Hung‐Li Wang

2.7k total citations
63 papers, 2.2k citations indexed

About

Hung‐Li Wang is a scholar working on Cellular and Molecular Neuroscience, Molecular Biology and Neurology. According to data from OpenAlex, Hung‐Li Wang has authored 63 papers receiving a total of 2.2k indexed citations (citations by other indexed papers that have themselves been cited), including 49 papers in Cellular and Molecular Neuroscience, 45 papers in Molecular Biology and 16 papers in Neurology. Recurrent topics in Hung‐Li Wang's work include Neuropeptides and Animal Physiology (20 papers), Receptor Mechanisms and Signaling (20 papers) and Parkinson's Disease Mechanisms and Treatments (14 papers). Hung‐Li Wang is often cited by papers focused on Neuropeptides and Animal Physiology (20 papers), Receptor Mechanisms and Signaling (20 papers) and Parkinson's Disease Mechanisms and Treatments (14 papers). Hung‐Li Wang collaborates with scholars based in Taiwan, United States and Netherlands. Hung‐Li Wang's co-authors include Tu‐Hsueh Yeh, Tony Wu, Allen H. Li, An-Hsun Chou, Ying‐Ling Chen, Yi‐Hsin Weng, Ying-Ling Chen, Chin-Song Lu, Jin‐Chung Chen and Pin Ouyang and has published in prestigious journals such as Langmuir, Journal of Neurophysiology and Brain Research.

In The Last Decade

Hung‐Li Wang

63 papers receiving 2.1k citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
Hung‐Li Wang Taiwan 30 1.4k 1.3k 498 368 229 63 2.2k
Curt Mazur United States 22 2.0k 1.5× 819 0.6× 899 1.8× 427 1.2× 197 0.9× 45 3.4k
Tu‐Hsueh Yeh Taiwan 29 1.2k 0.9× 875 0.7× 903 1.8× 269 0.7× 373 1.6× 74 2.3k
Kinya Hisanaga Japan 20 934 0.7× 772 0.6× 462 0.9× 453 1.2× 214 0.9× 48 2.2k
Mariaelena Repici Italy 19 924 0.7× 629 0.5× 287 0.6× 336 0.9× 291 1.3× 37 1.9k
Gregory R. Stewart United States 24 1.1k 0.8× 1.0k 0.8× 227 0.5× 815 2.2× 160 0.7× 36 2.2k
Kay Seidel Germany 30 1.5k 1.1× 1.7k 1.3× 1.1k 2.2× 392 1.1× 350 1.5× 50 2.7k
Yitao Liu United States 11 1.0k 0.8× 1.0k 0.8× 205 0.4× 276 0.8× 464 2.0× 14 2.0k
Iddo Magen Israel 24 598 0.4× 617 0.5× 840 1.7× 402 1.1× 215 0.9× 38 2.0k
Marianna Storto Italy 29 1.2k 0.9× 1.3k 1.0× 214 0.4× 457 1.2× 326 1.4× 60 2.5k
Hideki Hida Japan 29 879 0.6× 811 0.6× 371 0.7× 212 0.6× 498 2.2× 81 2.2k

Countries citing papers authored by Hung‐Li Wang

Since Specialization
Citations

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

Fields of papers citing papers by Hung‐Li Wang

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Hung‐Li Wang. 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 Hung‐Li Wang. The network helps show where Hung‐Li Wang may publish in the future.

Co-authorship network of co-authors of Hung‐Li Wang

This figure shows the co-authorship network connecting the top 25 collaborators of Hung‐Li Wang. A scholar is included among the top collaborators of Hung‐Li Wang 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 Hung‐Li Wang. Hung‐Li Wang 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.
Wang, Hung‐Li, Yi‐Chuan Cheng, Tu‐Hsueh Yeh, et al.. (2023). HCH6-1, an antagonist of formyl peptide receptor-1, exerts anti-neuroinflammatory and neuroprotective effects in cellular and animal models of Parkinson’s disease. Biochemical Pharmacology. 212. 115524–115524. 9 indexed citations
2.
Chen, Yi‐Chun, Shih‐Cheng Chang, Yun‐Shien Lee, et al.. (2023). TOMM40 Genetic Variants Cause Neuroinflammation in Alzheimer’s Disease. International Journal of Molecular Sciences. 24(4). 4085–4085. 20 indexed citations
3.
Wang, Hung‐Li, Ying‐Zu Huang, Yi‐Hsin Weng, et al.. (2020). Alda-1, an activator of ALDH2, ameliorates Achilles tendinopathy in cellular and mouse models. Biochemical Pharmacology. 175. 113919–113919. 23 indexed citations
4.
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6.
Wang, Hung‐Li, et al.. (2013). XLID CUL4B mutants are defective in promoting TSC2 degradation and positively regulating mTOR signaling in neocortical neurons. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1832(4). 585–593. 15 indexed citations
7.
Wang, Hung‐Li, et al.. (2011). PARK6 PINK1 mutants are defective in maintaining mitochondrial membrane potential and inhibiting ROS formation of substantia nigra dopaminergic neurons. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1812(6). 674–684. 103 indexed citations
8.
Wang, Hung‐Li, et al.. (2010). Polyglutamine-expanded ataxin-7 upregulates Bax expression by activating p53 in cerebellar and inferior olivary neurons. Experimental Neurology. 224(2). 486–494. 22 indexed citations
9.
Chou, An-Hsun, et al.. (2010). HDAC inhibitor sodium butyrate reverses transcriptional downregulation and ameliorates ataxic symptoms in a transgenic mouse model of SCA3. Neurobiology of Disease. 41(2). 481–488. 83 indexed citations
10.
Chou, An‐Hsun, Chia‐Yang Chen, Siying Chen, et al.. (2009). Polyglutamine-expanded ataxin-7 causes cerebellar dysfunction by inducing transcriptional dysregulation. Neurochemistry International. 56(2). 329–339. 48 indexed citations
11.
Chou, An-Hsun, et al.. (2008). Polyglutamine-expanded ataxin-3 causes cerebellar dysfunction of SCA3 transgenic mice by inducing transcriptional dysregulation. Neurobiology of Disease. 31(1). 89–101. 143 indexed citations
12.
13.
Peng, Tsung‐I, et al.. (2005). Visualizing common deletion of mitochondrial DNA-augmented mitochondrial reactive oxygen species generation and apoptosis upon oxidative stress. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1762(2). 241–255. 59 indexed citations
14.
Chou, An-Hsun, et al.. (2005). Polyglutamine-expanded ataxin-3 activates mitochondrial apoptotic pathway by upregulating Bax and downregulating Bcl-xL. Neurobiology of Disease. 21(2). 333–345. 80 indexed citations
15.
Pommier, Blandine, Cynthia Marie‐Claire, Sophie Da Nascimento, et al.. (2003). Further evidence that the CCK2receptor is coupled to two transduction pathways using site‐directed mutagenesis. Journal of Neurochemistry. 85(2). 454–461. 20 indexed citations
16.
Wang, Hung‐Li, et al.. (2002). Identification of two C-terminal amino acids, Ser355 and Thr357, required for short-term homologous desensitization of μ-opioid receptors. Biochemical Pharmacology. 64(2). 257–266. 32 indexed citations
17.
Li, Allen H., et al.. (2001). Neurotensin excitation of serotonergic neurons in the rat nucleus raphe magnus: ionic and molecular mechanisms. Neuropharmacology. 40(8). 1073–1083. 25 indexed citations
18.
Wu, Tony, Allen Li, & Hung‐Li Wang. (1995). Neurotensin increases the cationic conductance of rat substantia nigra dopaminergic neurons through the inositol 1,4,5-trisphosphate-calcium pathway. Brain Research. 683(2). 242–250. 41 indexed citations
19.
Wu, Tony & Hung‐Li Wang. (1994). CCK-8 excites substantia nigra dopaminergic neurons by increasing a cationic conductance. Neuroscience Letters. 170(2). 229–232. 19 indexed citations
20.
Dichter, Marc A., Hung‐Li Wang, & Terry Reisine. (1990). Electrophysiological effects of somatostatin-14 and somatostatin-28 on mammalian central nervous system neurons. Metabolism. 39(9). 86–90. 15 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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