Rika Kato

410 total citations
10 papers, 206 citations indexed

About

Rika Kato is a scholar working on Molecular Biology, Immunology and Rheumatology. According to data from OpenAlex, Rika Kato has authored 10 papers receiving a total of 206 indexed citations (citations by other indexed papers that have themselves been cited), including 4 papers in Molecular Biology, 4 papers in Immunology and 2 papers in Rheumatology. Recurrent topics in Rika Kato's work include T-cell and B-cell Immunology (4 papers), Immune Cell Function and Interaction (3 papers) and Immunotherapy and Immune Responses (2 papers). Rika Kato is often cited by papers focused on T-cell and B-cell Immunology (4 papers), Immune Cell Function and Interaction (3 papers) and Immunotherapy and Immune Responses (2 papers). Rika Kato collaborates with scholars based in Japan and United States. Rika Kato's co-authors include Yumi Tsuchida, Keishi Fujio, Kazuhiko Yamamoto, Shinichiro Nakachi, Shuji Sumitomo, Haruka Tsuchiya, Yasuo Nagafuchi, Keiichi Sakurai, Norio Hanata and Hiroko Kanda and has published in prestigious journals such as Journal of Biological Chemistry, Scientific Reports and Frontiers in Immunology.

In The Last Decade

Rika Kato

10 papers receiving 204 citations

Peers

Rika Kato
Muyao Guo China
Alexander A. Girgis United States
Kevin Schifferli United States
Liat Izhak United States
Mary Birchler United States
Aziza Elmesmari United Kingdom
Pawel A. Kabala Netherlands
A Orfao Spain
Rika Kato
Citations per year, relative to Rika Kato Rika Kato (= 1×) peers Nathalie Gunera-Saad

Countries citing papers authored by Rika Kato

Since Specialization
Citations

This map shows the geographic impact of Rika Kato'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 Rika Kato with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Rika Kato more than expected).

Fields of papers citing papers by Rika Kato

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Rika Kato. 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 Rika Kato. The network helps show where Rika Kato may publish in the future.

Co-authorship network of co-authors of Rika Kato

This figure shows the co-authorship network connecting the top 25 collaborators of Rika Kato. A scholar is included among the top collaborators of Rika Kato 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 Rika Kato. Rika Kato is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

10 of 10 papers shown
1.
Kato, Rika, Shuhei Kusano, Hitoshi Endo, et al.. (2023). A Small Compound, HYGIC, Promotes Hypocotyl Growth Through Ectopic Ethylene Response. Plant and Cell Physiology. 64(10). 1167–1177. 1 indexed citations
2.
Kobayashi, Yuka, Rika Kato, Hitoshi Endo, et al.. (2023). Identification of a pluripotency-inducing small compound, PLU, that induces callus formation via Heat Shock Protein 90-mediated activation of auxin signaling. Frontiers in Plant Science. 14. 1099587–1099587. 2 indexed citations
3.
Fujitani, Kazuko, Asako Otomo, Taro Tachibana, et al.. (2020). PACT/PRKRA and p53 regulate transcriptional activity of DMRT1. Genetics and Molecular Biology. 43(2). e20190017–e20190017. 7 indexed citations
4.
Kato, Rika, Shuji Sumitomo, Yumi Tsuchida, et al.. (2019). CD4+CD25+LAG3+ T Cells With a Feature of Th17 Cells Associated With Systemic Lupus Erythematosus Disease Activity. Frontiers in Immunology. 10. 1619–1619. 24 indexed citations
5.
Nakachi, Shinichiro, Shuji Sumitomo, Yumi Tsuchida, et al.. (2017). Interleukin-10-producing LAG3+ regulatory T cells are associated with disease activity and abatacept treatment in rheumatoid arthritis. Arthritis Research & Therapy. 19(1). 97–97. 52 indexed citations
6.
Sumitomo, Shuji, Yasuo Nagafuchi, Yumi Tsuchida, et al.. (2017). A gene module associated with dysregulated TCR signaling pathways in CD4+ T cell subsets in rheumatoid arthritis. Journal of Autoimmunity. 89. 21–29. 19 indexed citations
7.
Nagafuchi, Yasuo, Hirofumi Shoda, Shuji Sumitomo, et al.. (2016). Immunophenotyping of rheumatoid arthritis reveals a linkage between HLA-DRB1 genotype, CXCR4 expression on memory CD4+ T cells and disease activity. Scientific Reports. 6(1). 29338–29338. 45 indexed citations
8.
Sumitomo, Shuji, Shinichiro Nakachi, Tomohisa Okamura, et al.. (2016). Identification of tonsillar CD4+CD25−LAG3+ T cells as naturally occurring IL-10-producing regulatory T cells in human lymphoid tissue. Journal of Autoimmunity. 76. 75–84. 12 indexed citations
9.
Kodera, Yoshio, Rika Kato, Tatsuya Saito, et al.. (2014). Establishment of a Strategy for the Discovery and Verification of Low-Abundance Biomarker Peptides in Plasma Using Two Types of Stable-Isotope Tags. Mass Spectrometry. 3(Special_Issue_3). S0044–S0044. 4 indexed citations
10.
Kariya, Yoshinobu, Rika Kato, Satsuki Itoh, et al.. (2008). N-Glycosylation of Laminin-332 Regulates Its Biological Functions. Journal of Biological Chemistry. 283(48). 33036–33045. 40 indexed citations

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.

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