David E. Nowak
Impact in
- Cancer Research top 10%
- NF-κB Signaling Pathways
- Immunology top 10%
- Immune Response and Inflammation
- interferon and immune responses
- Immune Cell Function and Interaction
Papers in
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- NF-κB Signaling Pathways 4
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- Ion Transport and Channel Regulation 2
- Genomics and Chromatin Dynamics 1
- Receptor Mechanisms and Signaling 1
- Ion channel regulation and function 1
- Co-authors
- Bing Tian (5 shared papers)Allan R. Brasier (5 shared papers)Mohammad Jamaluddin (2 shared papers)Shaofei Wang (1 shared paper)István Boldogh (1 shared paper)Leoncio Vergara (1 shared paper)Sanjeev Choudhary (1 shared paper)Xinhua Li (1 shared paper)
- Journals
- FEBS Journal (1 paper)BMC Genomics (1 paper)Journal of Theoretical Biology (1 paper)BioTechniques (1 paper)Journal of Biological Chemistry (1 paper)
- Partner nations
- United StatesAustraliaPoland
In The Last Decade
David E. Nowak
7 papers receiving 823 citations
Peers
Comparison fields: 5 of 84
- Cancer Research 256
- Immunology 289
- Molecular Biology 445
- Oncology 129
- Aging 7
Countries citing papers authored by David E. Nowak
This map shows the geographic impact of David E. Nowak'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 David E. Nowak with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites David E. Nowak more than expected).
Fields of papers citing papers by David E. Nowak
This network shows the impact of papers produced by David E. Nowak. 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 David E. Nowak. The network helps show where David E. Nowak may publish in the future.
Co-authors
The 19 scholars most cited alongside David E. Nowak, 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 | 2005 | 224 | |
| 2 | 2005 | 205 | |
| 3 | 2008 | 160 | |
| 4 | 2005 | 158 | |
| 5 | 2000 | 59 | |
| 6 | 2004 | 21 | |
| 7 | 2012 | 3 |
About David E. Nowak
David E. Nowak is a scholar working on Cancer Research, Molecular Biology, Immunology, Oncology and Pediatrics, Perinatology and Child Health, having authored 7 papers that have together received 830 indexed citations. Recurring topics across this work include NF-κB Signaling Pathways (4 papers), Immune Response and Inflammation (3 papers), Ion Transport and Channel Regulation (2 papers), Cytokine Signaling Pathways and Interactions (2 papers), Genomics and Chromatin Dynamics (1 paper), Receptor Mechanisms and Signaling (1 paper), Ion channel regulation and function (1 paper) and Ion Channels and Receptors (1 paper). The work is most often cited by research in Cancer Research (256 citations), Immunology (289 citations), Molecular Biology (445 citations), Oncology (129 citations) and Aging (7 citations). David E. Nowak has collaborated with scholars based in United States, Australia and Poland. Frequent co-authors include Bing Tian, Allan R. Brasier, Mohammad Jamaluddin, Shaofei Wang, István Boldogh, Leoncio Vergara, Sanjeev Choudhary, Xinhua Li, Steven A. Weinman and Lori Showalter. Their work appears in journals such as FEBS Journal, BMC Genomics, Journal of Theoretical Biology, BioTechniques 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.