: It is shown that mice lacking RSK2 develop a progressive skeletal disease, osteopenia due to impaired osteoblast function and normal osteoclast differentiation, and c-Fos protein levels are reduced, which are thought to be responsible for decreased proliferation and increased apoptosis of transformed osteoblasts.
Elevated Fra-1 expression causes severe lipodystrophy.
Julia Luther,Frank Driessler,Matthias Megges,Andreas Hess,Bettina Herbort,Vice Mandic,Mario M. Zaiss,Anne Reichardt,Christine Zech,Jan Tuckermann,Cornelis F. Calkhoven,Erwin F. Wagner,Georg Schett,Jean-Pierre David +13 more
TL;DR: To the known common systemic control of fat and bone mass, a new cell-autonomous level of control of cell fate decision by which the osteogenic transcription factor Fra-1 opposes adipocyte differentiation by inhibiting C/EBPα is added.