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Trends in Molecular Medicine|October 30, 2016
Is it Time to Fold the Cysts Away?Matteus Krappitz, Anna-Rachel Gallagher, Sorin Fedeles
Journal of Visualized Experiments : Jove|July 22, 2014
Demonstration of proteolytic activation of the epithelial sodium channel (ENaC) by combining current measurements with detection of cleavage fragmentsMatteus Krappitz, Christoph Korbmacher, Silke Haerteis
The Journal of General Physiology|September 12, 2012
Plasmin and chymotrypsin have distinct preferences for channel activating cleavage sites in the γ subunit of the human epithelial sodium channelSilke Haerteis, Matteus Krappitz, Alexei Diakov, et al.
European Journal of Ophthalmology|January 24, 2024
Transcriptome Analysis of Choroidal Endothelium Links Androgen Receptor Role to Central Serous ChorioretinopathySandrine H Künzel, Dominika Pohlmann, Lynn Zur Bonsen, et al.
Pflugers Archiv : European Journal of Physiology|August 7, 2012
Proteolytic activation of the epithelial sodium channel (ENaC) by the cysteine protease cathepsin-SSilke Haerteis, Matteus Krappitz, Marko Bertog, et al.
American Journal of Physiology. Renal Physiology|July 15, 2025
Valosin-containing protein in ciliary morphology: a novel target in ADPKDCarlotta Pioppini, Rishi Bhardwaj, Ria Schönauer, et al.
The Journal of Biological Chemistry|May 21, 2014
Proteolytic activation of the human epithelial sodium channel by trypsin IV and trypsin I involves distinct cleavage sitesSilke Haerteis, Annabel Krappitz, Matteus Krappitz, et al.
Journal of Cell Science|November 17, 2020
Disrupting polycystin-2 EF hand Ca2+ affinity does not alter channel function or contribute to polycystic kidney diseaseThuy N Vien, Leo C T Ng, Jessica M Smith, et al.
Biorxiv : the Preprint Server for Biology|February 20, 2025
In vivo base editing reduces liver cysts in autosomal dominant polycystic kidney diseaseAntonia Ibel, Rishi Bhardwaj, Duygu Elif Yilmaz, et al.
Journal of the American Society of Nephrology : JASN|October 21, 2022
XBP1 Activation Reduces Severity of Polycystic Kidney Disease due to a Nontruncating Polycystin-1 Mutation in MiceMatteus Krappitz, Rishi Bhardwaj, Ke Dong, et al.
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