John E. Pawlowski

25 papers receiving 1.2k citations

Peers

John E. Pawlowski
Comparison fields: 5 of 87
  • Cell Biology 376
  • Endocrinology, Diabetes and Metabolism 282
  • Biochemistry 76
  • Reproductive Medicine 79
  • Behavioral Neuroscience 31
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Citations per year

Countries citing papers authored by John E. Pawlowski

Since Specialization
Citations

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

Fields of papers citing papers by John E. Pawlowski

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by John E. Pawlowski. 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 John E. Pawlowski. The network helps show where John E. Pawlowski may publish in the future.

Co-authors

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

All Works

20 of 20 papers shown

Showing the 20 most-cited of 26 papers — load more, or switch the sort, to bring in the rest.

#Work
1 2002151
2 1991139
3 1994126
4 199998
5 198880
6 199677
7 199472
8 199971
9 199659
10 200456
11 199754
12 200747
13 200242
14 199132
15 199228
16
NF-kappa B does not modulate sensitivity of renal carcinoma cells to TNF alpha-related apoptosis-inducing ligand (TRAIL).
200126
17
Rat dihydrodiol dehydrogenase: complexity of gene structure and tissue-specific and sexually dimorphic gene expression.
199419
18 199113
19 199411
20 20229

About John E. Pawlowski

John E. Pawlowski is a scholar working on Molecular Biology, Cell Biology, Endocrinology, Diabetes and Metabolism, Epidemiology and Immunology, having authored 26 papers that have together received 1.2k indexed citations. Recurring topics across this work include Aldose Reductase and Taurine (8 papers), Hormonal Regulation and Hypertension (5 papers), Ovarian function and disorders (2 papers), Reproductive System and Pregnancy (2 papers), Cancer-related gene regulation (2 papers), Herpesvirus Infections and Treatments (2 papers), Hypothalamic control of reproductive hormones (2 papers) and Diet, Metabolism, and Disease (2 papers). The work is most often cited by research in Cell Biology (376 citations), Endocrinology, Diabetes and Metabolism (282 citations), Biochemistry (76 citations), Reproductive Medicine (79 citations) and Behavioral Neuroscience (31 citations). John E. Pawlowski has collaborated with scholars based in United States, Germany and Poland. Frequent co-authors include T.M. Penning, Margaret E. Wierman, Susan S. Hoog, Melissa P. Allen, David S. Taylor, Christopher J. Molloy, Pedro M. Alzari, Mary Lewis, Mei Xu and Elizabeth M. Wilson. Their work appears in journals such as Journal of Biological Chemistry, Inflammation Research, Journal of Clinical Investigation, Proceedings of the National Academy of Sciences and Endocrinology.

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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