Ameeta Kelekar
- Physiology top 1%
- Cancer Research top 5%
- Cancer, Hypoxia, and Metabolism 6
- Molecular Biology top 5%
- Cell death mechanisms and regulation 13
- RNA Interference and Gene Delivery 3
- Metabolism, Diabetes, and Cancer 3
- Immunology top 5%
- Immune Cell Function and Interaction 4
- Epidemiology top 5%
- Autophagy in Disease and Therapy 8
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- Cancer-related Molecular Pathways 6
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- Virus-based gene therapy research 5
- Co-authors
- Craig B. ThompsonMichael D. ColeMaura McDonnellMd. Joynal AbedinUte LehmannIndira V. SubramanianJohn E. HarlanBrian S. Chang
- Partner nations
- United StatesJapanSpain
In The Last Decade
Ameeta Kelekar
43 papers receiving 3.5k citations
Hit Papers
Peers
Comparison fields: 5 of 116
- Physiology 207
- Cancer Research 514
- Molecular Biology 2.3k
- Immunology 632
- Epidemiology 864
Countries citing papers authored by Ameeta Kelekar
This map shows the geographic impact of Ameeta Kelekar'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 Ameeta Kelekar with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Ameeta Kelekar more than expected).
Fields of papers citing papers by Ameeta Kelekar
This network shows the impact of papers produced by Ameeta Kelekar. 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 Ameeta Kelekar. The network helps show where Ameeta Kelekar may publish in the future.
Co-authorship network
The 25 scholars most cited alongside Ameeta Kelekar, 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 | 19 | |
| 2 | 2018 | 193 | |
| 3 | 2017 | 81 | |
| 4 | 2017 | 24 | |
| 5 | EGLN1 Inhibition and Rerouting of α-Ketoglutarate Suffice for Remote Ischemic Protection | 2016 | 1 |
| 6 | 2016 | 107 | |
| 7 | 2016 | 33 | |
| 8 | 2015 | 7 | |
| 9 | 2015 | 13 | |
| 10 | 2011 | 90 | |
| 11 | 2009 | 90 | |
| 12 | 2009 | 21 | |
| 13 | 2007 | 84 | |
| 14 | 2006 | 426 | |
| 15 | 2006 | 124 | |
| 16 | 2005 | 2 | |
| 17 | 2005 | 179 | |
| 18 | 2003 | 94 | |
| 19 | 2001 | 120 | |
| 20 | 1990 | 7 |
About Ameeta Kelekar
Ameeta Kelekar is a scholar working on Biological Psychiatry, Cancer Research and Oncology, having authored 43 papers that have together received 3.5k indexed citations. Recurring topics across this work include Cell death mechanisms and regulation (13 papers), Autophagy in Disease and Therapy (8 papers), Cancer-related Molecular Pathways (6 papers), Cancer, Hypoxia, and Metabolism (6 papers), Virus-based gene therapy research (5 papers), Immune Cell Function and Interaction (4 papers), RNA Interference and Gene Delivery (3 papers) and Metabolism, Diabetes, and Cancer (3 papers). The work is most often cited by research in Physiology (207 citations), Cancer Research (514 citations) and Molecular Biology (2.3k citations). Ameeta Kelekar has collaborated with scholars based in United States, Japan and Spain. Frequent co-authors include Craig B. Thompson, Michael D. Cole, Maura McDonnell, Md. Joynal Abedin, Ute Lehmann, Indira V. Subramanian, John E. Harlan, Brian S. Chang, Stephen W. Fesik and Sundaram Ramakrishnan. Their work appears in journals such as Nature, Cell 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.