Beth Apsel
Impact in
- Molecular Biology top 10%
- PI3K/AKT/mTOR signaling in cancer
- Protein Kinase Regulation and GTPase Signaling
- Polyamine Metabolism and Applications
- Genetics top 10%
- Chronic Lymphocytic Leukemia Research
Papers in ⓘ
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- PI3K/AKT/mTOR signaling in cancer 3
- Polyamine Metabolism and Applications 1
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- Inflammatory mediators and NSAID effects 2
- Co-authors
- Kevan M. Shokat (3 shared papers)Zachary A. Knight (3 shared papers)Morris E. Feldman (1 shared paper)Davide Ruggero (1 shared paper)Robbie Loewith (1 shared paper)Randy Hoffman (1 shared paper)Roger Williams (1 shared paper)Tamim Nazif (1 shared paper)
- Journals
- The Journal of Immunology (1 paper)British Journal of Pharmacology (1 paper)PLoS Biology (1 paper)Nature Chemical Biology (1 paper)Tetrahedron Letters (1 paper)
- Partner nations
- United StatesSwitzerlandSpain
In The Last Decade
Beth Apsel
7 papers receiving 1.5k citations
Hit Papers
Peers
Comparison fields: 5 of 89
- Molecular Biology 1.1k
- Genetics 133
- Hematology 94
- Immunology 161
- Cancer Research 113
Countries citing papers authored by Beth Apsel
This map shows the geographic impact of Beth Apsel'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 Beth Apsel with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Beth Apsel more than expected).
Fields of papers citing papers by Beth Apsel
This network shows the impact of papers produced by Beth Apsel. 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 Beth Apsel. The network helps show where Beth Apsel may publish in the future.
Co-authors
The 25 scholars most cited alongside Beth Apsel, 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 | Active-Site Inhibitors of mTOR Target Rapamycin-Resistant Outputs of mTORC1 and mTORC2 Hit paper breakdown → | 2009 | 889 |
| 2 | 2008 | 339 | |
| 3 | 2006 | 91 | |
| 4 | 2008 | 76 | |
| 5 | 2003 | 71 | |
| 6 | 2003 | 38 | |
| 7 | 2004 | 16 |
About Beth Apsel
Beth Apsel is a scholar working on Molecular Biology, Pharmacology, Organic Chemistry, Genetics and Immunology, having authored 7 papers that have together received 1.5k indexed citations. Recurring topics across this work include PI3K/AKT/mTOR signaling in cancer (3 papers), Inflammatory mediators and NSAID effects (2 papers), Chronic Lymphocytic Leukemia Research (2 papers), NF-κB Signaling Pathways (2 papers), Polyamine Metabolism and Applications (1 paper), Mast cells and histamine (1 paper), Synthetic Organic Chemistry Methods (1 paper) and Synthesis and Biological Evaluation (1 paper). The work is most often cited by research in Molecular Biology (1.1k citations), Genetics (133 citations), Hematology (94 citations), Immunology (161 citations) and Cancer Research (113 citations). Beth Apsel has collaborated with scholars based in United States, Switzerland and Spain. Frequent co-authors include Kevan M. Shokat, Zachary A. Knight, Morris E. Feldman, Davide Ruggero, Robbie Loewith, Randy Hoffman, Roger Williams, Tamim Nazif, Jimmy A. Blair and Beatriz González. Their work appears in journals such as The Journal of Immunology, British Journal of Pharmacology, PLoS Biology, Nature Chemical Biology and Tetrahedron Letters.
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.