Zobrazeno 1 - 10
of 160
pro vyhledávání: '"Emile, de Heer"'
Autor:
Angela Schulz, Nicola Victoria Müller, Nina Anne van de Lest, Andreas Eisenreich, Martina Schmidbauer, Andrei Barysenka, Bettina Purfürst, Anje Sporbert, Theodor Lorenzen, Alexander M Meyer, Laura Herlan, Anika Witten, Frank Rühle, Weibin Zhou, Emile de Heer, Marion Scharpfenecker, Daniela Panáková, Monika Stoll, Reinhold Kreutz
Publikováno v:
eLife, Vol 8 (2019)
Unraveling the genetic susceptibility of complex diseases such as chronic kidney disease remains challenging. Here, we used inbred rat models of kidney damage associated with elevated blood pressure for the comprehensive analysis of a major albuminur
Externí odkaz:
https://doaj.org/article/3ce65e8761e146108e0f630955c54002
Autor:
Alessia Calcagnì, Lotte kors, Eric Verschuren, Rossella De Cegli, Nicolina Zampelli, Edoardo Nusco, Stefano Confalonieri, Giovanni Bertalot, Salvatore Pece, Carmine Settembre, Gabriel G Malouf, Jaklien C Leemans, Emile de Heer, Marco Salvatore, Dorien JM Peters, Pier Paolo Di Fiore, Andrea Ballabio
Publikováno v:
eLife, Vol 5 (2016)
TFE-fusion renal cell carcinomas (TFE-fusion RCCs) are caused by chromosomal translocations that lead to overexpression of the TFEB and TFE3 genes (Kauffman et al., 2014). The mechanisms leading to kidney tumor development remain uncharacterized and
Externí odkaz:
https://doaj.org/article/32edca15298541028482d193be8401b5
Autor:
Dorrith Schonkeren, Godelieve Swings, Drucilla Roberts, Frans Claas, Emile de Heer, Sicco Scherjon
Publikováno v:
PLoS ONE, Vol 7, Iss 3, p e32347 (2012)
In pregnancies achieved after egg donation (ED) tolerance towards a completely allogeneic fetus is mediated by several complex immunoregulatory mechanisms, of which numerous aspects are still unknown. A distinct lesion not described previously in the
Externí odkaz:
https://doaj.org/article/e793c318b9094052a7d1d35936020ce6
Autor:
Amaya García de Vinuesa, Lise Høj Thomsen, Jenny Norlin, Lisbeth Nielsen Fink, Peter ten Dijke, Troels Krarup Hansen, Emile de Heer, Morten Fog-Tonnesen, Alexander Rosendahl
Publikováno v:
Renal Failure
Thomsen, L H, Fog-Tonnesen, M, Nielsen Fink, L, Norlin, J, García de Vinuesa, A, Hansen, T K, de Heer, E, Ten Dijke, P & Rosendahl, A 2017, ' Disparate phospho-Smad2 levels in advanced type 2 diabetes patients with diabetic nephropathy and early experimental db/db mouse model ', Renal Failure, vol. 39, no. 1, pp. 629-642 . https://doi.org/10.1080/0886022X.2017.1361837
Renal Failure, 39(1), 629-642
Thomsen, L H, Fog-Tonnesen, M, Nielsen Fink, L, Norlin, J, García de Vinuesa, A, Hansen, T K, de Heer, E, Ten Dijke, P & Rosendahl, A 2017, ' Disparate phospho-Smad2 levels in advanced type 2 diabetes patients with diabetic nephropathy and early experimental db/db mouse model ', Renal Failure, vol. 39, no. 1, pp. 629-642 . https://doi.org/10.1080/0886022X.2017.1361837
Renal Failure, 39(1), 629-642
Uncontrolled activation of transforming growth factor beta (TGF-β) family members is hypothesized to participate in type 2 diabetes (T2D) dependent diabetic nephropathy (DN). We evaluated and compared downstream activation of the Smad2-signaling pat
Autor:
Leendert A. van Es, Jimmy F.P. Berbée, Pascal Bus, Hans J. Baelde, Emile de Heer, Ron Wolterbeek, Jan A. Bruijn, Patrick C.N. Rensen, Rosalie Bor, Louis M. Havekes, Louise Pierneef
Publikováno v:
The Journal of Pathology. 241:589-599
Diabetic nephropathy is the leading cause of end-stage renal disease. Diabetic patients have increased plasma concentrations of apolipoprotein C-I (apoCI), and meta-analyses found that a polymorphism in APOC1 is associated with an increased risk of d
Autor:
Troels Krarup Hansen, Emile de Heer, Lisbeth Nielsen Fink, Amaya García de Vinuesa, Jenny Norlin, Morten Fog-Tonnesen, Alexander Rosendahl, Peter ten Dijke, Lise Høj Thomsen
Publikováno v:
Nephron
Nephron, 135(4), 291-306
Thomsen, L H, Fog-Tonnesen, M, Fink, L N, Norlin, J, de Vinuesa, A G, Hansen, T K, de Heer, E, ten Dijke, P & Rosendahl, A 2017, ' Smad2 Phosphorylation in Diabetic Kidney Tubule Epithelial Cells Is Associated with Modulation of Several Transforming Growth Factor-beta Family Members ', Nephron Clinical Practice, vol. 135, no. 4, pp. 291-306 . https://doi.org/10.1159/000453337
Nephron, 135(4), 291-306
Thomsen, L H, Fog-Tonnesen, M, Fink, L N, Norlin, J, de Vinuesa, A G, Hansen, T K, de Heer, E, ten Dijke, P & Rosendahl, A 2017, ' Smad2 Phosphorylation in Diabetic Kidney Tubule Epithelial Cells Is Associated with Modulation of Several Transforming Growth Factor-beta Family Members ', Nephron Clinical Practice, vol. 135, no. 4, pp. 291-306 . https://doi.org/10.1159/000453337
Background: The role of transforming growth factor-β (TGF-β) has recently gained much attention in diabetic nephropathy and kidney fibrosis. In this study, we extend this to an assessment of transcriptional regulation of the entire TGF-β superfami
Autor:
Anika Witten, Martina Schmidbauer, Marion Scharpfenecker, Anje Sporbert, Weibin Zhou, Daniela Panáková, Nina A. van de Lest, Emile de Heer, Reinhold Kreutz, Nicola Victoria Müller, Andrei Barysenka, Laura Herlan, Frank Rühle, Alexander M Meyer, Angela Schulz, Monika Stoll, Andreas Eisenreich, Bettina Purfürst, Theodor Lorenzen
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::6c2cca0785022be13863bd0603a3bef8
https://doi.org/10.7554/elife.42068.040
https://doi.org/10.7554/elife.42068.040
Autor:
Debbie Zittema, Esther Meijer, Harry van Goor, Dorien J.M. Peters, Ron T. Gansevoort, Emile de Heer, Irina B. Versteeg, Kimberley A. M. Veraar
Publikováno v:
American Journal of Nephrology, 44(3), 194-203
American Journal of Nephrology, 44(3), 194-203. KARGER
American Journal of Nephrology, 44(3), 194-203. KARGER
Background: In autosomal dominant polycystic kidney disease, renoprotective treatment with a vasopressin V2 receptor antagonist (V2RA) is given in a fixed dose (FD). Disease progression and drug habituation could diminish treatment efficacy. We inves
Autor:
Fatiha el Bouazzaoui, Emile de Heer, Olli Ritvos, Dorien J.M. Peters, Kimberley Veraar, Sebastian B.T. Jianu, Wouter N. Leonhard, Arja Pasternack, Martijn H. Breuning, Steven J. Kunnen, Peter ten Dijke, Willem M.H. Hoogaars, Anna J. Plugge
Publikováno v:
Journal of the American Society of Nephrology, 27(12), 3589-3599
Journal of the American Society of Nephrology, 27(12), 3589-3599. American Society of Nephrology
Journal of the American Society of Nephrology
Leonhard, W M, Kunnen, S J, Plugge, A J, Pasternack, A, Jianu, B, Veraar, K, El Bouazzaoui, F, Hoogaars, W, ten Dijke, P, Breuning, M H, de Heer, E, Ritvos, O & Peters, D J 2016, ' Inhibition of Activin Signaling Slows Progression of Polycystic Kidney Disease. ', Journal of the American Society of Nephrology, vol. 27, no. 12, pp. 3589-3599 . https://doi.org/10.1681/ASN.2015030287
Journal of the American Society of Nephrology, 27(12), 3589-3599. American Society of Nephrology
Journal of the American Society of Nephrology
Leonhard, W M, Kunnen, S J, Plugge, A J, Pasternack, A, Jianu, B, Veraar, K, El Bouazzaoui, F, Hoogaars, W, ten Dijke, P, Breuning, M H, de Heer, E, Ritvos, O & Peters, D J 2016, ' Inhibition of Activin Signaling Slows Progression of Polycystic Kidney Disease. ', Journal of the American Society of Nephrology, vol. 27, no. 12, pp. 3589-3599 . https://doi.org/10.1681/ASN.2015030287
Autosomal dominant polycystic kidney disease (ADPKD), characterized by the formation of numerous kidney cysts, is caused by PKD1 or PKD2 mutations and affects 0.1% of the population. Although recent clinical studies indicate that reduction of cAMP le