Shelya X. Zeng
- Oncology top 2%
- Cancer-related Molecular Pathways 45
- Cancer Research top 5%
- Cancer, Hypoxia, and Metabolism 8
- Molecular Biology top 5%
- RNA modifications and cancer 19
- Ubiquitin and proteasome pathways 16
- Epigenetics and DNA Methylation 12
- DNA Repair Mechanisms 7
- RNA Research and Splicing 6
- Geriatrics and Gerontology top 5%
- Biotechnology top 5%
- Cancer Research and Treatments 6
- Journals
- Proceedings of the National Academy of Sciences (1 paper)Journal of Biological Chemistry (10 papers)Nature Communications (1 paper)
- Partner nations
- United StatesChinaSouth Korea
In The Last Decade
Shelya X. Zeng
59 papers receiving 2.2k citations
Peers
Comparison fields: 5 of 100
- Oncology 999
- Cancer Research 508
- Molecular Biology 1.7k
- Geriatrics and Gerontology 91
- Biotechnology 135
Countries citing papers authored by Shelya X. Zeng
This map shows the geographic impact of Shelya X. Zeng'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 Shelya X. Zeng with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Shelya X. Zeng more than expected).
Fields of papers citing papers by Shelya X. Zeng
This network shows the impact of papers produced by Shelya X. Zeng. 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 Shelya X. Zeng. The network helps show where Shelya X. Zeng may publish in the future.
Co-authorship network
The 25 scholars most cited alongside Shelya X. Zeng, 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 | 2025 | 0 | |
| 2 | 2025 | 2 | |
| 3 | 2025 | 0 | |
| 4 | 2021 | 13 | |
| 5 | 2021 | 2 | |
| 6 | MCTS1 Directly Binds to TWF1 and Synergistically Modulate Cyclin D1 and C-Myc Translation in Luminal A/B Breast Cancer Cells | 2020 | 3 |
| 7 | 2020 | 30 | |
| 8 | 2017 | 19 | |
| 9 | 2017 | 15 | |
| 10 | 2016 | 33 | |
| 11 | 2016 | 13 | |
| 12 | 2015 | 13 | |
| 13 | 2014 | 12 | |
| 14 | 2012 | 24 | |
| 15 | 2012 | 16 | |
| 16 | 2009 | 19 | |
| 17 | 2007 | 58 | |
| 18 | 2006 | 47 | |
| 19 | 2005 | 39 | |
| 20 | 2004 | 409 |
About Shelya X. Zeng
Shelya X. Zeng is a scholar working on Oncology, Cancer Research and Molecular Biology, having authored 61 papers that have together received 2.2k indexed citations. Recurring topics across this work include Cancer-related Molecular Pathways (45 papers), RNA modifications and cancer (19 papers), Ubiquitin and proteasome pathways (16 papers), Epigenetics and DNA Methylation (12 papers), Cancer, Hypoxia, and Metabolism (8 papers), DNA Repair Mechanisms (7 papers), Cancer Research and Treatments (6 papers) and RNA Research and Splicing (6 papers). The work is most often cited by research in Oncology (999 citations), Cancer Research (508 citations) and Molecular Biology (1.7k citations). Shelya X. Zeng has collaborated with scholars based in United States, China and South Korea. Frequent co-authors include Hua Lu, Yetao Jin, Mu‐Shui Dai, Xiao‐Xin Sun, Larry L. David, Xiang Zhou, Peng Liao, Qi Zhang, Jun‐Ming Liao and Yu Zhang. Their work appears in journals such as Proceedings of the National Academy of Sciences, Journal of Biological Chemistry and Nature Communications.
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.