James M. Willard

647 citations
23 papers · 519 · h-index 15

Impact in

Papers in

    • Receptor Mechanisms and Signaling 4
    • Enzyme function and inhibition 4
    • Ion channel regulation and function 3
    • Biochemical Acid Research Studies 3
    • Amino Acid Enzymes and Metabolism 2

James M. Willard

23 papers receiving 447 citations

Peers

James M. Willard
Comparison fields: 5 of 75
  • Biochemistry 70
  • Clinical Biochemistry 38
  • Agronomy and Crop Science 54
  • Cellular and Molecular Neuroscience 89
  • Molecular Biology 308
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Countries citing papers authored by James M. Willard

Since Specialization
Citations

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

Fields of papers citing papers by James M. Willard

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by James M. Willard. 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 James M. Willard. The network helps show where James M. Willard may publish in the future.

Co-authors

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

All Works

20 of 20 papers shown

Showing the 20 most-cited of 23 papers — load more, or switch the sort, to bring in the rest.

#Work
1 199570
2 196957
3 196947
4 200838
5 199035
6 196835
7 199229
8 199124
9 196823
10 201420
11 202219
12 196918
13 196515
14 199214
15 196914
16 197214
17 197313
18 199210
19 197110
20 19756

About James M. Willard

James M. Willard is a scholar working on Molecular Biology, Biochemistry, Cellular and Molecular Neuroscience, Nutrition and Dietetics and Cell Biology, having authored 23 papers that have together received 519 indexed citations. Recurring topics across this work include Neuroscience and Neuropharmacology Research (4 papers), Receptor Mechanisms and Signaling (4 papers), Enzyme function and inhibition (4 papers), Biochemical Acid Research Studies (3 papers), Microbial Metabolites in Food Biotechnology (3 papers), Ion channel regulation and function (3 papers), Metabolism and Genetic Disorders (2 papers) and Amino Acid Enzymes and Metabolism (2 papers). The work is most often cited by research in Biochemistry (70 citations), Clinical Biochemistry (38 citations), Agronomy and Crop Science (54 citations), Cellular and Molecular Neuroscience (89 citations) and Molecular Biology (308 citations). James M. Willard has collaborated with scholars based in United States and Israel. Frequent co-authors include Harland G. Wood, Martin Gibbs, Robert E. Oswald, J. N. Stellflug, D. R. White, R.G. Sasser, Irwin A. Rose, Janet L. Schottel, Naomi L. Kruhlak and Edward L. O'Connell. Their work appears in journals such as Biochemistry, Journal of Biological Chemistry, Journal of Animal Science, Molecular Pharmacology and PLANT PHYSIOLOGY.

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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