Mingbiao Wei
Impact in
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- Colorectal Cancer Surgical Treatments
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- RNA Research and Splicing
- RNA modifications and cancer
- DNA Repair Mechanisms
- Epigenetics and DNA Methylation
- Genomics and Chromatin Dynamics
- CRISPR and Genetic Engineering
Papers in
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- DNA Repair Mechanisms 2
- Epigenetics and DNA Methylation 2
- Genomics and Chromatin Dynamics 1
- Glycosylation and Glycoproteins Research 1
- Cancer-related gene regulation 1
- Oncology 2
- Co-authors
- Xiang‐Bo Wan (4 shared papers)Yunlong Wang (3 shared papers)Lili Feng (3 shared papers)Weiwei Xiao (1 shared paper)Shu Zhang (1 shared paper)Hui Chang (1 shared paper)Li Li (1 shared paper)Yuanhong Gao (1 shared paper)
- Journals
- Nature Communications (1 paper)Clinical and Translational Medicine (1 paper)American Journal of Cancer Research (1 paper)Radiation Oncology (1 paper)Oncogene (1 paper)
- Partner nations
- ChinaTaiwanUnited States
In The Last Decade
Mingbiao Wei
6 papers receiving 132 citations
Peers
Comparison fields: 5 of 29
- Oncology 45
- Molecular Biology 72
- Cancer Research 13
- Biochemistry 5
- Immunology 8
Countries citing papers authored by Mingbiao Wei
This map shows the geographic impact of Mingbiao Wei'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 Mingbiao Wei with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Mingbiao Wei more than expected).
Fields of papers citing papers by Mingbiao Wei
This network shows the impact of papers produced by Mingbiao Wei. 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 Mingbiao Wei. The network helps show where Mingbiao Wei may publish in the future.
Co-authors
The 25 scholars most cited alongside Mingbiao Wei, 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 | 46 | |
| 2 | 2021 | 44 | |
| 3 | 2022 | 14 | |
| 4 | Glycosylation of Siglec15 promotes immunoescape and tumor growth. | 2021 | 13 |
| 5 | 2023 | 11 | |
| 6 | 2019 | 4 |
About Mingbiao Wei
Mingbiao Wei is a scholar working on Molecular Biology, Oncology, Pathology and Forensic Medicine, Biotechnology and Immunology, having authored 6 papers that have together received 132 indexed citations. Recurring topics across this work include DNA Repair Mechanisms (2 papers), Epigenetics and DNA Methylation (2 papers), Genomics and Chromatin Dynamics (1 paper), Glycosylation and Glycoproteins Research (1 paper), Cancer Research and Treatments (1 paper), Cancer-related gene regulation (1 paper), Galectins and Cancer Biology (1 paper) and Genetic factors in colorectal cancer (1 paper). The work is most often cited by research in Oncology (45 citations), Molecular Biology (72 citations), Cancer Research (13 citations), Biochemistry (5 citations) and Immunology (8 citations). Mingbiao Wei has collaborated with scholars based in China, Taiwan and United States. Frequent co-authors include Xiang‐Bo Wan, Yunlong Wang, Lili Feng, Weiwei Xiao, Shu Zhang, Hui Chang, Li Li, Yuanhong Gao, Mien‐Chie Hung and Caolitao Qin. Their work appears in journals such as Nature Communications, Clinical and Translational Medicine, American Journal of Cancer Research, Radiation Oncology and Oncogene.
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.