Michael Willenbrock

432 citations
5 papers · 191 · h-index 4

Impact in

Papers in

    • Cell death mechanisms and regulation 1
    • Wnt/β-catenin signaling in development and cancer 1
    • Mitochondrial Function and Pathology 1
    • NF-κB Signaling Pathways 3

Michael Willenbrock

5 papers receiving 189 citations

Peers

Michael Willenbrock
Comparison fields: 5 of 53
  • Immunology and Allergy 53
  • Aging 5
  • Physiology 47
  • Cell Biology 29
  • Molecular Biology 115
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Pei-Chieh Tien United States
G. Vuagniaux Switzerland
Sonia Rodríguez‐Fdez Spain
Ellen L. van Agtmaal Netherlands
Marina Badenes Portugal
Jesús Gómez-Escudero Spain
Rebecca L. Daugherty United States
T.C. Lee United States
Federica Fusella Italy
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Citations per field
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Pei-Chieh Tien · 1×
Citations per year

Countries citing papers authored by Michael Willenbrock

Since Specialization
Citations

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

Fields of papers citing papers by Michael Willenbrock

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authors

The 25 scholars most cited alongside Michael Willenbrock, 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 Michael Willenbrock Line = papers co-authored together Michael Willenbrock links everyone, so they are left out of the graph.

All Works

5 of 5 papers shown
#Work
1 201289
2 202151
3 201943
4 20235
5 20233

About Michael Willenbrock

Michael Willenbrock is a scholar working on Molecular Biology, Cancer Research, Immunology, Critical Care and Intensive Care Medicine and Neurology, having authored 5 papers that have together received 191 indexed citations. Recurring topics across this work include NF-κB Signaling Pathways (3 papers), Immune Response and Inflammation (2 papers), Cell death mechanisms and regulation (1 paper), PARP inhibition in cancer therapy (1 paper), Monoclonal and Polyclonal Antibodies Research (1 paper), Wnt/β-catenin signaling in development and cancer (1 paper), Parkinson's Disease Mechanisms and Treatments (1 paper) and Mitochondrial Function and Pathology (1 paper). The work is most often cited by research in Immunology and Allergy (53 citations), Aging (5 citations), Physiology (47 citations), Cell Biology (29 citations) and Molecular Biology (115 citations). Michael Willenbrock has collaborated with scholars based in Germany and Moldova. Frequent co-authors include Dirk Schmidt‐Arras, Johannes Prox, Ralf Schwanbeck, Paul Säftig, Tobias Lehmann, Michael Schwake, Silvio Weber, Claus Scheidereit, Uta E. Höpken and Clemens A. Schmitt. Their work appears in journals such as iScience, The EMBO Journal, Cellular and Molecular Life Sciences, Journal of Cachexia Sarcopenia and Muscle and Cell chemical biology.

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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