Zobrazeno 1 - 4
of 4
pro vyhledávání: '"Thomas Dörffel"'
Autor:
Bernhard N. Bohnert, Irene Gonzalez-Menendez, Thomas Dörffel, Jonas C. Schneider, Mengyun Xiao, Andrea Janessa, M. Zaher Kalo, Birgit Fehrenbacher, Martin Schaller, Nicolas Casadei, Kerstin Amann, Christoph Daniel, Andreas L. Birkenfeld, Florian Grahammer, Lahoucine Izem, Edward F. Plow, Leticia Quintanilla-Martinez, Ferruh Artunc
Publikováno v:
Disease Models & Mechanisms, Vol 14, Iss 9 (2021)
Susceptibility to doxorubicin-induced nephropathy (DIN), a toxic model for the induction of proteinuria in mice, is related to the single-nucleotide polymorphism (SNP) C6418T of the Prkdc gene encoding for the DNA-repair enzyme DNA-PKcs. In addition,
Externí odkaz:
https://doaj.org/article/f61afe8bfcdd4d3ca25f47e7366b3a1a
Autor:
Antje Semrau, Carsten Calaminus, Sophie Daiminger, Ferruh Artunc, Franz Iglauer, Mai J Le, Almuth Falkenau, Bernhard N. Bohnert, Sandro Aidone, Thomas Dörffel
Publikováno v:
Laboratory Animals
Doxorubicin-induced nephropathy in mice is a model for studying experimental nephrotic syndrome. It corresponds to puromycin aminonucleoside nephrosis in rats. In this model, susceptible 129 S1/SvImJ mice are administered a rapid intravenous injectio
Autor:
Bernhard N, Bohnert, Irene, Gonzalez-Menendez, Thomas, Dörffel, Jonas C, Schneider, Mengyun, Xiao, Andrea, Janessa, M Zaher, Kalo, Birgit, Fehrenbacher, Martin, Schaller, Nicolas, Casadei, Kerstin, Amann, Christoph, Daniel, Andreas L, Birkenfeld, Florian, Grahammer, Lahoucine, Izem, Edward F, Plow, Leticia, Quintanilla-Martinez, Ferruh, Artunc
Publikováno v:
Dis. Model. Mech. 14:dmm049038 (2021)
Disease Models & Mechanisms, Vol 14, Iss 9 (2021)
Disease Models & Mechanisms, Vol 14, Iss 9 (2021)
Susceptibility to doxorubicin-induced nephropathy (DIN), a toxic model for the induction of proteinuria in mice, is related to the single-nucleotide polymorphism (SNP) C6418T of the Prkdc gene encoding for the DNA-repair enzyme DNA-PKcs. In addition,
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid_dedup__::413f17e9719f112cebf89ac4e01467b4
https://push-zb.helmholtz-muenchen.de/frontdoor.php?source_opus=62887
https://push-zb.helmholtz-muenchen.de/frontdoor.php?source_opus=62887
Autor:
Alvin H. Schmaier, Daniel Essigke, Regina Nacken, Ferruh Artunc, Andrea Janessa, Anja Schork, Hans-Ulrich Häring, Marko Bertog, Edward P. Feener, Mengyun Xiao, Thomas Dörffel, Matthias Wörn, Christoph Korbmacher, Silke Haerteis, Bernhard N. Bohnert
Publikováno v:
Acta Physiol. 224:e13060 (2018)
AIM Recent work has demonstrated that activation of the epithelial sodium channel (ENaC) by aberrantly filtered serine proteases causes sodium retention in nephrotic syndrome. The aim of this study was to elucidate a potential role of plasma kallikre