Sung-Ung Kang
- Molecular Biology
- Neurology top 5%
- Cellular and Molecular Neuroscience top 10%
- Epidemiology
- Physiology top 10%
- Co-authors
- Valina L. DawsonTed M. DawsonHaisong JiangYunjong LeeByoung Dae LeeSenthilkumar S. KaruppagounderHo Chul KangJoo‐Ho Shin
- Topics
- Parkinson's Disease Mechanisms and Treatments (7 papers)Neuroinflammation and Neurodegeneration Mechanisms (3 papers)CRISPR and Genetic Engineering (3 papers)
- Partner nations
- United StatesSouth KoreaAustria
In The Last Decade
Sung-Ung Kang
22 papers receiving 1.1k citations
Hit Papers
Peers
Comparison fields: 5 of 97
- Molecular Biology 587
- Neurology 319
- Cellular and Molecular Neuroscience 226
- Epidemiology 216
- Physiology 201
Countries citing papers authored by Sung-Ung Kang
This map shows the geographic impact of Sung-Ung Kang'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 Sung-Ung Kang with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Sung-Ung Kang more than expected).
Fields of papers citing papers by Sung-Ung Kang
This network shows the impact of papers produced by Sung-Ung Kang. 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 Sung-Ung Kang. The network helps show where Sung-Ung Kang may publish in the future.
Co-authorship network of co-authors of Sung-Ung Kang
This figure shows the co-authorship network connecting the top 25 collaborators of Sung-Ung Kang. A scholar is included among the top collaborators of Sung-Ung Kang based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Sung-Ung Kang. Sung-Ung Kang is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
| # | Work | Indexed citations |
|---|---|---|
| 1 | 2 | |
| 2 | 2 | |
| 3 | 0 | |
| 4 | 2 | |
| 5 | 6 | |
| 6 | 16 | |
| 7 | 29 | |
| 8 | Neuronal NLRP3 is a parkin substrate that drives neurodegeneration in Parkinson’s diseasebreakdown → | 139 |
| 9 | 7 | |
| 10 | 11 | |
| 11 | 8 | |
| 12 | 25 | |
| 13 | 64 | |
| 14 | 19 | |
| 15 | 89 | |
| 16 | 191 | |
| 17 | 175 | |
| 18 | 49 | |
| 19 | 44 | |
| 20 | 41 |
About Sung-Ung Kang
Sung-Ung Kang is a scholar working on Neurology, Neurology and Cellular and Molecular Neuroscience, having authored 23 papers that have together received 1.1k indexed citations. Recurring topics across this work include Parkinson's Disease Mechanisms and Treatments (7 papers), Neuroinflammation and Neurodegeneration Mechanisms (3 papers) and CRISPR and Genetic Engineering (3 papers). The work is most often cited by research in Neurology (319 citations), Neurology (158 citations) and Cellular and Molecular Neuroscience (226 citations). Sung-Ung Kang has collaborated with scholars based in United States, South Korea and Austria. Frequent co-authors include Valina L. Dawson, Ted M. Dawson, Haisong Jiang, Yunjong Lee, Byoung Dae Lee, Senthilkumar S. Karuppagounder, Ho Chul Kang, Joo‐Ho Shin, Yun-Il Lee and Gert Lübec. Their work appears in journals such as Proceedings of the National Academy of Sciences, Nucleic Acids Research 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.