Mariko Taniguchi‐Ikeda
- Molecular Biology
- Genetics
- Pediatrics, Perinatology and Child Health top 10%
- Genetics
- Immunology and Allergy top 10%
- Co-authors
- Kazumoto IijimaIchiro MoriokaTatsushi TodaHiroki KurahashiKandai NozuHiroaki NagaseKazuhiro KobayashiMotoi Kanagawa
- Topics
- Muscle Physiology and Disorders (17 papers)Mitochondrial Function and Pathology (8 papers)Cell Adhesion Molecules Research (6 papers)
- Partner nations
- JapanUnited StatesUnited Kingdom
In The Last Decade
Mariko Taniguchi‐Ikeda
59 papers receiving 756 citations
Peers
Comparison fields: 5 of 81
- Molecular Biology 430
- Genetics 150
- Pediatrics, Perinatology and Child Health 144
- Genetics 77
- Immunology and Allergy 70
Countries citing papers authored by Mariko Taniguchi‐Ikeda
This map shows the geographic impact of Mariko Taniguchi‐Ikeda'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 Mariko Taniguchi‐Ikeda with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Mariko Taniguchi‐Ikeda more than expected).
Fields of papers citing papers by Mariko Taniguchi‐Ikeda
This network shows the impact of papers produced by Mariko Taniguchi‐Ikeda. 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 Mariko Taniguchi‐Ikeda. The network helps show where Mariko Taniguchi‐Ikeda may publish in the future.
Co-authorship network of co-authors of Mariko Taniguchi‐Ikeda
This figure shows the co-authorship network connecting the top 25 collaborators of Mariko Taniguchi‐Ikeda. A scholar is included among the top collaborators of Mariko Taniguchi‐Ikeda 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 Mariko Taniguchi‐Ikeda. Mariko Taniguchi‐Ikeda 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 | 5 | |
| 3 | 8 | |
| 4 | 1 | |
| 5 | 8 | |
| 6 | 12 | |
| 7 | 13 | |
| 8 | 1 | |
| 9 | 18 | |
| 10 | 1 | |
| 11 | 6 | |
| 12 | 9 | |
| 13 | 13 | |
| 14 | 9 | |
| 15 | 21 | |
| 16 | 6 | |
| 17 | 25 | |
| 18 | 15 | |
| 19 | 7 | |
| 20 | 132 |
About Mariko Taniguchi‐Ikeda
Mariko Taniguchi‐Ikeda is a scholar working on Immunology and Allergy, Genetics and Pediatrics, Perinatology and Child Health, having authored 60 papers that have together received 760 indexed citations. Recurring topics across this work include Muscle Physiology and Disorders (17 papers), Mitochondrial Function and Pathology (8 papers) and Cell Adhesion Molecules Research (6 papers). The work is most often cited by research in Immunology and Allergy (70 citations), Pediatrics, Perinatology and Child Health (144 citations) and Genetics (77 citations). Mariko Taniguchi‐Ikeda has collaborated with scholars based in Japan, United States and United Kingdom. Frequent co-authors include Kazumoto Iijima, Ichiro Morioka, Tatsushi Toda, Hiroki Kurahashi, Kandai Nozu, Hiroaki Nagase, Kazuhiro Kobayashi, Motoi Kanagawa, Atsushi Kuga and Toshifumi Yokota. Their work appears in journals such as Nature, Scientific Reports and Human Molecular Genetics.
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.