Lukas Sušac
Impact in
- Aging top 10%
- Physiology top 10%
- Telomeres, Telomerase, and Senescence
Papers in
-
- DNA Repair Mechanisms 4
- Receptor Mechanisms and Signaling 3
- Protein Structure and Dynamics 2
-
- Telomeres, Telomerase, and Senescence 5
- Adenosine and Purinergic Signaling 2
- Co-authors
- Yaqiang Wang (6 shared papers)Juli Feigon (6 shared papers)Kurt Wüthrich (5 shared papers)Z. Hong Zhou (3 shared papers)Raymond C. Stevens (3 shared papers)Robert Tampé (6 shared papers)Tatiana Didenko (1 shared paper)Matthew T. Eddy (1 shared paper)
- Journals
- Nature Communications (2 papers)Nature (2 papers)Cell (2 papers)Proceedings of the National Academy of Sciences (2 papers)FEBS Journal (1 paper)
- Partner nations
- United StatesGermanySwitzerland
In The Last Decade
Lukas Sušac
15 papers receiving 567 citations
Peers
Comparison fields: 5 of 63
- Aging 28
- Physiology 167
- Physiology 28
- Molecular Biology 407
- Immunology 84
Countries citing papers authored by Lukas Sušac
This map shows the geographic impact of Lukas Sušac'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 Lukas Sušac with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Lukas Sušac more than expected).
Fields of papers citing papers by Lukas Sušac
This network shows the impact of papers produced by Lukas Sušac. 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 Lukas Sušac. The network helps show where Lukas Sušac may publish in the future.
Co-authors
The 25 scholars most cited alongside Lukas Sušac, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.
All Works
| # | Work | ||
|---|---|---|---|
| 1 | 2018 | 103 | |
| 2 | 2018 | 87 | |
| 3 | 2022 | 84 | |
| 4 | 2019 | 60 | |
| 5 | 2021 | 49 | |
| 6 | 2014 | 37 | |
| 7 | 2022 | 34 | |
| 8 | 2022 | 32 | |
| 9 | 2015 | 22 | |
| 10 | 2020 | 21 | |
| 11 | 2023 | 18 | |
| 12 | 2024 | 9 | |
| 13 | 2015 | 8 | |
| 14 | 2016 | 4 | |
| 15 | 2021 | 1 | |
| 16 | 2026 | 0 | |
| 17 | 2026 | 0 |
About Lukas Sušac
Lukas Sušac is a scholar working on Molecular Biology, Physiology, Ecology, Cellular and Molecular Neuroscience and Physiology, having authored 17 papers that have together received 569 indexed citations. Recurring topics across this work include Telomeres, Telomerase, and Senescence (5 papers), DNA Repair Mechanisms (4 papers), Polar Research and Ecology (3 papers), Receptor Mechanisms and Signaling (3 papers), Adenosine and Purinergic Signaling (2 papers), Immunotherapy and Immune Responses (2 papers), Protein Structure and Dynamics (2 papers) and Trace Elements in Health (2 papers). The work is most often cited by research in Aging (28 citations), Physiology (167 citations), Physiology (28 citations), Molecular Biology (407 citations) and Immunology (84 citations). Lukas Sušac has collaborated with scholars based in United States, Germany and Switzerland. Frequent co-authors include Yaqiang Wang, Juli Feigon, Kurt Wüthrich, Z. Hong Zhou, Raymond C. Stevens, Robert Tampé, Tatiana Didenko, Matthew T. Eddy, Jiansen Jiang and Henry Chan. Their work appears in journals such as Nature Communications, Nature, Cell, Proceedings of the National Academy of Sciences and FEBS Journal.
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.