G
G. Schulze-Tanzil
Researcher at Free University of Berlin
Publications - 19
Citations - 2111
G. Schulze-Tanzil is an academic researcher from Free University of Berlin. The author has contributed to research in topics: Chondrocyte & Extracellular matrix. The author has an hindex of 15, co-authored 19 publications receiving 1961 citations. Previous affiliations of G. Schulze-Tanzil include Franklin Institute.
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Journal ArticleDOI
Mechanisms of magnesium-stimulated adhesion of osteoblastic cells to commonly used orthopaedic implants.
Hala Zreiqat,C. R. Howlett,Andrew C.W. Zannettino,Peter J. Evans,G. Schulze-Tanzil,C. Knabe,Mehdi Shakibaei +6 more
TL;DR: It is concluded that Mg(2+) supplementation of bioceramic substrata may be a promising way to improve integration of implants in orthopaedic and dental surgery.
Journal ArticleDOI
Redifferentiation of dedifferentiated human chondrocytes in high-density cultures.
G. Schulze-Tanzil,P. de Souza,H. Villegas Castrejon,Thilo John,H. J. Merker,Annette Scheid,Mehdi Shakibaei +6 more
TL;DR: It is concluded that the growth of dedifferentiated chondrocytes in high-density culture promotes their redifferentiation and reveals their chondrogenic potential.
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Simulated microgravity alters differentiation and increases apoptosis in human follicular thyroid carcinoma cells
Daniela Grimm,Johann Bauer,Peter Kossmehl,Mehdi Shakibaei,Johann Schönberger,Holger Pickenhahn,G. Schulze-Tanzil,Roland Vetter,Christoph Eilles,Martin Paul,Augusto Cogoli +10 more
TL;DR: Clinorotation elevates intermediate filaments, cell adhesion molecules, and extracellular matrix proteins and simultaneously induces apoptosis in follicular thyroid cancer cells, which could provide a regulatory basis for the finding that astronauts show low thyroid hormone levels after space flight.
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Inhibition of mitogen-activated protein kinase kinase induces apoptosis of human chondrocytes.
Mehdi Shakibaei,G. Schulze-Tanzil,Philippe de Souza,Thilo John,Masyar Rahmanzadeh,Rahim Rahmanzadeh,H. J. Merker +6 more
TL;DR: The blocked mitogen-activated protein kinase/extracellular signal-regulated kinase (Erk) (MEK), a kinase upstream of the kinase Erk by using U0126, indicates that the MEK/Erk signal transduction pathway is involved in the maintenance of chondrocytes differentiation and survival.
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Loss of chondrogenic potential in dedifferentiated chondrocytes correlates with deficient Shc-Erk interaction and apoptosis.
TL;DR: The loss of chondrogenic potential by chondrocytes maintained in monolayer culture is associated with a decrease in the synthesis of cartilage markers and with a suppressed activation of key signaling proteins in the Ras-mitogen-activated protein kinase pathway (Shc and Erk1/2).