Udo Maier
Impact in
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- Protein Kinase Regulation and GTPase Signaling
- PI3K/AKT/mTOR signaling in cancer
- Receptor Mechanisms and Signaling
- Ion channel regulation and function
- Metabolism, Diabetes, and Cancer
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- Chronic Lymphocytic Leukemia Research
Papers in
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- Protein Kinase Regulation and GTPase Signaling 5
- Ion channel regulation and function 1
- Cell death mechanisms and regulation 1
- Metabolism, Diabetes, and Cancer 1
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- Neuroscience and Neuropharmacology Research 2
- Co-authors
- Bernd Nürnberg (5 shared papers)А. Г. Бабич (2 shared papers)Torsten Exner (2 shared papers)Daniela Leopoldt (2 shared papers)Reinhard Wetzker (1 shared paper)Theodor Hanck (1 shared paper)Nathalie Macrez (2 shared papers)Jean Mironneau (1 shared paper)
In The Last Decade
Udo Maier
7 papers receiving 569 citations
Peers
Comparison fields: 5 of 53
- Molecular Biology 462
- Genetics 58
- Immunology and Allergy 32
- Cellular and Molecular Neuroscience 88
- Cell Biology 70
Countries citing papers authored by Udo Maier
This map shows the geographic impact of Udo Maier'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 Udo Maier with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Udo Maier more than expected).
Fields of papers citing papers by Udo Maier
This network shows the impact of papers produced by Udo Maier. 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 Udo Maier. The network helps show where Udo Maier may publish in the future.
Co-authors
The 25 scholars most cited alongside Udo Maier, 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 | 1999 | 194 | |
| 2 | 1998 | 171 | |
| 3 | 1999 | 102 | |
| 4 | 2000 | 67 | |
| 5 | 2006 | 24 | |
| 6 | 1999 | 14 | |
| 7 | 2024 | 1 | |
| 8 | 2025 | 0 |
About Udo Maier
Udo Maier is a scholar working on Molecular Biology, Cellular and Molecular Neuroscience, Oncology, Genetics and Computational Theory and Mathematics, having authored 8 papers that have together received 573 indexed citations. Recurring topics across this work include Protein Kinase Regulation and GTPase Signaling (5 papers), Neuroscience and Neuropharmacology Research (2 papers), Ion channel regulation and function (1 paper), Cell death mechanisms and regulation (1 paper), Peptidase Inhibition and Analysis (1 paper), Metabolism, Diabetes, and Cancer (1 paper), Cellular transport and secretion (1 paper) and Cancer-related Molecular Pathways (1 paper). The work is most often cited by research in Molecular Biology (462 citations), Genetics (58 citations), Immunology and Allergy (32 citations), Cellular and Molecular Neuroscience (88 citations) and Cell Biology (70 citations). Udo Maier has collaborated with scholars based in Germany, France and Portugal. Frequent co-authors include Bernd Nürnberg, А. Г. Бабич, Torsten Exner, Daniela Leopoldt, Reinhard Wetzker, Theodor Hanck, Nathalie Macrez, Jean Mironneau, Patricia Viard and Peter Gierschik. Their work appears in journals such as Journal of Biological Chemistry, Molecular Therapy — Methods & Clinical Development, European Journal of Cell Biology, The FASEB Journal and Combinatorial Chemistry & High Throughput Screening.
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.