Silva Sütt
Impact in
- Cell Biology top 10%
- Endoplasmic Reticulum Stress and Disease
Papers in
-
- Receptor Mechanisms and Signaling 4
-
- Endoplasmic Reticulum Stress and Disease 7
- Co-authors
- Eero Vasar (15 shared papers)Sulev Kõks (11 shared papers)Sirli Raud (11 shared papers)Hendrik Luuk (8 shared papers)Jürgen Innos (7 shared papers)Margit Mahlapuu (6 shared papers)Mario Plaas (7 shared papers)Esther Nuñez‐Durán (5 shared papers)
In The Last Decade
Silva Sütt
21 papers receiving 394 citations
Peers
Comparison fields: 5 of 58
- Cell Biology 157
- Aging 11
- Behavioral Neuroscience 16
- Biological Psychiatry 8
- Developmental Neuroscience 13
Countries citing papers authored by Silva Sütt
This map shows the geographic impact of Silva Sütt'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 Silva Sütt with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Silva Sütt more than expected).
Fields of papers citing papers by Silva Sütt
This network shows the impact of papers produced by Silva Sütt. 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 Silva Sütt. The network helps show where Silva Sütt may publish in the future.
Co-authors
The 25 scholars most cited alongside Silva Sütt, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.
All Works
Showing the 20 most-cited of 21 papers — load more, or switch the sort, to bring in the rest.
| # | Work | ||
|---|---|---|---|
| 1 | 2008 | 62 | |
| 2 | 2016 | 42 | |
| 3 | 2017 | 37 | |
| 4 | 2016 | 37 | |
| 5 | 2009 | 36 | |
| 6 | 2017 | 23 | |
| 7 | 2012 | 19 | |
| 8 | 2014 | 18 | |
| 9 | 2007 | 16 | |
| 10 | 2013 | 16 | |
| 11 | 2018 | 15 | |
| 12 | 2021 | 12 | |
| 13 | 2014 | 11 | |
| 14 | 2014 | 9 | |
| 15 | 2014 | 9 | |
| 16 | 2013 | 8 | |
| 17 | 2007 | 7 | |
| 18 | 2017 | 7 | |
| 19 | 2009 | 5 | |
| 20 | 2007 | 5 |
About Silva Sütt
Silva Sütt is a scholar working on Molecular Biology, Cell Biology, Cellular and Molecular Neuroscience, Genetics and Surgery, having authored 21 papers that have together received 397 indexed citations. Recurring topics across this work include Endoplasmic Reticulum Stress and Disease (7 papers), Genetics and Neurodevelopmental Disorders (4 papers), Receptor Mechanisms and Signaling (4 papers), Neurotransmitter Receptor Influence on Behavior (4 papers), Neuroscience and Neuropharmacology Research (3 papers), Diet, Metabolism, and Disease (3 papers), Pancreatic function and diabetes (3 papers) and Genetics, Aging, and Longevity in Model Organisms (2 papers). The work is most often cited by research in Cell Biology (157 citations), Aging (11 citations), Behavioral Neuroscience (16 citations), Biological Psychiatry (8 citations) and Developmental Neuroscience (13 citations). Silva Sütt has collaborated with scholars based in Estonia, Sweden and Germany. Frequent co-authors include Eero Vasar, Sulev Kõks, Sirli Raud, Hendrik Luuk, Jürgen Innos, Margit Mahlapuu, Mario Plaas, Esther Nuñez‐Durán, Marcus Ståhlman and Manoj Amrutkar. Their work appears in journals such as Behavioural Brain Research, Journal of Endocrinology, Biochemical and Biophysical Research Communications, Molecular Metabolism and Frontiers in Neuroscience.
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.