Matteus Krappitz

425 total citations
10 papers, 324 citations indexed

About

Matteus Krappitz is a scholar working on Molecular Biology, Genetics and Nephrology. According to data from OpenAlex, Matteus Krappitz has authored 10 papers receiving a total of 324 indexed citations (citations by other indexed papers that have themselves been cited), including 7 papers in Molecular Biology, 4 papers in Genetics and 3 papers in Nephrology. Recurrent topics in Matteus Krappitz's work include Genetic and Kidney Cyst Diseases (4 papers), Ion Transport and Channel Regulation (4 papers) and Ion channel regulation and function (3 papers). Matteus Krappitz is often cited by papers focused on Genetic and Kidney Cyst Diseases (4 papers), Ion Transport and Channel Regulation (4 papers) and Ion channel regulation and function (3 papers). Matteus Krappitz collaborates with scholars based in Germany, United States and Australia. Matteus Krappitz's co-authors include Christoph Korbmacher, Silke Haerteis, Nigel W. Bunnett, Pierangelo Geppetti, Romke Bron, Carlos U. Corvera, Daniel P. Poole, Serena Materazzi, Martin Steinhoff and Yvette Wilson and has published in prestigious journals such as Journal of Biological Chemistry, Gastroenterology and Journal of Cell Science.

In The Last Decade

Matteus Krappitz

8 papers receiving 319 citations

Peers

Matteus Krappitz

MB

ONCOL

SS

SURGE

PRM

Hanan AlSaeid Alshenawy Egypt

Hsin‐Yuan Su United States

Liqiong Xue China

Waka Yokoyama Japan

Serhan Karvar United States

Geping Wu China

Baoyong Zhou China

Henrik Søndergaard Denmark

Yan‐Wen Shu China

Hanan AlSaeid Alshenawy Egypt

Matteus Krappitz

134 ×1.0

MB

83 ×0.9

ONCOL

10 ×0.2

SS

46 ×0.9

SURGE

68 ×1.3

PRM

Citations per year, relative to Matteus Krappitz Matteus Krappitz (= 1×) peers Hanan AlSaeid Alshenawy

Countries citing papers authored by Matteus Krappitz

Since Specialization

Citations

This map shows the geographic impact of Matteus Krappitz's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Matteus Krappitz with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Matteus Krappitz more than expected).

Fields of papers citing papers by Matteus Krappitz

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Matteus Krappitz. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Matteus Krappitz. The network helps show where Matteus Krappitz may publish in the future.

Co-authorship network of co-authors of Matteus Krappitz

This figure shows the co-authorship network connecting the top 25 collaborators of Matteus Krappitz. A scholar is included among the top collaborators of Matteus Krappitz based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Matteus Krappitz. Matteus Krappitz is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

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10 of 10 papers shown

1.

Yılmaz, Duygu Elif, Ria Schönauer, Kai‐Uwe Eckardt, et al.. (2025). In vivo base editing reduces liver cysts in autosomal dominant polycystic kidney disease. Molecular Therapy. 33(11). 5373–5382.

2.

Künzel, Sandrine H., Dominika Pohlmann, Matteus Krappitz, et al.. (2024). Transcriptome Analysis of Choroidal Endothelium Links Androgen Receptor Role to Central Serous Chorioretinopathy. European Journal of Ophthalmology. 34(5). 1532–1540.

3.

Krappitz, Matteus, Ke Dong, Duygu Elif Yılmaz, et al.. (2022). XBP1 Activation Reduces Severity of Polycystic Kidney Disease due to a Nontruncating Polycystin-1 Mutation in Mice. Journal of the American Society of Nephrology. 34(1). 110–121. 7 indexed citations

4.

Vien, Thuy N., Leo Ng, Jessica M. Smith, et al.. (2020). Disrupting polycystin-2 EF hand Ca2+ affinity does not alter channel function or contribute to polycystic kidney disease. Journal of Cell Science. 133(24). 12 indexed citations

5.

Krappitz, Matteus, Anna‐Rachel Gallagher, & Sorin V. Fedeles. (2016). Is it Time to Fold the Cysts Away?. Trends in Molecular Medicine. 22(12). 997–999. 3 indexed citations

6.

Lieu, TinaMarie, Peishen Zhao, Daniel P. Poole, et al.. (2014). The Bile Acid Receptor TGR5 Activates the TRPA1 Channel to Induce Itch in Mice. Gastroenterology. 147(6). 1417–1428. 176 indexed citations

7.

Haerteis, Silke, Matteus Krappitz, Jane Murphy, et al.. (2014). Proteolytic Activation of the Human Epithelial Sodium Channel by Trypsin IV and Trypsin I Involves Distinct Cleavage Sites. Journal of Biological Chemistry. 289(27). 19067–19078. 28 indexed citations

8.

Krappitz, Matteus, Christoph Korbmacher, & Silke Haerteis. (2014). Demonstration of Proteolytic Activation of the Epithelial Sodium Channel (ENaC) by Combining Current Measurements with Detection of Cleavage Fragments. Journal of Visualized Experiments. 3 indexed citations

9.

Haerteis, Silke, Matteus Krappitz, Marko Bertog, et al.. (2012). Proteolytic activation of the epithelial sodium channel (ENaC) by the cysteine protease cathepsin-S. Pflügers Archiv - European Journal of Physiology. 464(4). 353–365. 55 indexed citations

10.

Haerteis, Silke, et al.. (2012). Plasmin and chymotrypsin have distinct preferences for channel activating cleavage sites in the γ subunit of the human epithelial sodium channel. The Journal of General Physiology. 140(4). 375–389. 40 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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