Yūko Fujioka
- Epidemiology top 0.5%
- Molecular Biology top 2%
- Cell Biology top 0.5%
- Plant Science top 5%
- Physiology top 0.5%
- Co-authors
- Yoshinori OhsumiFuyuhiko InagakiNobuo N. NodaNobuo SuzukiTakao HanadaYoshinobu IchimuraHiroyuki KumetaToshifumi Takao
- Topics
- Autophagy in Disease and Therapy (36 papers)Endoplasmic Reticulum Stress and Disease (16 papers)Ubiquitin and proteasome pathways (8 papers)
- Cited by
- PhysiologyEpidemiologyCell Biology
- Partner nations
- JapanUnited StatesFrance
In The Last Decade
Yūko Fujioka
54 papers receiving 4.8k citations
Hit Papers
Peers
Comparison fields: 5 of 112
- Epidemiology 3.3k
- Molecular Biology 2.6k
- Cell Biology 1.5k
- Plant Science 517
- Physiology 513
Countries citing papers authored by Yūko Fujioka
This map shows the geographic impact of Yūko Fujioka'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 Yūko Fujioka with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Yūko Fujioka more than expected).
Fields of papers citing papers by Yūko Fujioka
This network shows the impact of papers produced by Yūko Fujioka. 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 Yūko Fujioka. The network helps show where Yūko Fujioka may publish in the future.
Co-authorship network of co-authors of Yūko Fujioka
This figure shows the co-authorship network connecting the top 25 collaborators of Yūko Fujioka. A scholar is included among the top collaborators of Yūko Fujioka 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 Yūko Fujioka. Yūko Fujioka is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 1 | |
| 2 | 27 | |
| 3 | 19 | |
| 4 | 31 | |
| 5 | 74 | |
| 6 | Phase separation organizes the site of autophagosome formationbreakdown → | 284 |
| 7 | 101 | |
| 8 | 78 | |
| 9 | 101 | |
| 10 | 52 | |
| 11 | 148 | |
| 12 | 116 | |
| 13 | 90 | |
| 14 | 3 | |
| 15 | The Atg12-Atg5 Conjugate Has a Novel E3-like Activity for Protein Lipidation in Autophagybreakdown → | 884 |
| 16 | 7 | |
| 17 | 13 | |
| 18 | 99 | |
| 19 | 113 | |
| 20 | 35 |
About Yūko Fujioka
Yūko Fujioka is a scholar working on Cell Biology, Physiology and Epidemiology, having authored 55 papers that have together received 4.8k indexed citations. Recurring topics across this work include Autophagy in Disease and Therapy (36 papers), Endoplasmic Reticulum Stress and Disease (16 papers) and Ubiquitin and proteasome pathways (8 papers). The work is most often cited by research in Physiology (513 citations), Epidemiology (3.3k citations) and Cell Biology (1.5k citations). Yūko Fujioka has collaborated with scholars based in Japan, United States and France. Frequent co-authors include Yoshinori Ohsumi, Fuyuhiko Inagaki, Nobuo N. Noda, Nobuo Suzuki, Takao Hanada, Yoshinobu Ichimura, Hiroyuki Kumeta, Toshifumi Takao, Yoshinori Satomi and Kenji Satoo. Their work appears in journals such as Nature, Journal of the American Chemical Society and Journal of Biological Chemistry.
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.