Bruno Di Jeso
- Molecular Biology top 10%
- Cell Biology top 5%
- Endocrinology, Diabetes and Metabolism top 5%
- Physiology top 10%
- Immunology
- Co-authors
- Peter ArvanLuca UlianichSilvestro FormisanoEduardo ConsiglioAntonio LeonardiJaemin LeePasquale VitoFrancesco Bèguinot
- Topics
- Endoplasmic Reticulum Stress and Disease (15 papers)Erythrocyte Function and Pathophysiology (9 papers)Cell death mechanisms and regulation (7 papers)
- Journals
- Proceedings of the National Academy of SciencesNucleic Acids ResearchJournal of Biological Chemistry
- Partner nations
- ItalyUnited StatesAustralia
In The Last Decade
Bruno Di Jeso
55 papers receiving 1.5k citations
Peers
Comparison fields: 5 of 113
- Molecular Biology 774
- Cell Biology 393
- Endocrinology, Diabetes and Metabolism 325
- Physiology 258
- Immunology 173
Countries citing papers authored by Bruno Di Jeso
This map shows the geographic impact of Bruno Di Jeso'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 Bruno Di Jeso with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Bruno Di Jeso more than expected).
Fields of papers citing papers by Bruno Di Jeso
This network shows the impact of papers produced by Bruno Di Jeso. 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 Bruno Di Jeso. The network helps show where Bruno Di Jeso may publish in the future.
Co-authorship network of co-authors of Bruno Di Jeso
This figure shows the co-authorship network connecting the top 25 collaborators of Bruno Di Jeso. A scholar is included among the top collaborators of Bruno Di Jeso 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 Bruno Di Jeso. Bruno Di Jeso is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 10 | |
| 2 | 0 | |
| 3 | 7 | |
| 4 | 36 | |
| 5 | 35 | |
| 6 | 41 | |
| 7 | 54 | |
| 8 | 88 | |
| 9 | 13 | |
| 10 | 18 | |
| 11 | 12 | |
| 12 | 23 | |
| 13 | 24 | |
| 14 | 13 | |
| 15 | 3 | |
| 16 | 12 | |
| 17 | 4 | |
| 18 | 4 | |
| 19 | 12 | |
| 20 | 33 |
About Bruno Di Jeso
Bruno Di Jeso is a scholar working on Cell Biology, Physiology and Molecular Biology, having authored 56 papers that have together received 1.5k indexed citations. Recurring topics across this work include Endoplasmic Reticulum Stress and Disease (15 papers), Erythrocyte Function and Pathophysiology (9 papers) and Cell death mechanisms and regulation (7 papers). The work is most often cited by research in Cell Biology (393 citations), Endocrinology, Diabetes and Metabolism (325 citations) and Physiology (66 citations). Bruno Di Jeso has collaborated with scholars based in Italy, United States and Australia. Frequent co-authors include Peter Arvan, Luca Ulianich, Silvestro Formisano, Eduardo Consiglio, Antonio Leonardi, Jaemin Lee, Pasquale Vito, Francesco Bèguinot, Domenico Liguoro and Claudia Miele. Their work appears in journals such as Proceedings of the National Academy of Sciences, Nucleic Acids Research and Journal of Biological Chemistry.
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.