Seung Kwak

6.0k total citations
55 papers, 2.7k citations indexed

About

Seung Kwak is a scholar working on Molecular Biology, Cellular and Molecular Neuroscience and Behavioral Neuroscience. According to data from OpenAlex, Seung Kwak has authored 55 papers receiving a total of 2.7k indexed citations (citations by other indexed papers that have themselves been cited), including 41 papers in Molecular Biology, 34 papers in Cellular and Molecular Neuroscience and 7 papers in Behavioral Neuroscience. Recurrent topics in Seung Kwak's work include Genetic Neurodegenerative Diseases (30 papers), Mitochondrial Function and Pathology (18 papers) and RNA Research and Splicing (8 papers). Seung Kwak is often cited by papers focused on Genetic Neurodegenerative Diseases (30 papers), Mitochondrial Function and Pathology (18 papers) and RNA Research and Splicing (8 papers). Seung Kwak collaborates with scholars based in United States, United Kingdom and Germany. Seung Kwak's co-authors include Jack E. Dixon, K J Martell, D.J. Hakes, Jong‐Min Lee, Peter Holmans, James F. Gusella, Lesley Jones, Huda Akil, Marcy E. MacDonald and David Howland and has published in prestigious journals such as Nature, Proceedings of the National Academy of Sciences and Journal of Biological Chemistry.

In The Last Decade

Seung Kwak

55 papers receiving 2.6k citations

Peers

Seung Kwak
John Marshall United States
M. Galbiati Italy
Rosanna Parlato Germany
Dona M. Chikaraishi United States
Jianhua Xu United States
Nicole Faucon Biguet France
Andrea Levi Italy
A. Lamouroux France
Natalia V. Gounko Belgium
Yun‐Li Ma Taiwan
John Marshall United States
Seung Kwak
Citations per year, relative to Seung Kwak Seung Kwak (= 1×) peers John Marshall

Countries citing papers authored by Seung Kwak

Since Specialization
Citations

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

Fields of papers citing papers by Seung Kwak

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Seung Kwak

This figure shows the co-authorship network connecting the top 25 collaborators of Seung Kwak. A scholar is included among the top collaborators of Seung Kwak 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 Seung Kwak. Seung Kwak 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.
Ciosi, Marc, Sarah A. Cumming, Afroditi Chatzi, et al.. (2021). Approaches to Sequence the HTT CAG Repeat Expansion and Quantify Repeat Length Variation. Journal of Huntington s Disease. 10(1). 53–74. 18 indexed citations
2.
Hong, Eun Pyo, Marcy E. MacDonald, Vanessa C. Wheeler, et al.. (2021). Huntington’s Disease Pathogenesis: Two Sequential Components. Journal of Huntington s Disease. 10(1). 35–51. 54 indexed citations
3.
Lee, Yejin, Douglas Barker, Kevin Correia, et al.. (2021). Mutations causing Lopes-Maciel-Rodan syndrome are huntingtin hypomorphs. Human Molecular Genetics. 30(3-4). 135–148. 20 indexed citations
4.
Loupe, Jacob M., Ricardo Mouro Pinto, Kyung‐Hee Kim, et al.. (2020). Promotion of somatic CAG repeat expansion by Fan1 knock-out in Huntington’s disease knock-in mice is blocked by Mlh1 knock-out. Human Molecular Genetics. 29(18). 3044–3053. 50 indexed citations
5.
Oh, Hyejin, Seung Kwak, Susan L. Cotman, et al.. (2018). Novel DNA Aptamers that Bind to Mutant Huntingtin and Modify Its Activity. Molecular Therapy — Nucleic Acids. 11. 416–428. 13 indexed citations
6.
Chao, Michael J., Tammy Gillis, Ranjit Singh Atwal, et al.. (2017). Haplotype-based stratification of Huntington's disease. European Journal of Human Genetics. 25(11). 1202–1209. 18 indexed citations
7.
Shankaran, Mahalakshmi, Valerio Leoni, Claudio Caccia, et al.. (2016). Early and brain region-specific decrease of de novo cholesterol biosynthesis in Huntington's disease: A cross-validation study in Q175 knock-in mice. Neurobiology of Disease. 98. 66–76. 37 indexed citations
8.
Carroll, Jeffrey B., Amy Deik, Elisa Fossale, et al.. (2015). HdhQ111 Mice Exhibit Tissue Specific Metabolite Profiles that Include Striatal Lipid Accumulation. PLoS ONE. 10(8). e0134465–e0134465. 16 indexed citations
9.
Carty, Nikisha, Karsten Tillack, Christina Thiede, et al.. (2015). Characterization of HTT Inclusion Size, Location, and Timing in the zQ175 Mouse Model of Huntington´s Disease: An In Vivo High-Content Imaging Study. PLoS ONE. 10(4). e0123527–e0123527. 44 indexed citations
10.
Cheng, Aiwu, Thiruma V. Arumugam, Dong Liu, et al.. (2007). Pancortin-2 Interacts with WAVE1 and Bcl-xL in a Mitochondria-Associated Protein Complex That Mediates Ischemic Neuronal Death. Journal of Neuroscience. 27(7). 1519–1528. 46 indexed citations
11.
Kim, Yong, Jee Young Sung, Ilaria Ceglia, et al.. (2006). Phosphorylation of WAVE1 regulates actin polymerization and dendritic spine morphology. Nature. 442(7104). 814–817. 251 indexed citations
12.
Holzbaur, Erika L.F., David Howland, N Weber, et al.. (2006). Myostatin inhibition slows muscle atrophy in rodent models of amyotrophic lateral sclerosis. Neurobiology of Disease. 23(3). 697–707. 74 indexed citations
13.
Heinrich, Julia, et al.. (2005). Disruption of ShcA signaling halts cell proliferation — characterization of ShcC residues that influence signaling pathways using yeast. Cellular Signalling. 18(6). 795–806. 13 indexed citations
14.
Pausch, Mark H., Margaret Lai, Eugene Tseng, et al.. (2004). Functional expression of human and mouse P2Y12 receptors in Saccharomyces cerevisiae. Biochemical and Biophysical Research Communications. 324(1). 171–177. 40 indexed citations
15.
Barton, Michael D., John Dunlop, George Psaltis, et al.. (2002). Modified GFAP promoter auto-regulates tet-activator expression for increased transactivation and reduced tTA-associated toxicity. Molecular Brain Research. 101(1-2). 71–81. 23 indexed citations
16.
Martell, K J, et al.. (1995). hVH‐5: A Protein Tyrosine Phosphatase Abundant in Brain that Inactivates Mitogen‐Activated Protein Kinase. Journal of Neurochemistry. 65(4). 1823–1833. 89 indexed citations
17.
Martell, K J, Seung Kwak, D.J. Hakes, Jack E. Dixon, & Jeffrey M. Trent. (1994). Chromosomal Localization of Four Human VH1-like Protein-Tyrosine Phosphatases. Genomics. 22(2). 462–464. 21 indexed citations
18.
Kwak, Seung, et al.. (1993). Diurnal CRH mRNA Rhythm in the Hypothalamus: Decreased Expression in the Evening Is Not Dependent on Endogenous Glucocorticoids. Neuroendocrinology. 57(1). 96–105. 52 indexed citations
19.
Walton, Kevin M., K J Martell, Seung Kwak, Jack E. Dixon, & Brian L. Largent. (1993). A novel receptor-type protein tyrosine phosphatase is expressed during neurogenesis in the olfactory neuroepithelium. Neuron. 11(2). 387–400. 69 indexed citations
20.

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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