Zobrazeno 1 - 6
of 6
pro vyhledávání: '"Jonas C Schneider"'
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:
Bernhard N, Bohnert, Daniel, Essigke, Andrea, Janessa, Jonas C, Schneider, Matthias, Wörn, M Zaher, Kalo, Mengyun, Xiao, Lingsi, Kong, Kingsley, Omage, Jörg, Hennenlotter, Bastian, Amend, Andreas L, Birkenfeld, Ferruh, Artunc
Publikováno v:
American journal of physiology. Renal physiology. 321(4)
Proteolytic activation of the renal epithelial Na
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:
Ferruh Artunc, Lingsi Kong, Bernhard N. Bohnert, Andreas L. Birkenfeld, Matthias Wörn, Andrea Janessa, Daniel Essigke, Mengyun Xiao, Joerg Hennenlotter, Jonas C Schneider, Bastian Amend, M. Zaher Kalo, Kingsley Omage
Publikováno v:
Am. J. Physiol.-Renal Physiol. 321, F480-F493 (2021)
Proteolytic activation of the renal epithelial sodium channel ENaC involves cleavage events in its α- and γ-subunits and is thought to mediate sodium retention in nephrotic syndrome (NS). However, detection of proteolytically processed ENaC in kidn
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::11cd4867f8627bc1f2bcd602d63427bd
https://push-zb.helmholtz-muenchen.de/frontdoor.php?source_opus=62888
https://push-zb.helmholtz-muenchen.de/frontdoor.php?source_opus=62888
Autor:
Ferruh Artunc, Bernhard N. Bohnert, Jonas C. Schneider, Tobias Staudner, Florian Sure, Alexandr V. Ilyaskin, Matthias Wörn, Daniel Essigke, Andrea Janessa, Nis V. Nielsen, Andreas L. Birkenfeld, Michael Etscheid, Silke Haerteis, Christoph Korbmacher, Sandip M. Kanse
Publikováno v:
Pflügers Archiv, 2022(474):217-229
Pflugers Archiv
Pflugers Arch. 474, 217-229 (2022)
Pflugers Archiv
Pflugers Arch. 474, 217-229 (2022)
Proteolytic activation of the epithelial sodium channel (ENaC) by aberrantly filtered serine proteases is thought to contribute to renal sodium retention in nephrotic syndrome. However, the identity of the responsible proteases remains elusive. This
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f45650f55637d2b812841cb6d95a7372
https://repository.publisso.de/resource/frl:6431670
https://repository.publisso.de/resource/frl:6431670
Autor:
Ferruh Artunc, Sophie Daiminger, Tobias Staudner, Daniel Essigke, Matthias Wörn, Christoph Korbmacher, Florian Sure, Firas Batbouta, Bernhard N. Bohnert, Sandip M. Kanse, Andrea Janessa, Jonas C Schneider, Alexandr V. Ilyaskin, Silke Haerteis
Publikováno v:
Acta Physiol. 227:e13286 (2019)
Aim In nephrotic syndrome, aberrantly filtered plasminogen (plg) is converted to active plasmin by tubular urokinase-type plasminogen activator (uPA) and thought to lead to sodium retention by proteolytic activation of the epithelial sodium channel (