Eugene E. Quist

865 citations
32 papers · 818 · h-index 15

Impact in

  • Physiology top 10%
    • Erythrocyte Function and Pathophysiology
    • Ion channel regulation and function
    • Lipid Membrane Structure and Behavior
    • Protein Kinase Regulation and GTPase Signaling
    • Receptor Mechanisms and Signaling

Papers in

Eugene E. Quist

31 papers receiving 730 citations

Peers

Eugene E. Quist
Comparison fields: 5 of 102
  • Physiology 266
  • Physiology 43
  • Molecular Biology 431
  • Cell Biology 94
  • Pharmacology 77
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Citations per field
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Citations per year

Countries citing papers authored by Eugene E. Quist

Since Specialization
Citations

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

Fields of papers citing papers by Eugene E. Quist

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authors

The 22 scholars most cited alongside Eugene E. Quist, 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 Eugene E. Quist Line = papers co-authored together Eugene E. Quist links everyone, so they are left out of the graph.

All Works

20 of 20 papers shown

Showing the 20 most-cited of 32 papers — load more, or switch the sort, to bring in the rest.

#Work
1 1980145
2 197590
3 197568
4 197267
5 197853
6 198045
7 198237
8 197735
9 198927
10 199424
11 197622
12 198320
13 198320
14 198319
15 198516
16 198215
17 197314
18 198014
19 198513
20 199411

About Eugene E. Quist

Eugene E. Quist is a scholar working on Physiology, Cardiology and Cardiovascular Medicine, Molecular Biology, Cell Biology and Surgery, having authored 32 papers that have together received 818 indexed citations. Recurring topics across this work include Erythrocyte Function and Pathophysiology (11 papers), Ion channel regulation and function (7 papers), Pancreatic function and diabetes (7 papers), Cardiac electrophysiology and arrhythmias (6 papers), Protein Kinase Regulation and GTPase Signaling (5 papers), Receptor Mechanisms and Signaling (4 papers), Cellular transport and secretion (3 papers) and Cardiovascular Function and Risk Factors (2 papers). The work is most often cited by research in Physiology (266 citations), Physiology (43 citations), Molecular Biology (431 citations), Cell Biology (94 citations) and Pharmacology (77 citations). Eugene E. Quist has collaborated with scholars based in United States and Canada. Frequent co-authors include Basil D. Roufogalis, Lowell E. Hokin, Nimman Satumtira, Patricia A. Powell, Robert J. Zeleznikar, Lester R. Drewes, Thomas J. FitzGerald, V. Wickson, Lillian A. Repesh and Donna L. Coyle. Their work appears in journals such as Archives of Biochemistry and Biophysics, Biochemical and Biophysical Research Communications, Molecular Pharmacology, Biochemical Pharmacology and Journal of Cardiovascular Pharmacology.

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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