Shih‐Shun Chen

1.2k total citations
34 papers, 987 citations indexed

About

Shih‐Shun Chen is a scholar working on Molecular Biology, Oncology and Plant Science. According to data from OpenAlex, Shih‐Shun Chen has authored 34 papers receiving a total of 987 indexed citations (citations by other indexed papers that have themselves been cited), including 23 papers in Molecular Biology, 5 papers in Oncology and 5 papers in Plant Science. Recurrent topics in Shih‐Shun Chen's work include Cell death mechanisms and regulation (7 papers), Endoplasmic Reticulum Stress and Disease (4 papers) and Ubiquitin and proteasome pathways (3 papers). Shih‐Shun Chen is often cited by papers focused on Cell death mechanisms and regulation (7 papers), Endoplasmic Reticulum Stress and Disease (4 papers) and Ubiquitin and proteasome pathways (3 papers). Shih‐Shun Chen collaborates with scholars based in Taiwan, United States and China. Shih‐Shun Chen's co-authors include Meng‐Liang Lin, Jing‐Gung Chung, Ying‐Hue Lee, Meng-Liang Lin, Vijayakumar Muppala, Peter F. Johnson, Jinfeng Chen, Nan‐Shih Liao, Hong‐Lin Su and Szu-Cheng Kuo and has published in prestigious journals such as Blood, The Journal of Immunology and Molecular and Cellular Biology.

In The Last Decade

Shih‐Shun Chen

33 papers receiving 971 citations

Peers

Shih‐Shun Chen
Ying Shi China
Pia Rauch Germany
Oliver Voß United States
Joydeep Ghosh United States
Girish Rachakonda United States
Shih‐Shun Chen
Citations per year, relative to Shih‐Shun Chen Shih‐Shun Chen (= 1×) peers Alexandre E. Nowill

Countries citing papers authored by Shih‐Shun Chen

Since Specialization
Citations

This map shows the geographic impact of Shih‐Shun Chen'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 Shih‐Shun Chen with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Shih‐Shun Chen more than expected).

Fields of papers citing papers by Shih‐Shun Chen

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Shih‐Shun Chen. 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 Shih‐Shun Chen. The network helps show where Shih‐Shun Chen may publish in the future.

Co-authorship network of co-authors of Shih‐Shun Chen

This figure shows the co-authorship network connecting the top 25 collaborators of Shih‐Shun Chen. A scholar is included among the top collaborators of Shih‐Shun Chen 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 Shih‐Shun Chen. Shih‐Shun Chen is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

20 of 20 papers shown
1.
Hsu, Pei‐Chen, Hung-Wen Tsai, Wen-Shin Chang, et al.. (2024). Impact of DNA Ligase 1 Genotypes on Childhood Acute Lymphocytic Leukemia. In Vivo. 39(1). 152–159.
2.
Lin, Meng-Liang, et al.. (2024). Impacts of Matrix Metalloproteinase-2 Promoter Genotypes on Breast Cancer Risk. Cancer Genomics & Proteomics. 21(5). 502–510. 3 indexed citations
3.
Tien, Ni, Chun‐Hsu Yao, Da‐Tian Bau, et al.. (2024). Naringin Induces ROS‐Stimulated G 1 Cell‐Cycle Arrest and Apoptosis in Nasopharyngeal Carcinoma Cells. Environmental Toxicology. 39(11). 5059–5073. 4 indexed citations
5.
Tien, Ni, et al.. (2023). Let-7g Upregulation Attenuated the KRAS–PI3K–Rac1–Akt Axis-Mediated Bioenergetic Functions. Cells. 12(18). 2313–2313. 3 indexed citations
6.
Chang, Jan‐Gowth, Ni Tien, Yi‐Chih Chang, Meng‐Liang Lin, & Shih‐Shun Chen. (2021). Oxidative Stress-Induced Unscheduled CDK1–Cyclin B1 Activity Impairs ER–Mitochondria-Mediated Bioenergetic Metabolism. Cells. 10(6). 1280–1280. 10 indexed citations
9.
Lin, Meng‐Liang, et al.. (2019). Citrate-Induced p85α–PTEN Complex Formation Causes G2/M Phase Arrest in Human Pharyngeal Squamous Carcinoma Cell Lines. International Journal of Molecular Sciences. 20(9). 2105–2105. 11 indexed citations
10.
Lin, Meng‐Liang, et al.. (2019). Downregulation of miR-144 by triptolide enhanced p85α−PTEN complex formation causing S phase arrest of human nasopharyngeal carcinoma cells. European Journal of Pharmacology. 855. 137–148. 11 indexed citations
11.
Lin, Meng-Liang, et al.. (2018). Suppression of Akt-mediated HDAC3 expression and CDK2 T39 phosphorylation by a bichalcone analog contributes to S phase retardation of cancer cells. European Journal of Pharmacology. 829. 141–150. 5 indexed citations
12.
13.
Lin, Meng‐Liang & Shih‐Shun Chen. (2017). Activation of Casein Kinase II by Gallic Acid Induces BIK–BAX/BAK-Mediated ER Ca++-ROS-Dependent Apoptosis of Human Oral Cancer Cells. Frontiers in Physiology. 8. 761–761. 18 indexed citations
14.
Chen, Shih‐Shun, et al.. (2016). Suppression of phospho‐p85α–GTP‐Rac1 lipid raft interaction by bichalcone analog attenuates cancer cell invasion. Molecular Carcinogenesis. 55(12). 2106–2120. 7 indexed citations
15.
16.
Lin, Meng‐Liang, et al.. (2015). CHM-1 Suppresses Formation of Cell Surface-associated GRP78-p85α Complexes, Inhibiting PI3K-AKT Signaling and Inducing Apoptosis of Human Nasopharyngeal Carcinoma Cells.. PubMed. 35(10). 5359–68. 10 indexed citations
19.

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.

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