Andrew M. Ellisdon
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- Genetic Neurodegenerative Diseases 8
- Molecular Biology top 10%
- Mitochondrial Function and Pathology 7
- Protein Kinase Regulation and GTPase Signaling 7
- Receptor Mechanisms and Signaling 5
- RNA Research and Splicing 4
- Cell Biology top 10%
- Endoplasmic Reticulum Stress and Disease 4
- Cellular transport and secretion 3
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- Neurological disorders and treatments 4
- Co-authors
- Stephen BottomleyMurray StewartMichelle L. HallsEd HurtJames C. WhisstockMary C. PearceLisa D. CabritaAlwin Köhler
- Partner nations
- AustraliaUnited StatesUnited Kingdom
In The Last Decade
Andrew M. Ellisdon
33 papers receiving 1.1k citations
Peers
Comparison fields: 5 of 82
- Cellular and Molecular Neuroscience 367
- Molecular Biology 893
- Cell Biology 133
- Neurology 90
- Immunology 113
Countries citing papers authored by Andrew M. Ellisdon
This map shows the geographic impact of Andrew M. Ellisdon'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 Andrew M. Ellisdon with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Andrew M. Ellisdon more than expected).
Fields of papers citing papers by Andrew M. Ellisdon
This network shows the impact of papers produced by Andrew M. Ellisdon. 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 Andrew M. Ellisdon. The network helps show where Andrew M. Ellisdon may publish in the future.
Co-authorship network
The 25 scholars most cited alongside Andrew M. Ellisdon, 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 | 2026 | 0 | |
| 2 | 2025 | 3 | |
| 3 | 2024 | 1 | |
| 4 | 2022 | 9 | |
| 5 | 2021 | 1 | |
| 6 | 2020 | 25 | |
| 7 | 2019 | 20 | |
| 8 | 2017 | 71 | |
| 9 | 2017 | 7 | |
| 10 | 2015 | 50 | |
| 11 | 2014 | 14 | |
| 12 | 2012 | 80 | |
| 13 | 2009 | 31 | |
| 14 | 2009 | 57 | |
| 15 | 2009 | 112 | |
| 16 | 2008 | 30 | |
| 17 | 2007 | 9 | |
| 18 | 2006 | 144 | |
| 19 | 2006 | 14 | |
| 20 | 2004 | 62 |
About Andrew M. Ellisdon
Andrew M. Ellisdon is a scholar working on Structural Biology, Cellular and Molecular Neuroscience and Cell Biology, having authored 34 papers that have together received 1.1k indexed citations. Recurring topics across this work include Genetic Neurodegenerative Diseases (8 papers), Mitochondrial Function and Pathology (7 papers), Protein Kinase Regulation and GTPase Signaling (7 papers), Receptor Mechanisms and Signaling (5 papers), Endoplasmic Reticulum Stress and Disease (4 papers), Neurological disorders and treatments (4 papers), RNA Research and Splicing (4 papers) and Cellular transport and secretion (3 papers). The work is most often cited by research in Cellular and Molecular Neuroscience (367 citations), Molecular Biology (893 citations) and Cell Biology (133 citations). Andrew M. Ellisdon has collaborated with scholars based in Australia, United States and United Kingdom. Frequent co-authors include Stephen Bottomley, Murray Stewart, Michelle L. Halls, Ed Hurt, James C. Whisstock, Mary C. Pearce, Lisa D. Cabrita, Alwin Köhler, Lyudmila Dimitrova-Paternoga and Michelle K.M. Chow. Their work appears in journals such as Nature, Cell and Proceedings of the National Academy of Sciences.
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.