Hsiang Wen

649 total citations
18 papers, 499 citations indexed

About

Hsiang Wen is a scholar working on Molecular Biology, Cellular and Molecular Neuroscience and Cell Biology. According to data from OpenAlex, Hsiang Wen has authored 18 papers receiving a total of 499 indexed citations (citations by other indexed papers that have themselves been cited), including 13 papers in Molecular Biology, 5 papers in Cellular and Molecular Neuroscience and 5 papers in Cell Biology. Recurrent topics in Hsiang Wen's work include Ubiquitin and proteasome pathways (5 papers), Mitochondrial Function and Pathology (3 papers) and Endoplasmic Reticulum Stress and Disease (3 papers). Hsiang Wen is often cited by papers focused on Ubiquitin and proteasome pathways (5 papers), Mitochondrial Function and Pathology (3 papers) and Endoplasmic Reticulum Stress and Disease (3 papers). Hsiang Wen collaborates with scholars based in United States and Portugal. Hsiang Wen's co-authors include Henry L. Paulson, Kevin A. Glenn, Rick F. Nelson, Yaohui Chai, Diana Zepeda‐Orozco, Prerna Rastogi, Bryan G. Allen, Kranti A. Mapuskar, Douglas R. Spitz and Massimo Attanasio and has published in prestigious journals such as Journal of Biological Chemistry, Journal of Neuroscience and PLoS ONE.

In The Last Decade

Hsiang Wen

18 papers receiving 492 citations

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name h Career Trend Papers Cites
Hsiang Wen United States 9 336 149 65 60 55 18 499
Dustin Shilling United States 11 177 0.5× 89 0.6× 76 1.2× 32 0.5× 75 1.4× 15 501
César Payán‐Gómez Colombia 13 281 0.8× 78 0.5× 27 0.4× 50 0.8× 33 0.6× 48 557
Xiao-Hong Lin China 11 165 0.5× 125 0.8× 32 0.5× 34 0.6× 16 0.3× 18 545
Elöd Körtvely Germany 13 302 0.9× 73 0.5× 42 0.6× 28 0.5× 7 0.1× 26 786
Takahisa Koga Japan 16 301 0.9× 52 0.3× 145 2.2× 30 0.5× 23 0.4× 24 651
Raffaella Calligaris Italy 11 412 1.2× 101 0.7× 93 1.4× 58 1.0× 30 0.5× 14 590
Katsuhiro Tsuchiya Japan 6 181 0.5× 78 0.5× 108 1.7× 80 1.3× 17 0.3× 16 367
Joseph F. Sanchez United States 11 349 1.0× 126 0.8× 36 0.6× 26 0.4× 19 0.3× 13 574
Zunxuan Chen United States 6 653 1.9× 59 0.4× 52 0.8× 27 0.5× 29 0.5× 7 802
Radha Desai United States 12 386 1.1× 91 0.6× 82 1.3× 33 0.6× 36 0.7× 14 545

Countries citing papers authored by Hsiang Wen

Since Specialization
Citations

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

Fields of papers citing papers by Hsiang Wen

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Hsiang Wen. 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 Hsiang Wen. The network helps show where Hsiang Wen may publish in the future.

Co-authorship network of co-authors of Hsiang Wen

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

All Works

18 of 18 papers shown
1.
Mapuskar, Kranti A., Casey Pulliam, Ann Tomanek‐Chalkley, et al.. (2024). The antioxidant and anti-inflammatory activities of avasopasem manganese in age-associated, cisplatin-induced renal injury. Redox Biology. 70. 103022–103022. 13 indexed citations
2.
Rauckhorst, Adam J., Hsiang Wen, JY Kim, et al.. (2023). Tubular mitochondrial pyruvate carrier disruption elicits redox adaptations that protect from acute kidney injury. Molecular Metabolism. 79. 101849–101849. 4 indexed citations
3.
Wen, Hsiang, et al.. (2022). Deletion of the voltage‐gated calcium channel, Ca V 1 .3, causes deficits in motor performance and associative learning. Genes Brain & Behavior. 21(2). e12791–e12791. 8 indexed citations
4.
Wen, Hsiang, et al.. (2022). Neuronal deletion of CaV1.2 is associated with sex-specific behavioral phenotypes in mice. Scientific Reports. 12(1). 22152–22152. 4 indexed citations
5.
Li, Mengshi, Diana Zepeda‐Orozco, Hsiang Wen, et al.. (2020). Preclinical evaluation of 203/212Pb-based theranostics-dosimetry and renal toxicity.. 61. 289–289. 3 indexed citations
6.
Mapuskar, Kranti A., Hsiang Wen, Danniele G. Holanda, et al.. (2018). Persistent increase in mitochondrial superoxide mediates cisplatin-induced chronic kidney disease. Redox Biology. 20. 98–106. 90 indexed citations
7.
Zepeda‐Orozco, Diana, et al.. (2017). Dataset for: EGF Regulation of Proximal Tubule Cell Proliferation and VEGF-A Secretion. Figshare. 1 indexed citations
8.
Zepeda‐Orozco, Diana, et al.. (2017). EGF regulation of proximal tubule cell proliferation and VEGF-A secretion. Physiological Reports. 5(18). e13453–e13453. 26 indexed citations
9.
Beauvais, Geneviève, Nicole M. Bode, Hsiang Wen, et al.. (2016). Disruption of Protein Processing in the Endoplasmic Reticulum of DYT1Knock-inMice Implicates Novel Pathways in Dystonia Pathogenesis. Journal of Neuroscience. 36(40). 10245–10256. 39 indexed citations
10.
Wen, Hsiang, et al.. (2015). FBG1 Is the Final Arbitrator of A1AT-Z Degradation. PLoS ONE. 10(8). e0135591–e0135591. 4 indexed citations
11.
Wen, Hsiang, et al.. (2014). Tissue Standards Using Stain Free Gels as a Superior Approach for Aging Research. International Journal of Biochemistry Research & Review. 5(1). 73–81. 1 indexed citations
12.
Wen, Hsiang, et al.. (2011). Using a ubiquitin ligase as an unfolded protein sensor. Biochemical and Biophysical Research Communications. 418(1). 44–48. 5 indexed citations
13.
Wen, Hsiang, et al.. (2010). FBG1 is a promiscuous ubiquitin ligase that sequesters APC2 and causes S-phase arrest. Cell Cycle. 9(22). 4506–4517. 8 indexed citations
14.
Glenn, Kevin A., et al.. (2008). Diversity in Tissue Expression, Substrate Binding, and SCF Complex Formation for a Lectin Family of Ubiquitin Ligases. Journal of Biological Chemistry. 283(19). 12717–12729. 64 indexed citations
15.
Nelson, Rick F., Kevin A. Glenn, Yuzhou Zhang, et al.. (2007). Selective Cochlear Degeneration in Mice Lacking the F-Box Protein, Fbx2, a Glycoprotein-Specific Ubiquitin Ligase Subunit. Journal of Neuroscience. 27(19). 5163–5171. 65 indexed citations
16.
Todi, Sokol V., Mário Laço, Brett J Winborn, et al.. (2007). Cellular Turnover of the Polyglutamine Disease Protein Ataxin-3 Is Regulated by Its Catalytic Activity. Journal of Biological Chemistry. 282(40). 29348–29358. 43 indexed citations
17.
Nelson, Rick F., Kevin A. Glenn, Victor M. Miller, Hsiang Wen, & Henry L. Paulson. (2006). A Novel Route for F-box Protein-mediated Ubiquitination Links CHIP to Glycoprotein Quality Control. Journal of Biological Chemistry. 281(29). 20242–20251. 40 indexed citations
18.
Chai, Yaohui, et al.. (2005). Defining the Role of Ubiquitin-interacting Motifs in the Polyglutamine Disease Protein, Ataxin-3. Journal of Biological Chemistry. 280(36). 32026–32034. 81 indexed citations

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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