Ee Wern Su

1.3k total citations · 1 hit paper
9 papers, 1.1k citations indexed

About

Ee Wern Su is a scholar working on Immunology, Molecular Biology and Oncology. According to data from OpenAlex, Ee Wern Su has authored 9 papers receiving a total of 1.1k indexed citations (citations by other indexed papers that have themselves been cited), including 8 papers in Immunology, 4 papers in Molecular Biology and 3 papers in Oncology. Recurrent topics in Ee Wern Su's work include Galectins and Cancer Biology (5 papers), Signaling Pathways in Disease (3 papers) and Peptidase Inhibition and Analysis (2 papers). Ee Wern Su is often cited by papers focused on Galectins and Cancer Biology (5 papers), Signaling Pathways in Disease (3 papers) and Peptidase Inhibition and Analysis (2 papers). Ee Wern Su collaborates with scholars based in United States and Egypt. Ee Wern Su's co-authors include Larry Kane, Vijay K. Kuchroo, William D. Hastings, Lisa Bregoli, Charles Lei, József Kármán, David E. Anderson, Rucha Chandwaskar, Nasim Kassam and Jeffrey N. Bruce and has published in prestigious journals such as Science, Nucleic Acids Research and The Journal of Immunology.

In The Last Decade

Ee Wern Su

9 papers receiving 1.1k citations

Hit Papers

Promotion of Tissue Inflammation by the Immune Receptor T... 2007 2026 2013 2019 2007 100 200 300 400 500

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name h Career Trend Papers Cites
Ee Wern Su United States 8 928 405 313 84 50 9 1.1k
Atsuko Sakata Japan 11 660 0.7× 149 0.4× 380 1.2× 40 0.5× 31 0.6× 20 850
Chie Hotta Japan 10 580 0.6× 132 0.3× 349 1.1× 25 0.3× 45 0.9× 13 776
Hanjie Li China 8 716 0.8× 509 1.3× 501 1.6× 31 0.4× 164 3.3× 9 1.2k
Bianca von Scheidt Australia 16 938 1.0× 918 2.3× 215 0.7× 77 0.9× 39 0.8× 21 1.3k
Hyun-Il Cho South Korea 15 700 0.8× 447 1.1× 389 1.2× 89 1.1× 118 2.4× 35 1.1k
Caroline Voskens Germany 18 653 0.7× 410 1.0× 196 0.6× 29 0.3× 131 2.6× 31 1.0k
Jan Kubach Germany 9 798 0.9× 156 0.4× 222 0.7× 21 0.3× 56 1.1× 9 1.0k
Venkateswara R. Simhadri United States 18 1.1k 1.1× 349 0.9× 412 1.3× 58 0.7× 116 2.3× 21 1.4k
Robin Handon United States 9 1.3k 1.4× 471 1.2× 194 0.6× 60 0.7× 54 1.1× 11 1.5k

Countries citing papers authored by Ee Wern Su

Since Specialization
Citations

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

Fields of papers citing papers by Ee Wern Su

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Ee Wern Su. 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 Ee Wern Su. The network helps show where Ee Wern Su may publish in the future.

Co-authorship network of co-authors of Ee Wern Su

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

All Works

9 of 9 papers shown
1.
Rubinstein, Mark P., Ee Wern Su, Samantha Suriano, et al.. (2015). Interleukin-12 enhances the function and anti-tumor activity in murine and human CD8+ T cells. Cancer Immunology Immunotherapy. 64(5). 539–549. 32 indexed citations
2.
Su, Ee Wern, Samantha Suriano, Christopher Johnson, et al.. (2015). IL-2Rα mediates temporal regulation of IL-2 signaling and enhances immunotherapy. Science Translational Medicine. 7(311). 311ra170–311ra170. 47 indexed citations
3.
Bishu, Shrinivas, et al.. (2014). Rheumatoid arthritis patients exhibit impaired Candida albicans-specific Th17 responses. Arthritis Research & Therapy. 16(1). R50–R50. 27 indexed citations
4.
Su, Ee Wern, Chen Zhu, Sarah G. Hainline, et al.. (2011). Phosphotyrosine-Dependent Coupling of Tim-3 to T-Cell Receptor Signaling Pathways. Molecular and Cellular Biology. 31(19). 3963–3974. 219 indexed citations
5.
Su, Ee Wern, et al.. (2010). Galectin-9 regulates T helper cell function independently of Tim-3. Glycobiology. 21(10). 1258–1265. 86 indexed citations
6.
Su, Ee Wern, et al.. (2009). Determination of Cytoplasmic Tyrosine Residues of Tim-3 Involved in Regulation of TCR signaling (35.30). The Journal of Immunology. 182(Supplement_1). 35.30–35.30. 1 indexed citations
7.
Su, Ee Wern, et al.. (2008). TIM-1 and TIM-3 proteins in immune regulation. Cytokine. 44(1). 9–13. 64 indexed citations
8.
Fogel, Gary B., V William Porto, Gábor Varga, et al.. (2008). Evolutionary computation for discovery of composite transcription factor binding sites. Nucleic Acids Research. 36(21). e142–e142. 22 indexed citations
9.
Anderson, Ana C., David E. Anderson, Lisa Bregoli, et al.. (2007). Promotion of Tissue Inflammation by the Immune Receptor Tim-3 Expressed on Innate Immune Cells. Science. 318(5853). 1141–1143. 580 indexed citations breakdown →

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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