G
Gerd Walz
Researcher at University of Freiburg
Publications - 76
Citations - 6189
Gerd Walz is an academic researcher from University of Freiburg. The author has contributed to research in topics: Podocyte & Cilium. The author has an hindex of 29, co-authored 76 publications receiving 5435 citations.
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Journal ArticleDOI
The mTOR pathway is regulated by polycystin-1, and its inhibition reverses renal cystogenesis in polycystic kidney disease.
Jonathan M. Shillingford,Noel S. Murcia,Claire H. Larson,Seng Hui Low,Ryan C. Hedgepeth,Nicole Brown,Christopher A Flask,Andrew C. Novick,David A. Goldfarb,Albrecht Kramer-Zucker,Gerd Walz,Klaus Piontek,Gregory G. Germino,Thomas Weimbs +13 more
TL;DR: It is shown that the cytoplasmic tail of PC1 interacts with tuberin, and the mTOR pathway is inappropriately activated in cyst-lining epithelial cells in human ADPKD patients and mouse models, indicating that PC1 has an important function in the regulation of the m TOR pathway and that this pathway provides a target for medical therapy of AD PKD.
Journal ArticleDOI
Mutations in INVS encoding inversin cause nephronophthisis type 2, linking renal cystic disease to the function of primary cilia and left-right axis determination.
Edgar A. Otto,Bernhard Schermer,Tomoko Obara,John F. O'Toole,Karl S. Hiller,Adelheid M. Mueller,Rainer G. Ruf,Julia Hoefele,Frank Beekmann,Daniel Landau,John W. Foreman,Judith A. Goodship,Tom Strachan,Andreas Kispert,Matthias T.F. Wolf,Marie F. Gagnadoux,Hubert Nivet,Corinne Antignac,Gerd Walz,Iain A. Drummond,Thomas Benzing,Friedhelm Hildebrandt +21 more
TL;DR: The interaction and colocalization in cilia of inversin, nephrocystin and β-tubulin connect pathogenetic aspects of NPHP to PKD, to primary cilia function and to left-right axis determination.
Journal ArticleDOI
Autophagy influences glomerular disease susceptibility and maintains podocyte homeostasis in aging mice
Björn Hartleben,Markus Gödel,Catherine Meyer-Schwesinger,Shuya Liu,Theresa Ulrich,Sven Köbler,Thorsten Wiech,Florian Grahammer,Sebastian J. Arnold,Maja T. Lindenmeyer,Clemens D. Cohen,Hermann Pavenstädt,Dontscho Kerjaschki,Noboru Mizushima,Andrey S. Shaw,Gerd Walz,Tobias B. Huber +16 more
TL;DR: It is postulate that constitutive and induced autophagy is a major protective mechanism against podocyte aging and glomerular injury, representing a putative target to ameliorate human glomersular disease and aging-related loss of renal function.
Journal ArticleDOI
The centrosomal protein nephrocystin-6 is mutated in Joubert syndrome and activates transcription factor ATF4
John A. Sayer,John A. Sayer,Edgar A. Otto,John F. O'Toole,Gudrun Nürnberg,Michael A. Kennedy,Christian Becker,Hans Christian Hennies,Juliana Helou,Massimo Attanasio,Blake V. Fausett,Boris Utsch,Hemant Khanna,Yan Liu,Iain A. Drummond,Isao Kawakami,Takehiro Kusakabe,Motoyuki Tsuda,Li Ma,Hwankyu Lee,Ronald G. Larson,Susan J. Allen,Christopher J. Wilkinson,Erich A. Nigg,Chengchao Shou,Concepción Lillo,David S. Williams,Bernd Hoppe,Markus J. Kemper,Thomas J. Neuhaus,Melissa A. Parisi,Ian A. Glass,Marianne Petry,Andreas Kispert,Joachim Gloy,Athina Ganner,Gerd Walz,Xueliang Zhu,Daniel Goldman,Peter Nürnberg,Anand Swaroop,Michel R. Leroux,Friedhelm Hildebrandt +42 more
TL;DR: These findings help establish the link between centrosome function, tissue architecture and transcriptional control in the pathogenesis of cystic kidney disease, retinal degeneration, and central nervous system development.
Journal ArticleDOI
Role of mTOR in podocyte function and diabetic nephropathy in humans and mice
Markus Gödel,Björn Hartleben,Nadja Herbach,Shuya Liu,Stefan Zschiedrich,Shun Lu,Andrea Debreczeni-Mór,Maja T. Lindenmeyer,Maria Pia Rastaldi,Götz Hartleben,Thorsten Wiech,Alessia Fornoni,Robert G. Nelson,Matthias Kretzler,Rüdiger Wanke,Hermann Pavenstädt,Dontscho Kerjaschki,Clemens D. Cohen,Michael N. Hall,Markus A. Rüegg,Ken Inoki,Gerd Walz,Tobias B. Huber,Tobias B. Huber +23 more
TL;DR: It is suggested that mTOR inhibition can protect podocytes and prevent progressive diabetic nephropathy and demonstrate the requirement for tightly balanced mTOR activity in podocyte homeostasis.