Koh‐ichi Nagata
- Molecular Biology top 5%
- Cell Biology top 1%
- Cellular and Molecular Neuroscience top 5%
- Genetics top 5%
- Physiology top 10%
- Co-authors
- Hidenori ItoYoshinori NozawaMasaki InagakiRika MorishitaIkuko IwamotoHidenori TabataTomiko AsanoNanako Hamada
- Topics
- Protein Kinase Regulation and GTPase Signaling (29 papers)Genetics and Neurodevelopmental Disorders (26 papers)Cellular transport and secretion (22 papers)
- Partner nations
- JapanUnited StatesUnited Kingdom
In The Last Decade
Koh‐ichi Nagata
148 papers receiving 3.2k citations
Peers
Comparison fields: 5 of 112
- Molecular Biology 2.1k
- Cell Biology 1.1k
- Cellular and Molecular Neuroscience 554
- Genetics 528
- Physiology 223
Countries citing papers authored by Koh‐ichi Nagata
This map shows the geographic impact of Koh‐ichi Nagata'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 Koh‐ichi Nagata with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Koh‐ichi Nagata more than expected).
Fields of papers citing papers by Koh‐ichi Nagata
This network shows the impact of papers produced by Koh‐ichi Nagata. 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 Koh‐ichi Nagata. The network helps show where Koh‐ichi Nagata may publish in the future.
Co-authorship network of co-authors of Koh‐ichi Nagata
This figure shows the co-authorship network connecting the top 25 collaborators of Koh‐ichi Nagata. A scholar is included among the top collaborators of Koh‐ichi Nagata 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 Koh‐ichi Nagata. Koh‐ichi Nagata 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 | 1 | |
| 3 | 0 | |
| 4 | 0 | |
| 5 | 1 | |
| 6 | 4 | |
| 7 | 0 | |
| 8 | 2 | |
| 9 | 4 | |
| 10 | 7 | |
| 11 | 7 | |
| 12 | 13 | |
| 13 | 9 | |
| 14 | 25 | |
| 15 | 15 | |
| 16 | Differential expression of Septin 9 isoforms in cells sensitive and resistant to microtubule stabilizing drugs. | 1 |
| 17 | 6 | |
| 18 | 2 | |
| 19 | 4 | |
| 20 | 22 |
About Koh‐ichi Nagata
Koh‐ichi Nagata is a scholar working on Cell Biology, Aging and Cellular and Molecular Neuroscience, having authored 157 papers that have together received 3.2k indexed citations. Recurring topics across this work include Protein Kinase Regulation and GTPase Signaling (29 papers), Genetics and Neurodevelopmental Disorders (26 papers) and Cellular transport and secretion (22 papers). The work is most often cited by research in Cell Biology (1.1k citations), Aging (65 citations) and Developmental Neuroscience (138 citations). Koh‐ichi Nagata has collaborated with scholars based in Japan, United States and United Kingdom. Frequent co-authors include Hidenori Ito, Yoshinori Nozawa, Masaki Inagaki, Rika Morishita, Ikuko Iwamoto, Hidenori Tabata, Tomiko Asano, Nanako Hamada, Shigeru Nakashima and Alan Hall. Their work appears in journals such as Journal of Biological Chemistry, Nature Communications and The Journal of Cell Biology.
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.