Attila Mócsai
- Immunology top 0.2%
- Molecular Biology top 2%
- Immunology and Allergy top 0.2%
- Oncology top 2%
- Hematology top 1%
- Co-authors
- Clifford A. LowellVictor L. J. TybulewiczJürgen RulandTamás NémethKrisztina FutosiSzabina FodorZoltán JakusMarkus Sperandio
- Topics
- Cell Adhesion Molecules Research (39 papers)Neutrophil, Myeloperoxidase and Oxidative Mechanisms (33 papers)Immune Response and Inflammation (25 papers)
- Partner nations
- HungaryGermanyUnited States
In The Last Decade
Attila Mócsai
111 papers receiving 9.6k citations
Hit Papers
Peers
Comparison fields: 5 of 133
- Immunology 5.4k
- Molecular Biology 3.4k
- Immunology and Allergy 1.8k
- Oncology 1.2k
- Hematology 856
Countries citing papers authored by Attila Mócsai
This map shows the geographic impact of Attila Mócsai'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 Attila Mócsai with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Attila Mócsai more than expected).
Fields of papers citing papers by Attila Mócsai
This network shows the impact of papers produced by Attila Mócsai. 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 Attila Mócsai. The network helps show where Attila Mócsai may publish in the future.
Co-authorship network of co-authors of Attila Mócsai
This figure shows the co-authorship network connecting the top 25 collaborators of Attila Mócsai. A scholar is included among the top collaborators of Attila Mócsai 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 Attila Mócsai. Attila Mócsai 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 | 2 | |
| 3 | 3 | |
| 4 | 1 | |
| 5 | 3 | |
| 6 | 3 | |
| 7 | 10 | |
| 8 | Neutrophils as emerging therapeutic targetsbreakdown → | 492 |
| 9 | 12 | |
| 10 | 33 | |
| 11 | 16 | |
| 12 | 32 | |
| 13 | 13 | |
| 14 | 154 | |
| 15 | 29 | |
| 16 | 258 | |
| 17 | 35 | |
| 18 | 330 | |
| 19 | Separation of blood and lymphatic vascular networks is regulated by the hematopoietic signaling proteins SLP-76 and Syk. | 1 |
| 20 | 49 |
About Attila Mócsai
Attila Mócsai is a scholar working on Immunology and Allergy, Immunology and Rheumatology, having authored 113 papers that have together received 9.7k indexed citations. Recurring topics across this work include Cell Adhesion Molecules Research (39 papers), Neutrophil, Myeloperoxidase and Oxidative Mechanisms (33 papers) and Immune Response and Inflammation (25 papers). The work is most often cited by research in Immunology and Allergy (1.8k citations), Immunology (5.4k citations) and Hematology (856 citations). Attila Mócsai has collaborated with scholars based in Hungary, Germany and United States. Frequent co-authors include Clifford A. Lowell, Victor L. J. Tybulewicz, Jürgen Ruland, Tamás Németh, Krisztina Futosi, Szabina Fodor, Zoltán Jakus, Markus Sperandio, Giorgio Berton and Erzsébet Ligeti. Their work appears in journals such as Nature, Science and Proceedings of the National Academy of Sciences.
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.