Zobrazeno 1 - 8 of 8 pro vyhledávání: '"Daniel, Essigke"'
1
Sodium retention in nephrotic syndrome is independent of the activation of the membrane-anchored serine protease prostasin (CAP1/PRSS8) and its enzymatic activity
Autor: Daniel Essigke, Bernhard N. Bohnert, Andrea Janessa, Matthias Wörn, Kingsley Omage, Hubert Kalbacher, Andreas L. Birkenfeld, Thomas H. Bugge, Roman Szabo, Ferruh Artunc
Publikováno v: Pflugers Arch. 474, 613-624 (2022)
Experimental nephrotic syndrome leads to activation of the epithelial sodium channel (ENaC) by proteolysis and promotes renal sodium retention. The membrane-anchored serine protease prostasin (CAP1/PRSS8) is expressed in the distal nephron and partic
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::01d8d5d02e57401897245ad5c43daed6
https://doi.org/10.1007/s00424-022-02682-y
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4
Zymogen-locked mutant prostasin (Prss8) leads to incomplete proteolytic activation of the epithelial sodium channel (ENaC) and severely compromises triamterene tolerance in mice
Autor: Daniel Essigke, Kerstin Amann, Thomas H. Bugge, Ferruh Artunc, Roman Szabo, Matthias Wörn, Andreas L. Birkenfeld, Bernhard N. Bohnert, Mengyun Xiao, Christoph Korbmacher, Christoph Daniel, Alexandr V. Ilyaskin
Publikováno v: Acta Physiol. 232:e13640 (2021)
Acta Physiol (Oxf)
Aim The serine protease prostasin (Prss8) is expressed in the distal tubule and stimulates proteolytic activation of the epithelial sodium channel (ENaC) in co-expression experiments in vitro. The aim of this study was to explore the role of prostasi
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::39dc782ab0453a3ed5733647de3f1fed
https://pubmed.ncbi.nlm.nih.gov/33721422
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5
Experimental nephrotic syndrome leads to proteolytic activation of the epithelial sodium channel (ENaC) in the mouse kidney
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
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6
Proteolytic activation of the epithelial sodium channel (ENaC) by factor VII activating protease (FSAP) and its relevance for sodium retention in nephrotic mice
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)
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
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7
Plasminogen deficiency does not prevent sodium retention in a genetic mouse model of experimental nephrotic syndrome
Autor: Christoph Daniel, Ferruh Artunc, Mengyun Xiao, Daniel Essigke, Bernhard N. Bohnert, Matthias Wörn, Kerstin Amann, Oliver Kretz, Andrea Janessa, Andreas L. Birkenfeld, Hande Aypek, Edward F. Plow, Ute Aukschun, Tobias B. Huber, Florian Grahammer
Publikováno v: Acta Physiol (Oxf)
Acta Physiol. 231:e13512 (2020)
AIM: Sodium retention is the hallmark of nephrotic syndrome (NS) and mediated by the proteolytic activation of the epithelial sodium channel (ENaC) by aberrantly filtered serine proteases. Plasmin is highly abundant in nephrotic urine and has been pr
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6c1cd5e0927ebafc8f2f548beb69f8f0
https://pubmed.ncbi.nlm.nih.gov/32455507
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8
Plasma kallikrein activates the epithelial sodium channel in vitro but is not essential for volume retention in nephrotic mice
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
Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f0152dc92a1c9df5658ef7aae1c13ba3
https://pubmed.ncbi.nlm.nih.gov/29489063
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