Beate Enigk

679 citations
15 papers · 559 · h-index 14

Impact in

Papers in

    • TGF-β signaling in diseases 2
    • Peroxisome Proliferator-Activated Receptors 1
    • Epigenetics and DNA Methylation 1
    • FOXO transcription factor regulation 1
    • Genetic Associations and Epidemiology 4

Beate Enigk

15 papers receiving 551 citations

Peers

Beate Enigk
Comparison fields: 5 of 67
  • Endocrine and Autonomic Systems 45
  • Biochemistry 33
  • Physiology 134
  • Epidemiology 133
  • Endocrinology, Diabetes and Metabolism 63
Replace Marie S. Isidor with:
Marie S. Isidor Denmark
Gerard C. van der Zon Netherlands
F. Lasnier France
Isabelle Scerri Switzerland
Michaela Keuper Germany
Xuelin Cui United States
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Citations per field
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Citations per year

Countries citing papers authored by Beate Enigk

Since Specialization
Citations

This map shows the geographic impact of Beate Enigk'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 Beate Enigk with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Beate Enigk more than expected).

Fields of papers citing papers by Beate Enigk

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Beate Enigk. 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 Beate Enigk. The network helps show where Beate Enigk may publish in the future.

Co-authors

The 25 scholars most cited alongside Beate Enigk, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.

Border = papers with Beate Enigk Line = papers co-authored together Beate Enigk links everyone, so they are left out of the graph.

All Works

15 of 15 papers shown
#Work
1 200779
2 200969
3 200963
4 200656
5 200953
6 200648
7 201140
8 201131
9 200725
10 200920
11 200917
12 201017
13 200715
14 201113
15 201313

About Beate Enigk

Beate Enigk is a scholar working on Molecular Biology, Genetics, Endocrinology, Diabetes and Metabolism, Endocrine and Autonomic Systems and Epidemiology, having authored 15 papers that have together received 559 indexed citations. Recurring topics across this work include Genetic Associations and Epidemiology (4 papers), TGF-β signaling in diseases (2 papers), Diabetes Treatment and Management (2 papers), Adipokines, Inflammation, and Metabolic Diseases (2 papers), Peroxisome Proliferator-Activated Receptors (1 paper), Circadian rhythm and melatonin (1 paper), Epigenetics and DNA Methylation (1 paper) and FOXO transcription factor regulation (1 paper). The work is most often cited by research in Endocrine and Autonomic Systems (45 citations), Biochemistry (33 citations), Physiology (134 citations), Epidemiology (133 citations) and Endocrinology, Diabetes and Metabolism (63 citations). Beate Enigk has collaborated with scholars based in Germany, United States and United Kingdom. Frequent co-authors include Péter Kovács, Michael Stümvoll, Yvonne Böttcher, Anke Tönjes, Matthias Blüher, Dorit Schleinitz, Nora Klöting, Kerstin Dietrich, Antje Körner and Wieland Kieß. Their work appears in journals such as Diabetes, The Journal of Clinical Endocrinology & Metabolism, Pharmacogenomics, Diabetic Medicine and PLoS ONE.

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.

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