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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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Porphobilinogen deaminase deficiency in mice causes a neuropathy resembling that of human hepatic porphyria

TL;DR: To study the pathogenesis of the neurologic symptoms of AIP, Pbgd-deficient mice are generated by gene targeting and reveal decreased motor function and-histo-pathological findings include axonal neuropathy and neurologic muscle atrophy.
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IgD can largely substitute for loss of IgM function in B cells

TL;DR: It is concluded that IgD is largely able to substitute for IgM functions in mice deficient in B cells, and survived infection with vesicular stomatitis virus by developing neutralizing immunoglobulins, but they were more susceptible than wild-type controls with delayed specific Immunoglobulin responses.
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Efficient targeting of the IL-4 gene in a BALB/c embryonic stem cell line

TL;DR: This newly-characterized BALB/c-ES cell line thus provides an alternative to the traditional 129-derived and the recently described C57BL/6 embryonic stem cell lines, and will be useful in disrupting genes involved in the immune system.
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Wnt signalling inhibits neural differentiation of embryonic stem cells by controlling bone morphogenetic protein expression.

TL;DR: This work studied the effect of wnt signalling in embryonic stem cells by either inactivating APC or by introducing a dominant active form of beta-catenin, finding that neural differentiation could be partially restored by the addition of the BMP antagonist noggin.
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Acute rejection of vascular heart allografts by perforin‐deficient mice

TL;DR: Data indicate that perforin is not essential in the cell‐mediated acute rejection of a fully mismatched heart allograft, and Perforin‐dependent effector mechanisms appeared to be limiting in the T cellmediated rejection of heart allogsrafts differing only at a single major histocompatibility complex class I antigen.