Giuseppe Cannino
- Molecular Biology
- Health, Toxicology and Mutagenesis top 5%
- Cancer Research
- Nutrition and Dietetics top 10%
- Physiology
- Co-authors
- Anna Maria RinaldiClaudio LuparelloAndrea RasolaIonica MasgrasHoward T. JacobsCarlo Maria Di LiegroCarlos Sànchez‐MartìnFrancesco Ciscato
- Topics
- Mitochondrial Function and Pathology (16 papers)ATP Synthase and ATPases Research (13 papers)Cancer, Hypoxia, and Metabolism (5 papers)
In The Last Decade
Giuseppe Cannino
29 papers receiving 991 citations
Peers
Comparison fields: 5 of 102
- Molecular Biology 610
- Health, Toxicology and Mutagenesis 194
- Cancer Research 133
- Nutrition and Dietetics 130
- Physiology 91
Countries citing papers authored by Giuseppe Cannino
This map shows the geographic impact of Giuseppe Cannino'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 Giuseppe Cannino with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Giuseppe Cannino more than expected).
Fields of papers citing papers by Giuseppe Cannino
This network shows the impact of papers produced by Giuseppe Cannino. 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 Giuseppe Cannino. The network helps show where Giuseppe Cannino may publish in the future.
Co-authorship network of co-authors of Giuseppe Cannino
This figure shows the co-authorship network connecting the top 25 collaborators of Giuseppe Cannino. A scholar is included among the top collaborators of Giuseppe Cannino 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 Giuseppe Cannino. Giuseppe Cannino is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 15 | |
| 2 | 29 | |
| 3 | 28 | |
| 4 | 25 | |
| 5 | 64 | |
| 6 | 11 | |
| 7 | 4 | |
| 8 | 76 | |
| 9 | 73 | |
| 10 | 13 | |
| 11 | 36 | |
| 12 | 39 | |
| 13 | 15 | |
| 14 | 16 | |
| 15 | 179 | |
| 16 | 41 | |
| 17 | 76 | |
| 18 | Mitochondrial protein expression in rattus norvegicus and human cells | 9 |
| 19 | Mitochondrial protein expression in Ratt and in human cells | 3 |
| 20 | 13 |
About Giuseppe Cannino
Giuseppe Cannino is a scholar working on Aging, Geriatrics and Gerontology and Cancer Research, having authored 29 papers that have together received 1.0k indexed citations. Recurring topics across this work include Mitochondrial Function and Pathology (16 papers), ATP Synthase and ATPases Research (13 papers) and Cancer, Hypoxia, and Metabolism (5 papers). The work is most often cited by research in Aging (34 citations), Health, Toxicology and Mutagenesis (194 citations) and Molecular Biology (610 citations). Giuseppe Cannino has collaborated with scholars based in Italy, Finland and Brazil. Frequent co-authors include Anna Maria Rinaldi, Claudio Luparello, Andrea Rasola, Ionica Masgras, Howard T. Jacobs, Carlo Maria Di Liegro, Carlos Sànchez‐Martìn, Francesco Ciscato, Éric Dufour and Giorgio Colombo. Their work appears in journals such as Journal of Biological Chemistry, PLoS ONE and Molecular and Cellular Biology.
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.