Jonathan Grim
Impact in
- Oncology top 5%
- Cancer-related Molecular Pathways
- Hematology top 5%
- Acute Myeloid Leukemia Research
Papers in
-
- Acute Myeloid Leukemia Research 2
- Oncology 4
- Peptidase Inhibition and Analysis 2
- Cancer-related Molecular Pathways 2
- Co-authors
- Bruce E. ClurmanMarkus WelckerAmir OrianRobert N. EisenmanJianping JinJ. Wade HarperKeith R. LoebJames M. Roberts
- Journals
- Genes & Development (1 paper)The Prostate (1 paper)Future Oncology (1 paper)Current Biology (1 paper)The Journal of Experimental Medicine (1 paper)
- Partner nations
- United StatesAustriaJapan
In The Last Decade
Jonathan Grim
9 papers receiving 2.1k citations
Hit Papers
Peers
Comparison fields: 5 of 81
- Oncology 766
- Hematology 283
- Molecular Biology 1.7k
- Cell Biology 331
- Genetics 159
Countries citing papers authored by Jonathan Grim
This map shows the geographic impact of Jonathan Grim'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 Jonathan Grim with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Jonathan Grim more than expected).
Fields of papers citing papers by Jonathan Grim
This network shows the impact of papers produced by Jonathan Grim. 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 Jonathan Grim. The network helps show where Jonathan Grim may publish in the future.
Co-authorship network
The 25 scholars most cited alongside Jonathan Grim, 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 | 2022 | 45 | |
| 2 | 2017 | 4 | |
| 3 | 2012 | 88 | |
| 4 | FBW7 mutations in leukemic cells mediate NOTCH pathway activation and resistance to γ-secretase inhibitors Hit paper breakdown → | 2007 | 523 |
| 5 | 2005 | 27 | |
| 6 | The Fbw7 tumor suppressor regulates glycogen synthase kinase 3 phosphorylation-dependent c-Myc protein degradation Hit paper breakdown → | 2004 | 756 |
| 7 | 2004 | 257 | |
| 8 | 2003 | 146 | |
| 9 | 2003 | 302 |
About Jonathan Grim
Jonathan Grim is a scholar working on Hematology, Oncology, Cell Biology, Genetics and Molecular Biology, having authored 9 papers that have together received 2.1k indexed citations. Recurring topics across this work include Ubiquitin and proteasome pathways (3 papers), Acute Myeloid Leukemia Research (2 papers), Peptidase Inhibition and Analysis (2 papers), Cancer-related Molecular Pathways (2 papers), RNA modifications and cancer (1 paper), DNA Repair Mechanisms (1 paper), Estrogen and related hormone effects (1 paper) and Antifungal resistance and susceptibility (1 paper). The work is most often cited by research in Oncology (766 citations), Hematology (283 citations), Molecular Biology (1.7k citations), Cell Biology (331 citations) and Genetics (159 citations). Jonathan Grim has collaborated with scholars based in United States, Austria and Japan. Frequent co-authors include Bruce E. Clurman, Markus Welcker, Amir Orian, Robert N. Eisenman, Jianping Jin, J. Wade Harper, Keith R. Loeb, James M. Roberts, Jeffrey D. Singer and Andrew Bloecher. Their work appears in journals such as Genes & Development, The Prostate, Future Oncology, Current Biology and The Journal of Experimental Medicine.
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.