Sara Caldarola
- Reproductive Medicine top 5%
- Molecular Biology top 10%
- RNA and protein synthesis mechanisms 6
- RNA modifications and cancer 5
- RNA Research and Splicing 4
- PI3K/AKT/mTOR signaling in cancer 3
- Muscle Physiology and Disorders 2
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- Peptidase Inhibition and Analysis 3
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- Autophagy in Disease and Therapy 3
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- Cancer Mechanisms and Therapy 3
- Co-authors
- Fabrizio LoreniFrancesco AmaldiValentina IadevaiaGianni CesareniStefano CannataStefania GonfloniMaurizio MatteiFrancesca Gioia Klinger
- Partner nations
- ItalyUnited KingdomDenmark
In The Last Decade
Sara Caldarola
19 papers receiving 1.1k citations
Peers
Comparison fields: 5 of 87
- Reproductive Medicine 126
- Molecular Biology 704
- Cancer Research 142
- Oncology 191
- Epidemiology 224
Countries citing papers authored by Sara Caldarola
This map shows the geographic impact of Sara Caldarola'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 Sara Caldarola with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Sara Caldarola more than expected).
Fields of papers citing papers by Sara Caldarola
This network shows the impact of papers produced by Sara Caldarola. 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 Sara Caldarola. The network helps show where Sara Caldarola may publish in the future.
Co-authorship network
The 25 scholars most cited alongside Sara Caldarola, 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 | 2018 | 4 | |
| 2 | 2016 | 20 | |
| 3 | 2016 | 15 | |
| 4 | 2015 | 247 | |
| 5 | Autophagy induction impairs migration and invasion by reversing EMT in human glioblastoma cells | 2015 | 2 |
| 6 | 2014 | 35 | |
| 7 | 2014 | 36 | |
| 8 | 2013 | 39 | |
| 9 | 2012 | 96 | |
| 10 | 2010 | 16 | |
| 11 | 2010 | 49 | |
| 12 | 2009 | 269 | |
| 13 | 2009 | 43 | |
| 14 | 2008 | 86 | |
| 15 | 2005 | 39 | |
| 16 | 2005 | 12 | |
| 17 | 2004 | 13 | |
| 18 | 2004 | 30 | |
| 19 | 2004 | 17 |
About Sara Caldarola
Sara Caldarola is a scholar working on Molecular Biology, Pathology and Forensic Medicine and Cellular and Molecular Neuroscience, having authored 19 papers that have together received 1.1k indexed citations. Recurring topics across this work include RNA and protein synthesis mechanisms (6 papers), RNA modifications and cancer (5 papers), RNA Research and Splicing (4 papers), Cancer Mechanisms and Therapy (3 papers), PI3K/AKT/mTOR signaling in cancer (3 papers), Autophagy in Disease and Therapy (3 papers), Peptidase Inhibition and Analysis (3 papers) and Muscle Physiology and Disorders (2 papers). The work is most often cited by research in Reproductive Medicine (126 citations), Molecular Biology (704 citations) and Cancer Research (142 citations). Sara Caldarola has collaborated with scholars based in Italy, United Kingdom and Denmark. Frequent co-authors include Fabrizio Loreni, Francesco Amaldi, Valentina Iadevaia, Gianni Cesareni, Stefano Cannata, Stefania Gonfloni, Maurizio Mattei, Francesca Gioia Klinger, Claudia Di Bartolomeo and Gerry Melino. Their work appears in journals such as FEBS Journal, Oncotarget, Molecular Oncology, Nature Medicine and Scientific Reports.
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.