Ryoji Yagi

3.5k total citations
30 papers, 2.7k citations indexed

About

Ryoji Yagi is a scholar working on Immunology, Molecular Biology and Oncology. According to data from OpenAlex, Ryoji Yagi has authored 30 papers receiving a total of 2.7k indexed citations (citations by other indexed papers that have themselves been cited), including 26 papers in Immunology, 7 papers in Molecular Biology and 3 papers in Oncology. Recurrent topics in Ryoji Yagi's work include Immune Cell Function and Interaction (20 papers), T-cell and B-cell Immunology (13 papers) and IL-33, ST2, and ILC Pathways (8 papers). Ryoji Yagi is often cited by papers focused on Immune Cell Function and Interaction (20 papers), T-cell and B-cell Immunology (13 papers) and IL-33, ST2, and ILC Pathways (8 papers). Ryoji Yagi collaborates with scholars based in United States, Japan and Finland. Ryoji Yagi's co-authors include Jinfang Zhu, Keji Zhao, William E. Paul, Gang Wei, Suveena Sharma, Toshinori Nakayama, W E Paul, Yasmine Belkaid, Daniel Northrup and Nicolas Bouladoux and has published in prestigious journals such as Proceedings of the National Academy of Sciences, Journal of Clinical Investigation and Nature Communications.

In The Last Decade

Ryoji Yagi

30 papers receiving 2.7k citations

Peers

Ryoji Yagi
Hiroaki Takatori Japan
Machteld M. Tiemessen Netherlands
Kotaro Suzuki Japan
Saskia Hemmers United States
Joel Tocker United States
Victor C. de Vries United States
Ken‐ichiro Seino Japan
Laurence E. Cheng United States
Richard J. DiPaolo United States
Sara Trifari United States
Hiroaki Takatori Japan
Ryoji Yagi
Citations per year, relative to Ryoji Yagi Ryoji Yagi (= 1×) peers Hiroaki Takatori

Countries citing papers authored by Ryoji Yagi

Since Specialization
Citations

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

Fields of papers citing papers by Ryoji Yagi

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Ryoji Yagi

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

All Works

20 of 20 papers shown
1.
Yagi, Ryoji, Yukihiro Endo, Ryo Koyama‐Nasu, et al.. (2021). IFNγ suppresses the expression of GFI1 and thereby inhibits Th2 cell proliferation. PLoS ONE. 16(11). e0260204–e0260204. 6 indexed citations
2.
Suzuki, Akane, Ryoji Yagi, Motoko Y. Kimura, et al.. (2020). Essential Role for CD30-Transglutaminase 2 Axis in Memory Th1 and Th17 Cell Generation. Frontiers in Immunology. 11. 1536–1536. 7 indexed citations
3.
Kimura, Motoko Y., Ryo Koyama‐Nasu, Ryoji Yagi, & Toshinori Nakayama. (2019). A new therapeutic target: the CD69-Myl9 system in immune responses. Seminars in Immunopathology. 41(3). 349–358. 36 indexed citations
4.
Kimura, Motoko Y., Koji Hayashizaki, Miho Shinzawa, et al.. (2018). CD69 prevents PLZFhi innate precursors from prematurely exiting the thymus and aborting NKT2 cell differentiation. Nature Communications. 9(1). 3749–3749. 12 indexed citations
5.
Fang, Difeng, Kairong Cui, Gangqing Hu, et al.. (2018). Bcl11b, a novel GATA3-interacting protein, suppresses Th1 while limiting Th2 cell differentiation. The Journal of Experimental Medicine. 215(5). 1449–1462. 46 indexed citations
6.
Northrup, Daniel, Ryoji Yagi, Kairong Cui, et al.. (2017). Histone demethylases UTX and JMJD3 are required for NKT cell development in mice. Cell & Bioscience. 7(1). 25–25. 30 indexed citations
7.
Yagi, Ryoji, Chao Zhong, Daniel Northrup, et al.. (2014). The Transcription Factor GATA3 Is Critical for the Development of All IL-7Rα-Expressing Innate Lymphoid Cells. Immunity. 40(3). 378–388. 303 indexed citations
8.
Junttila, Ilkka, L. Cynthia Watson, Laura Kummola, et al.. (2013). Efficient cytokine-induced IL-13 production by mast cells requires both IL-33 and IL-3. Journal of Allergy and Clinical Immunology. 132(3). 704–712.e10. 45 indexed citations
9.
Endo, Yusuke, Kiyoshi Hirahara, Ryoji Yagi, Damon J. Tumes, & Toshinori Nakayama. (2013). Pathogenic memory type Th2 cells in allergic inflammation. Trends in Immunology. 35(2). 69–78. 101 indexed citations
10.
Zhu, Jinfang, Dragana Janković, Andrew J. Oler, et al.. (2012). The Transcription Factor T-bet Is Induced by Multiple Pathways and Prevents an Endogenous Th2 Cell Program during Th1 Cell Responses. Immunity. 37(4). 660–673. 260 indexed citations
11.
Wei, Gang, Brian J. Abraham, Ryoji Yagi, et al.. (2011). Genome-wide Analyses of Transcription Factor GATA3-Mediated Gene Regulation in Distinct T Cell Types. Immunity. 35(2). 299–311. 258 indexed citations
12.
Yagi, Ryoji, Jinfang Zhu, & W E Paul. (2011). An updated view on transcription factor GATA3-mediated regulation of Th1 and Th2 cell differentiation. International Immunology. 23(7). 415–420. 186 indexed citations
13.
Wohlfert, Elizabeth A., John R. Grainger, Nicolas Bouladoux, et al.. (2011). GATA3 controls Foxp3+ regulatory T cell fate during inflammation in mice. Journal of Clinical Investigation. 121(11). 4503–4515. 421 indexed citations
14.
Yagi, Ryoji, Masamitsu Tanaka, Kazuki Sasaki, et al.. (2010). ARAP3 inhibits peritoneal dissemination of scirrhous gastric carcinoma cells by regulating cell adhesion and invasion. Oncogene. 30(12). 1413–1421. 24 indexed citations
15.
Tanaka, Shinya, Yasutaka Motomura, Yoshie Suzuki, et al.. (2010). The enhancer HS2 critically regulates GATA-3-mediated Il4 transcription in TH2 cells. Nature Immunology. 12(1). 77–85. 106 indexed citations
16.
Yagi, Ryoji, Ilkka Junttila, Gang Wei, et al.. (2010). The Transcription Factor GATA3 Actively Represses RUNX3 Protein-Regulated Production of Interferon-γ. Immunity. 32(4). 507–517. 125 indexed citations
17.
Hayashi, Keitaro, Waka Natsume, Toshio Watanabe, et al.. (2003). The Runx1 Transcription Factor Inhibits the Differentiation of Naive CD4 + T Cells into the Th2 Lineage by Repressing GATA3 Expression. The Journal of Experimental Medicine. 198(1). 51–61. 111 indexed citations
18.
Yagi, Ryoji, Wataru Suzuki, Noriyasu Seki, et al.. (2002). The IL-4 production capability of different strains of naive CD4+ T cells controls the direction of the Th cell response. International Immunology. 14(1). 1–11. 42 indexed citations
19.
Yagi, Ryoji, S. Tanaka, & Takayoshi Koike. (2000). Thapsigargin induces microglial transformation from amoeboid- to ramified- type in vivo. Glia. 29(1). 102–102. 20 indexed citations
20.
Yagi, Ryoji, Shuuitsu Tanaka, & Tatsuro Koike. (1999). Thapsigargin induces microglial transformation from amoeboid to ramified type in vitro. Glia. 28(1). 49–52. 19 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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