Nicholas G. Brown
- Molecular Biology top 5%
- Cell Biology top 2%
- Molecular Medicine top 2%
- Oncology top 10%
- Genetics
- Co-authors
- Brenda A. SchulmanJan‐Michael PetersTimothy PalzkillHolger StarkRyan T. VanderLindenFlorian WeissmannGeorg PetzoldEdmond R. Watson
- Topics
- Ubiquitin and proteasome pathways (28 papers)Microtubule and mitosis dynamics (20 papers)Antibiotic Resistance in Bacteria (11 papers)
- Journals
- NatureProceedings of the National Academy of SciencesJournal of the American Chemical Society
- Partner nations
- United StatesAustriaGermany
In The Last Decade
Nicholas G. Brown
57 papers receiving 2.0k citations
Peers
Comparison fields: 5 of 94
- Molecular Biology 1.6k
- Cell Biology 671
- Molecular Medicine 250
- Oncology 248
- Genetics 171
Countries citing papers authored by Nicholas G. Brown
This map shows the geographic impact of Nicholas G. Brown'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 Nicholas G. Brown with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Nicholas G. Brown more than expected).
Fields of papers citing papers by Nicholas G. Brown
This network shows the impact of papers produced by Nicholas G. Brown. 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 Nicholas G. Brown. The network helps show where Nicholas G. Brown may publish in the future.
Co-authorship network of co-authors of Nicholas G. Brown
This figure shows the co-authorship network connecting the top 25 collaborators of Nicholas G. Brown. A scholar is included among the top collaborators of Nicholas G. Brown 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 Nicholas G. Brown. Nicholas G. Brown is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 0 | |
| 2 | 3 | |
| 3 | 3 | |
| 4 | 24 | |
| 5 | 9 | |
| 6 | 9 | |
| 7 | 37 | |
| 8 | 25 | |
| 9 | 13 | |
| 10 | 71 | |
| 11 | 223 | |
| 12 | 108 | |
| 13 | 112 | |
| 14 | 49 | |
| 15 | 27 | |
| 16 | 92 | |
| 17 | 63 | |
| 18 | 18 | |
| 19 | 69 | |
| 20 | 36 |
About Nicholas G. Brown
Nicholas G. Brown is a scholar working on Molecular Medicine, Structural Biology and Cell Biology, having authored 60 papers that have together received 2.1k indexed citations. Recurring topics across this work include Ubiquitin and proteasome pathways (28 papers), Microtubule and mitosis dynamics (20 papers) and Antibiotic Resistance in Bacteria (11 papers). The work is most often cited by research in Molecular Medicine (250 citations), Cell Biology (671 citations) and Molecular Biology (1.6k citations). Nicholas G. Brown has collaborated with scholars based in United States, Austria and Germany. Frequent co-authors include Brenda A. Schulman, Jan‐Michael Peters, Timothy Palzkill, Holger Stark, Ryan T. VanderLinden, Florian Weissmann, Georg Petzold, Edmond R. Watson, David Haselbach and Renping Qiao. Their work appears in journals such as Nature, Proceedings of the National Academy of Sciences and Journal of the American Chemical Society.
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.