Marina Dusl
Impact in
- Neurology top 5%
- Myasthenia Gravis and Thymoma
- Neuroblastoma Research and Treatments
- Cell Biology top 10%
- Cellular transport and secretion
Papers in
-
- Myasthenia Gravis and Thymoma 7
-
- Ion channel regulation and function 2
- Co-authors
- Hanns Lochmüller (8 shared papers)Angela Abicht (8 shared papers)Juliane S. Müller (4 shared papers)Velina Guergueltcheva (4 shared papers)Angela Huebner (2 shared papers)Constanze Gallenmüller (2 shared papers)Maja von der Hagen (2 shared papers)Amina Chaouch (2 shared papers)
- Journals
- Neuromuscular Disorders (3 papers)Journal of Neurology (3 papers)Human Mutation (1 paper)International Journal of Molecular Sciences (1 paper)Human Molecular Genetics (1 paper)
- Partner nations
- GermanyUnited KingdomBulgaria
In The Last Decade
Marina Dusl
10 papers receiving 308 citations
Peers
Comparison fields: 5 of 40
- Neurology 218
- Cell Biology 127
- Genetics 26
- Molecular Biology 139
- Rheumatology 24
Countries citing papers authored by Marina Dusl
This map shows the geographic impact of Marina Dusl'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 Marina Dusl with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Marina Dusl more than expected).
Fields of papers citing papers by Marina Dusl
This network shows the impact of papers produced by Marina Dusl. 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 Marina Dusl. The network helps show where Marina Dusl may publish in the future.
Co-authors
The 25 scholars most cited alongside Marina Dusl, 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 | 2012 | 91 | |
| 2 | 2011 | 50 | |
| 3 | 2013 | 47 | |
| 4 | 2017 | 34 | |
| 5 | 2015 | 29 | |
| 6 | 2015 | 23 | |
| 7 | 2020 | 18 | |
| 8 | 2019 | 13 | |
| 9 | 2012 | 7 | |
| 10 | 2012 | 1 |
About Marina Dusl
Marina Dusl is a scholar working on Neurology, Molecular Biology, Cell Biology, Endocrinology, Diabetes and Metabolism and Oncology, having authored 10 papers that have together received 313 indexed citations. Recurring topics across this work include Myasthenia Gravis and Thymoma (7 papers), Cellular transport and secretion (5 papers), Cancer Treatment and Pharmacology (2 papers), Ion channel regulation and function (2 papers), Thyroid Cancer Diagnosis and Treatment (2 papers), Pituitary Gland Disorders and Treatments (1 paper), Genetic factors in colorectal cancer (1 paper) and Genetics and Neurodevelopmental Disorders (1 paper). The work is most often cited by research in Neurology (218 citations), Cell Biology (127 citations), Genetics (26 citations), Molecular Biology (139 citations) and Rheumatology (24 citations). Marina Dusl has collaborated with scholars based in Germany, United Kingdom and Bulgaria. Frequent co-authors include Hanns Lochmüller, Angela Abicht, Juliane S. Müller, Velina Guergueltcheva, Angela Huebner, Constanze Gallenmüller, Maja von der Hagen, Amina Chaouch, Ulrike Schara and Rolf Stucka. Their work appears in journals such as Neuromuscular Disorders, Journal of Neurology, Human Mutation, International Journal of Molecular Sciences and Human Molecular Genetics.
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.