Sébastien Nola
- Cell Biology top 5%
- Cellular transport and secretion 9
- Hippo pathway signaling and YAP/TAZ 5
- Endoplasmic Reticulum Stress and Disease 3
- Cellular Mechanics and Interactions 3
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- Wnt/β-catenin signaling in development and cancer 4
- Retinal Development and Disorders 3
- Receptor Mechanisms and Signaling 2
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- Autophagy in Disease and Therapy 3
- Co-authors
- Jean‐Paul BorgChristel NavarroMarie-Josée SantoniStéphane AudebertSylvie MarchettoDaniel IsnardonDaniel BirnbaumChristophe Ginestier
- Journals
- Journal of Biological Chemistry (2 papers)The Journal of Cell Biology (1 paper)The EMBO Journal (1 paper)
- Partner nations
- FranceUnited StatesArgentina
In The Last Decade
Sébastien Nola
18 papers receiving 590 citations
Peers
Comparison fields: 5 of 65
- Cell Biology 370
- Molecular Biology 443
- Physiology 24
- Aging 7
- Immunology and Allergy 23
Countries citing papers authored by Sébastien Nola
This map shows the geographic impact of Sébastien Nola'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 Sébastien Nola with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Sébastien Nola more than expected).
Fields of papers citing papers by Sébastien Nola
This network shows the impact of papers produced by Sébastien Nola. 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 Sébastien Nola. The network helps show where Sébastien Nola may publish in the future.
Co-authorship network
The 25 scholars most cited alongside Sébastien Nola, 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 | 2025 | 0 | |
| 2 | 2023 | 5 | |
| 3 | 2021 | 7 | |
| 4 | 2021 | 2 | |
| 5 | 2020 | 34 | |
| 6 | 2018 | 23 | |
| 7 | 2018 | 21 | |
| 8 | 2016 | 12 | |
| 9 | 2015 | 12 | |
| 10 | 2015 | 28 | |
| 11 | 2013 | 24 | |
| 12 | 2012 | 12 | |
| 13 | 2011 | 3 | |
| 14 | 2011 | 59 | |
| 15 | 2009 | 10 | |
| 16 | 2009 | 26 | |
| 17 | 2008 | 82 | |
| 18 | 2005 | 66 | |
| 19 | 2005 | 173 |
About Sébastien Nola
Sébastien Nola is a scholar working on Cell Biology, Physiology and Geriatrics and Gerontology, having authored 19 papers that have together received 599 indexed citations. Recurring topics across this work include Cellular transport and secretion (9 papers), Hippo pathway signaling and YAP/TAZ (5 papers), Wnt/β-catenin signaling in development and cancer (4 papers), Autophagy in Disease and Therapy (3 papers), Retinal Development and Disorders (3 papers), Endoplasmic Reticulum Stress and Disease (3 papers), Cellular Mechanics and Interactions (3 papers) and Receptor Mechanisms and Signaling (2 papers). The work is most often cited by research in Cell Biology (370 citations), Molecular Biology (443 citations) and Physiology (24 citations). Sébastien Nola has collaborated with scholars based in France, United States and Argentina. Frequent co-authors include Jean‐Paul Borg, Christel Navarro, Marie-Josée Santoni, Stéphane Audebert, Sylvie Marchetto, Daniel Isnardon, Daniel Birnbaum, Christophe Ginestier, André Le Bivic and Jean‐Pierre Arsanto. Their work appears in journals such as Journal of Biological Chemistry, The Journal of Cell Biology and The EMBO Journal.
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.