Daryl T. Baldwin
- Molecular Biology top 2%
- Immunology top 1%
- Cancer Research top 2%
- Oncology top 5%
- Epidemiology top 10%
- Co-authors
- Austin GurneyAudrey D. GoddardPaul J. GodowskiScot A. MarstersRobert PittiAvi AshkenaziWilliam I. WoodJames P. Sheridan
- Topics
- Cell death mechanisms and regulation (5 papers)NF-κB Signaling Pathways (5 papers)interferon and immune responses (4 papers)
- Partner nations
- United StatesFrance
In The Last Decade
Daryl T. Baldwin
10 papers receiving 3.8k citations
Hit Papers
Peers
Comparison fields: 5 of 106
- Molecular Biology 2.5k
- Immunology 2.0k
- Cancer Research 915
- Oncology 824
- Epidemiology 438
Countries citing papers authored by Daryl T. Baldwin
This map shows the geographic impact of Daryl T. Baldwin'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 Daryl T. Baldwin with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Daryl T. Baldwin more than expected).
Fields of papers citing papers by Daryl T. Baldwin
This network shows the impact of papers produced by Daryl T. Baldwin. 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 Daryl T. Baldwin. The network helps show where Daryl T. Baldwin may publish in the future.
Co-authorship network of co-authors of Daryl T. Baldwin
This figure shows the co-authorship network connecting the top 25 collaborators of Daryl T. Baldwin. A scholar is included among the top collaborators of Daryl T. Baldwin based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Daryl T. Baldwin. Daryl T. Baldwin is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 268 | |
| 2 | 328 | |
| 3 | 171 | |
| 4 | 81 | |
| 5 | 152 | |
| 6 | 197 | |
| 7 | Genomic amplification of a decoy receptor for Fas ligand in lung and colon cancerbreakdown → | 645 |
| 8 | A novel receptor for Apo2L/TRAIL contains a truncated death domainbreakdown → | 557 |
| 9 | Control of TRAIL-Induced Apoptosis by a Family of Signaling and Decoy Receptorsbreakdown → | 1474 |
| 10 | Regulation of IL-3, IL-4 and GM-CSF genes and signal transduction by their receptors. | 4 |
About Daryl T. Baldwin
Daryl T. Baldwin is a scholar working on Immunology, Cancer Research and Immunology and Allergy, having authored 10 papers that have together received 3.9k indexed citations. Recurring topics across this work include Cell death mechanisms and regulation (5 papers), NF-κB Signaling Pathways (5 papers) and interferon and immune responses (4 papers). The work is most often cited by research in Immunology (2.0k citations), Cancer Research (915 citations) and Molecular Biology (2.5k citations). Daryl T. Baldwin has collaborated with scholars based in United States and France. Frequent co-authors include Austin Gurney, Audrey D. Goddard, Paul J. Godowski, Scot A. Marsters, Robert Pitti, Avi Ashkenazi, William I. Wood, James P. Sheridan, Kevin P. Baker and Arthur Huang. Their work appears in journals such as Nature, Science 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.