David Caton
Impact in
Papers in
-
- Connexins and lens biology 5
- Nicotinic Acetylcholine Receptors Study 2
- Muscle Physiology and Disorders 1
- Surgery 5
- Pancreatic function and diabetes 4
- Co-authors
- Béatrice Cousin (4 shared papers)Louis Casteilla (4 shared papers)Alessandra Calabrese (6 shared papers)Luc Pénicaud (2 shared papers)Paolo Meda (4 shared papers)Danièle Noël (2 shared papers)Stéphane Roche (2 shared papers)Sylvain Lehmann (2 shared papers)
- Journals
- Experimental Cell Research (3 papers)Cell Communication & Adhesion (1 paper)PROTEOMICS (1 paper)Journal of Cellular Physiology (1 paper)Journal of Cell Science (1 paper)
- Partner nations
- SwitzerlandFranceUnited States
In The Last Decade
David Caton
11 papers receiving 922 citations
Peers
Comparison fields: 5 of 79
- Genetics 428
- Surgery 377
- Urology 48
- Endocrine and Autonomic Systems 52
- Physiology 173
Countries citing papers authored by David Caton
This map shows the geographic impact of David Caton'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 David Caton with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites David Caton more than expected).
Fields of papers citing papers by David Caton
This network shows the impact of papers produced by David Caton. 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 David Caton. The network helps show where David Caton may publish in the future.
Co-authors
The 25 scholars most cited alongside David Caton, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.
All Works
| # | Work | ||
|---|---|---|---|
| 1 | 2008 | 269 | |
| 2 | 2005 | 211 | |
| 3 | 2003 | 121 | |
| 4 | 2006 | 97 | |
| 5 | 2009 | 73 | |
| 6 | 2002 | 56 | |
| 7 | 2004 | 42 | |
| 8 | 2003 | 39 | |
| 9 | Beta-cell crosstalk: a further dimension in the stimulus-secretion coupling of glucose-induced insulin release. | 2002 | 24 |
| 10 | 2001 | 16 | |
| 11 | 2006 | 1 |
About David Caton
David Caton is a scholar working on Molecular Biology, Surgery, Genetics, Physiology and Cell Biology, having authored 11 papers that have together received 949 indexed citations. Recurring topics across this work include Connexins and lens biology (5 papers), Mesenchymal stem cell research (4 papers), Pancreatic function and diabetes (4 papers), Nicotinic Acetylcholine Receptors Study (2 papers), Adipose Tissue and Metabolism (2 papers), Electrospun Nanofibers in Biomedical Applications (1 paper), Muscle Physiology and Disorders (1 paper) and Endoplasmic Reticulum Stress and Disease (1 paper). The work is most often cited by research in Genetics (428 citations), Surgery (377 citations), Urology (48 citations), Endocrine and Autonomic Systems (52 citations) and Physiology (173 citations). David Caton has collaborated with scholars based in Switzerland, France and United States. Frequent co-authors include Béatrice Cousin, Louis Casteilla, Alessandra Calabrese, Luc Pénicaud, Paolo Meda, Danièle Noël, Stéphane Roche, Sylvain Lehmann, Christian Jørgensen and Mireille André. Their work appears in journals such as Experimental Cell Research, Cell Communication & Adhesion, PROTEOMICS, Journal of Cellular Physiology and Journal of Cell Science.
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.