Werner Machleidt
- Molecular Biology top 2%
- Cancer Research top 2%
- Cell Biology top 2%
- Oncology top 5%
- Physiology top 5%
- Co-authors
- Irmgard Assfalg‐MachleidtHans FritzVito TürkAnka RitonjaElmar WächterJoachim OttoWalter SebaldJože Brzin
- Topics
- Protease and Inhibitor Mechanisms (23 papers)Calpain Protease Function and Regulation (13 papers)Enzyme Production and Characterization (13 papers)
- Journals
- Proceedings of the National Academy of SciencesJournal of Biological ChemistryThe Journal of Experimental Medicine
- Partner nations
- GermanySloveniaUnited States
In The Last Decade
Werner Machleidt
107 papers receiving 4.5k citations
Peers
Comparison fields: 5 of 120
- Molecular Biology 2.6k
- Cancer Research 882
- Cell Biology 675
- Oncology 604
- Physiology 416
Countries citing papers authored by Werner Machleidt
This map shows the geographic impact of Werner Machleidt'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 Werner Machleidt with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Werner Machleidt more than expected).
Fields of papers citing papers by Werner Machleidt
This network shows the impact of papers produced by Werner Machleidt. 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 Werner Machleidt. The network helps show where Werner Machleidt may publish in the future.
Co-authorship network of co-authors of Werner Machleidt
This figure shows the co-authorship network connecting the top 25 collaborators of Werner Machleidt. A scholar is included among the top collaborators of Werner Machleidt 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 Werner Machleidt. Werner Machleidt is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 10 | |
| 2 | 9 | |
| 3 | 55 | |
| 4 | 180 | |
| 5 | 191 | |
| 6 | 24 | |
| 7 | 31 | |
| 8 | 31 | |
| 9 | 69 | |
| 10 | 39 | |
| 11 | 17 | |
| 12 | 35 | |
| 13 | 61 | |
| 14 | 14 | |
| 15 | 55 | |
| 16 | 36 | |
| 17 | 20 | |
| 18 | 34 | |
| 19 | 75 | |
| 20 | 20 |
About Werner Machleidt
Werner Machleidt is a scholar working on Biotechnology, Cancer Research and Cell Biology, having authored 107 papers that have together received 4.7k indexed citations. Recurring topics across this work include Protease and Inhibitor Mechanisms (23 papers), Calpain Protease Function and Regulation (13 papers) and Enzyme Production and Characterization (13 papers). The work is most often cited by research in Cancer Research (882 citations), Biotechnology (366 citations) and Cell Biology (675 citations). Werner Machleidt has collaborated with scholars based in Germany, Slovenia and United States. Frequent co-authors include Irmgard Assfalg‐Machleidt, Hans Fritz, Vito Türk, Anka Ritonja, Elmar Wächter, Joachim Otto, Walter Sebald, Jože Brzin, Ursula Borchart and Ennes A. Auerswald. Their work appears in journals such as Proceedings of the National Academy of Sciences, Journal of Biological Chemistry and The Journal of Experimental Medicine.
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.