H
Holger M. Reichardt
Researcher at University of Göttingen
Publications - 150
Citations - 12072
Holger M. Reichardt is an academic researcher from University of Göttingen. The author has contributed to research in topics: Glucocorticoid receptor & T cell. The author has an hindex of 53, co-authored 146 publications receiving 11024 citations. Previous affiliations of Holger M. Reichardt include German Cancer Research Center & Karlsruhe Institute of Technology.
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Journal ArticleDOI
Resetting of circadian time in peripheral tissues by glucocorticoid signaling.
Aurélio Balsalobre,Steven A. Brown,Lysiane Marcacci,François Tronche,Christoph Kellendonk,Holger M. Reichardt,Günther Schütz,Ueli Schibler +7 more
TL;DR: It is shown that the glucocorticoid hormone analog dexamethasone induces circadian gene expression in cultured rat-1 fibroblasts and transiently changes the phase of circadian gene Expression in liver, kidney, and heart, however, dexamETHasone does not affect cyclic geneexpression in neurons of the suprachiasmatic nucleus.
Journal ArticleDOI
DNA binding of the glucocorticoid receptor is not essential for survival
Holger M. Reichardt,Klaus H. Kaestner,Jan Tuckermann,Oliver Kretz,Oliver Wessely,Rudolf Bock,Peter Gass,Wolfgang Schmid,Peter Herrlich,Peter Angel,Günther Schütz +10 more
TL;DR: A point mutation A458T is introduced into the GR by gene targeting using the Cre/loxP system, impairs dimerization and therefore GRE-dependent transactivation while functions that require cross-talk with other transcription factors, such as transrepression of AP-1-driven genes, remain intact.
Journal ArticleDOI
Repression of inflammatory responses in the absence of DNA binding by the glucocorticoid receptor.
Holger M. Reichardt,Jan Tuckermann,Jan Tuckermann,Martin Göttlicher,Maja Vujic,Falk Weih,Peter Angel,Peter Herrlich,Günther Schütz +8 more
TL;DR: It is found that most actions of glucocorticoid receptor are exerted in the absence of the DNA‐binding ability of the GR: inhibition of the inflammatory response of locally irritated skin and of the systemic response to lipopolysaccharides.
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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.
Journal ArticleDOI
Glucocorticoids in T cell apoptosis and function.
TL;DR: This review summarizes the present knowledge on GC action, the mechanisms employed to induce apoptosis and the currently discussed models of how they may participate in thymocyte development.