Gustav Hagen
- Molecular Biology top 5%
- RNA Research and Splicing 2
- Genomics and Chromatin Dynamics 2
- RNA modifications and cancer 1
- RNA regulation and disease 1
- Virology top 5%
- HIV Research and Treatment 1
- Immunology top 10%
- Reproductive System and Pregnancy 2
- Immunology and Allergy top 10%
- Genetics top 10%
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- Reproductive Biology and Fertility 1
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- Erythrocyte Function and Pathophysiology 1
- Co-authors
- Guntram SuskeMiguel BeatoSusanne MüllerJörg DennigBarbara MajelloPasquale De LucaLuigi LaniaAnette Preiss
- Cited by
- Molecular BiologyVirologyImmunology
- Journals
- Nucleic Acids Research (3 papers)Journal of Biological Chemistry (2 papers)Annals of the New York Academy of Sciences (1 paper)
- Partner nations
- GermanyUnited StatesAustria
In The Last Decade
Gustav Hagen
8 papers receiving 1.8k citations
Hit Papers
Peers
Comparison fields: 5 of 82
- Molecular Biology 1.3k
- Virology 82
- Immunology 266
- Immunology and Allergy 72
- Genetics 304
Countries citing papers authored by Gustav Hagen
This map shows the geographic impact of Gustav Hagen'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 Gustav Hagen with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Gustav Hagen more than expected).
Fields of papers citing papers by Gustav Hagen
This network shows the impact of papers produced by Gustav Hagen. 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 Gustav Hagen. The network helps show where Gustav Hagen may publish in the future.
Co-authorship network
The 15 scholars most cited alongside Gustav Hagen, 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 | 1995 | 195 | |
| 2 | 1995 | 101 | |
| 3 | 1994 | 210 | |
| 4 | Sp1-mediated transcriptional activation is repressed by Sp3.breakdown → | 1994 | 653 |
| 5 | Cloning by recognition site screening of two novel GT box binding proteins: a family of Sp1 related genesbreakdown → | 1992 | 530 |
| 6 | 1991 | 8 | |
| 7 | 1990 | 87 | |
| 8 | 1954 | 1 |
About Gustav Hagen
Gustav Hagen is a scholar working on Virology, Immunology and Molecular Biology, having authored 8 papers that have together received 1.8k indexed citations. Recurring topics across this work include Reproductive System and Pregnancy (2 papers), RNA Research and Splicing (2 papers), Genomics and Chromatin Dynamics (2 papers), RNA modifications and cancer (1 paper), HIV Research and Treatment (1 paper), RNA regulation and disease (1 paper), Reproductive Biology and Fertility (1 paper) and Erythrocyte Function and Pathophysiology (1 paper). The work is most often cited by research in Molecular Biology (1.3k citations), Virology (82 citations) and Immunology (266 citations). Gustav Hagen has collaborated with scholars based in Germany, United States and Austria. Frequent co-authors include Guntram Suske, Miguel Beato, Susanne Müller, Jörg Dennig, Barbara Majello, Pasquale De Luca, Luigi Lania, Anette Preiss, Markus Wolf and Sikandar L. Katyal. Their work appears in journals such as Nucleic Acids Research, Journal of Biological Chemistry, Annals of the New York Academy of Sciences, Chemie Ingenieur Technik 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.