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Birgit Ledermann
Researcher at University of Zurich
Publications - 42
Citations - 11107
Birgit Ledermann is an academic researcher from University of Zurich. The author has contributed to research in topics: Embryonic stem cell & Stem cell. The author has an hindex of 35, co-authored 41 publications receiving 10771 citations. Previous affiliations of Birgit Ledermann include Novartis.
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Journal ArticleDOI
Cytotoxicity mediated by T cells and natural killer cells is greatly impaired in perforin-deficient mice
David Kägi,Birgit Ledermann,Kurt Bürki,Peter Seiler,Bernhard Odermatt,Kristin J. Olsen,Eckhard R. Podack,Rolf M. Zinkernagel,Hans Hengartner +8 more
TL;DR: Perforin-deficient mice have been generated by homologous recombination to determine whether the effects of CDS+ cytolytic T cells and natural killer cells are mediated by pore formation involving perform, and perforin is therefore a key effector molecule for T-cell- and natural Killer- cell-mediated cy tolysis.
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Fas and Perforin Pathways as Major Mechanisms of T Cell-Mediated Cytotoxicity
David Kägi,Françoise Vignaux,Birgit Ledermann,Kurt Bürki,Valérie Depraetere,Shigekazu Nagata,Hans Hengartner,Pierre Golstein +7 more
TL;DR: The perforin- and Fas-based mechanisms may account for all T cell-mediated cytotoxicity in short-term in vitro assays, and no third mechanism was detected.
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Two amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology
Christine Sturchler-Pierrat,Dorothee Abramowski,Mairead Duke,Karl-Heinz Wiederhold,Claudia Mistl,Sabin Rothacher,Birgit Ledermann,Kurt Bürki,Peter Frey,Paolo Paganetti,Caroline Waridel,Michael E. Calhoun,Mathias Jucker,Alphonse Probst,Matthias Staufenbiel,Bernd Sommer +15 more
TL;DR: These mice resemble major features of AD pathology and suggest a central role of A beta in the pathogenesis of the disease.
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Molecular Mechanisms of Lymphocyte-Mediated Cytotoxicity and Their Role in Immunological Protection and Pathogenesis In Vivo
TL;DR: Evidence for a role of Fas-dependent cytotoxicity as a T cell effector mechanism in vivo is lacking, and current data suggest that the main function of Fas may be in regulation of the immune response and apparently less at the level of an effector mechanisms in host defense.
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General anesthetic actions in vivo strongly attenuated by a point mutation in the GABA(A) receptor beta3 subunit.
Rachel Jurd,Margarete Arras,Sachar Lambert,Berthold Drexler,Roberta Siegwart,Florence Crestani,Michael Zaugg,Kaspar E. Vogt,Birgit Ledermann,Bernd Antkowiak,Uwe Rudolph +10 more
TL;DR: It is demonstrated that a single molecular target, and indeed a specific residue (N265) located within the GABAA receptor β3 subunit, is a major determinant of behavioral responses evoked by the intravenous anesthetics etomidate and propofol, whereas volatile anesthetic appear to act via a broader spectrum of molecular targets.