Donat Kögel
Impact in
- Molecular Biology top 2%
- Cell death mechanisms and regulation
- RNA Interference and Gene Delivery
- Mitochondrial Function and Pathology
- Cell Biology top 1%
- Endoplasmic Reticulum Stress and Disease
Papers in
- Cell Biology 27
- Endoplasmic Reticulum Stress and Disease 19
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- Cancer, Hypoxia, and Metabolism 9
- Co-authors
- Jochen H.M. PrehnSimone FuldaVolker SeifertAbdelhaq RamiC. ReimertzK H ScheidtmannHeiko DüßmannBenedikt Linder
- Journals
- Cancers (6 papers)Oncogene (5 papers)Neuroscience (5 papers)Autophagy (4 papers)Journal of Biological Chemistry (4 papers)
- Partner nations
- GermanyIrelandUnited States
In The Last Decade
Donat Kögel
121 papers receiving 5.9k citations
Peers
Comparison fields: 5 of 141
- Molecular Biology 3.8k
- Cell Biology 911
- Cancer Research 771
- Physiology 177
- Epidemiology 1.3k
Countries citing papers authored by Donat Kögel
This map shows the geographic impact of Donat Kögel'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 Donat Kögel with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Donat Kögel more than expected).
Fields of papers citing papers by Donat Kögel
This network shows the impact of papers produced by Donat Kögel. 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 Donat Kögel. The network helps show where Donat Kögel may publish in the future.
Co-authors
The 25 scholars most cited alongside Donat Kögel, 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 | 2023 | 0 | |
| 2 | 2023 | 7 | |
| 3 | 2022 | 8 | |
| 4 | 2022 | 10 | |
| 5 | 2022 | 4 | |
| 6 | 2021 | 74 | |
| 7 | 2021 | 9 | |
| 8 | 2021 | 1 | |
| 9 | 2021 | 16 | |
| 10 | 2021 | 11 | |
| 11 | 2020 | 47 | |
| 12 | 2020 | 6 | |
| 13 | 2019 | 39 | |
| 14 | 2019 | 84 | |
| 15 | 2019 | 26 | |
| 16 | 2018 | 74 | |
| 17 | 2018 | 90 | |
| 18 | 2016 | 64 | |
| 19 | 2013 | 30 | |
| 20 | 2010 | 115 |
About Donat Kögel
Donat Kögel is a scholar working on Cell Biology, Cancer Research, Molecular Biology, Epidemiology and Genetics, having authored 122 papers that have together received 5.9k indexed citations. Recurring topics across this work include Cell death mechanisms and regulation (35 papers), Autophagy in Disease and Therapy (32 papers), Endoplasmic Reticulum Stress and Disease (19 papers), Alzheimer's disease research and treatments (15 papers), RNA Interference and Gene Delivery (10 papers), Glioma Diagnosis and Treatment (10 papers), Cancer, Hypoxia, and Metabolism (9 papers) and Mitochondrial Function and Pathology (7 papers). The work is most often cited by research in Molecular Biology (3.8k citations), Cell Biology (911 citations), Cancer Research (771 citations), Physiology (177 citations) and Epidemiology (1.3k citations). Donat Kögel has collaborated with scholars based in Germany, Ireland and United States. Frequent co-authors include Jochen H.M. Prehn, Simone Fulda, Volker Seifert, Abdelhaq Rami, C. Reimertz, K H Scheidtmann, Heiko Düßmann, Benedikt Linder, Markus Rehm and Hans‐Georg König. Their work appears in journals such as Cancers, Oncogene, Neuroscience, Autophagy 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.