Marina Dusl

1.3k total citations
10 papers, 313 citations indexed

About

Marina Dusl is a scholar working on Neurology, Molecular Biology and Cell Biology. According to data from OpenAlex, Marina Dusl has authored 10 papers receiving a total of 313 indexed citations (citations by other indexed papers that have themselves been cited), including 8 papers in Neurology, 5 papers in Molecular Biology and 5 papers in Cell Biology. Recurrent topics in Marina Dusl's work include Myasthenia Gravis and Thymoma (7 papers), Cellular transport and secretion (5 papers) and Ion channel regulation and function (2 papers). Marina Dusl is often cited by papers focused on Myasthenia Gravis and Thymoma (7 papers), Cellular transport and secretion (5 papers) and Ion channel regulation and function (2 papers). Marina Dusl collaborates with scholars based in Germany, United Kingdom and Spain. Marina Dusl's co-authors include Angela Abicht, Hanns Lochmüller, Juliane S. Müller, Velina Guergueltcheva, Angela Huebner, Maja von der Hagen, Constanze Gallenmüller, Ulrike Schara, Amina Chaouch and Violeta Mihaylova and has published in prestigious journals such as International Journal of Molecular Sciences, Human Molecular Genetics and Cardiovascular Research.

In The Last Decade

Marina Dusl

10 papers receiving 308 citations

Peers

Marina Dusl
Amina Chaouch United Kingdom
Thomas L. Hilder United States
Annabel K. Wang United States
Sheng Yao China
Cathryn Poulton Netherlands
Martin A. Haagmans Netherlands
M Beis Canada
Angela D. Bhalla United States
Amina Chaouch United Kingdom
Marina Dusl
Citations per year, relative to Marina Dusl Marina Dusl (= 1×) peers Amina Chaouch

Countries citing papers authored by Marina Dusl

Since Specialization
Citations

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

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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-authorship network of co-authors of Marina Dusl

This figure shows the co-authorship network connecting the top 25 collaborators of Marina Dusl. A scholar is included among the top collaborators of Marina Dusl 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 Marina Dusl. Marina Dusl is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

10 of 10 papers shown
1.
Stendel, Claudia, Maria Cristina D’Adamo, Marina Dusl, et al.. (2020). Association of A Novel Splice Site Mutation in P/Q-Type Calcium Channels with Childhood Epilepsy and Late-Onset Slowly Progressive Non-Episodic Cerebellar Ataxia. International Journal of Molecular Sciences. 21(11). 3810–3810. 18 indexed citations
2.
Dusl, Marina, T. Moreno, Francina Munell, et al.. (2019). Congenital myasthenic syndrome caused by novel COL13A1 mutations. Journal of Neurology. 266(5). 1107–1112. 13 indexed citations
3.
McMacken, Grace, Roger G. Whittaker, Teresinha Evangelista, et al.. (2017). Congenital myasthenic syndrome with episodic apnoea: clinical, neurophysiological and genetic features in the long-term follow-up of 19 patients. Journal of Neurology. 265(1). 194–203. 34 indexed citations
4.
Dusl, Marina, Jan Senderek, Juliane S. Müller, et al.. (2015). A 3'-UTR mutation creates a microRNA target site in the GFPT1 gene of patients with congenital myasthenic syndrome. Human Molecular Genetics. 24(12). 3418–3426. 23 indexed citations
5.
Benito, Daniel Natera‐de, Juan J. Vílchez, Teresinha Evangelista, et al.. (2015). Long-term follow-up in patients with congenital myasthenic syndrome due to RAPSN mutations. Neuromuscular Disorders. 26(2). 153–159. 29 indexed citations
6.
Gallenmüller, Constanze, Wolfgang Müller‐Felber, Marina Dusl, et al.. (2013). Salbutamol-responsive limb-girdle congenital myasthenic syndrome due to a novel missense mutation and heteroallelic deletion in MUSK. Neuromuscular Disorders. 24(1). 31–35. 47 indexed citations
7.
Abicht, Angela, Marina Dusl, Constanze Gallenmüller, et al.. (2012). Congenital myasthenic syndromes: Achievements and limitations of phenotype-guided gene-after-gene sequencing in diagnostic practice: A study of 680 patients. Human Mutation. 33(10). 1474–1484. 91 indexed citations
8.
Kriegmair, Maximilian C., et al.. (2012). Cardiac differentiation in Xenopus is initiated by mespa. Cardiovascular Research. 97(3). 454–463. 7 indexed citations
9.
Chaouch, Mohamed Ali, Velina Guergueltcheva, Marina Dusl, et al.. (2012). P37 A retrospective clinical study of the treatment of slow-channel congenital myasthenic syndrome. Neuromuscular Disorders. 22. S16–S17. 1 indexed citations
10.
Chaouch, Amina, Juliane S. Müller, Velina Guergueltcheva, et al.. (2011). A retrospective clinical study of the treatment of slow-channel congenital myasthenic syndrome. Journal of Neurology. 259(3). 474–481. 50 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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