Lydia E. Matesic

3.3k total citations
32 papers, 2.5k citations indexed

About

Lydia E. Matesic is a scholar working on Molecular Biology, Immunology and Genetics. According to data from OpenAlex, Lydia E. Matesic has authored 32 papers receiving a total of 2.5k indexed citations (citations by other indexed papers that have themselves been cited), including 15 papers in Molecular Biology, 12 papers in Immunology and 5 papers in Genetics. Recurrent topics in Lydia E. Matesic's work include Immune Cell Function and Interaction (5 papers), Immune Response and Inflammation (5 papers) and T-cell and B-cell Immunology (5 papers). Lydia E. Matesic is often cited by papers focused on Immune Cell Function and Interaction (5 papers), Immune Response and Inflammation (5 papers) and T-cell and B-cell Immunology (5 papers). Lydia E. Matesic collaborates with scholars based in United States, United Kingdom and Canada. Lydia E. Matesic's co-authors include Neal G. Copeland, Nancy A. Jenkins, Ceshi Chen, Edward W. Harhaj, Shuichi Sato, James P. White, Matthew C. Kostek, James A. Carson, John Baynes and Xufeng Wu and has published in prestigious journals such as Proceedings of the National Academy of Sciences, Journal of Biological Chemistry and The EMBO Journal.

In The Last Decade

Lydia E. Matesic

31 papers receiving 2.5k citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
Lydia E. Matesic United States 21 1.6k 603 587 408 330 32 2.5k
Kazumi Ishidoh Japan 34 1.7k 1.1× 678 1.1× 510 0.9× 526 1.3× 616 1.9× 74 3.1k
Cristina López-Rodrı́guez Spain 26 1.6k 1.0× 932 1.5× 861 1.5× 307 0.8× 374 1.1× 48 3.1k
Kristopher Clark United Kingdom 24 1.4k 0.9× 463 0.8× 990 1.7× 234 0.6× 434 1.3× 42 3.1k
Imed‐Eddine Gallouzi Canada 34 3.3k 2.1× 366 0.6× 368 0.6× 389 1.0× 475 1.4× 65 3.9k
Toru Tanaka Japan 30 1.6k 1.0× 225 0.4× 429 0.7× 280 0.7× 363 1.1× 89 2.9k
Sean Bong Lee United States 36 2.8k 1.8× 424 0.7× 540 0.9× 264 0.6× 449 1.4× 83 4.1k
Miguel A. Vega Spain 31 1.5k 0.9× 273 0.5× 1.3k 2.3× 255 0.6× 436 1.3× 60 3.5k
Yoshiyuki Ohsawa Japan 26 2.1k 1.3× 717 1.2× 884 1.5× 731 1.8× 311 0.9× 42 3.5k
Hao Shi United States 27 1.1k 0.7× 261 0.4× 801 1.4× 328 0.8× 354 1.1× 73 2.4k
Jaesang Kim South Korea 28 2.3k 1.4× 419 0.7× 765 1.3× 307 0.8× 469 1.4× 63 3.8k

Countries citing papers authored by Lydia E. Matesic

Since Specialization
Citations

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

Fields of papers citing papers by Lydia E. Matesic

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Lydia E. Matesic. 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 Lydia E. Matesic. The network helps show where Lydia E. Matesic may publish in the future.

Co-authorship network of co-authors of Lydia E. Matesic

This figure shows the co-authorship network connecting the top 25 collaborators of Lydia E. Matesic. A scholar is included among the top collaborators of Lydia E. Matesic 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 Lydia E. Matesic. Lydia E. Matesic 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.
Lim, Kyungtae, Peng He, Weimin Lin, et al.. (2025). A novel human fetal lung-derived alveolar organoid model reveals mechanisms of surfactant protein C maturation relevant to interstitial lung disease. The EMBO Journal. 44(3). 639–664. 4 indexed citations
2.
3.
Zhang, Hengwei, et al.. (2013). Ubiquitin E3 Ligase Itch Negatively Regulates Osteoclast Formation by Promoting Deubiquitination of Tumor Necrosis Factor (TNF) Receptor-associated Factor 6. Journal of Biological Chemistry. 288(31). 22359–22368. 27 indexed citations
4.
Moreno‐García, Miguel E., Karen Sommer, Héctor Rincón‐Arano, et al.. (2013). Kinase-Independent Feedback of the TAK1/TAB1 Complex on BCL10 Turnover and NF-κB Activation. Molecular and Cellular Biology. 33(6). 1149–1163. 14 indexed citations
5.
White, James P., Melissa Puppa, Shuichi Sato, et al.. (2012). IL-6 regulation on skeletal muscle mitochondrial remodeling during cancer cachexia in the Apc Min/+ mouse. Skeletal Muscle. 2(1). 14–14. 180 indexed citations
6.
White, James P., John Baynes, Stephen Welle, et al.. (2011). The Regulation of Skeletal Muscle Protein Turnover during the Progression of Cancer Cachexia in the ApcMin/+ Mouse. PLoS ONE. 6(9). e24650–e24650. 210 indexed citations
7.
Rathinam, Chozhavendan, Lydia E. Matesic, & Richard A. Flavell. (2011). The E3 ligase Itch is a negative regulator of the homeostasis and function of hematopoietic stem cells. Nature Immunology. 12(5). 399–407. 69 indexed citations
8.
Zhao, Lan, Jian Huang, Hengwei Zhang, et al.. (2011). Tumor necrosis factor inhibits mesenchymal stem cell differentiation into osteoblasts via the ubiquitin E3 ligase Wwp1. Stem Cells. 29(10). 1601–1610. 123 indexed citations
9.
Yu, Jin, Anne B. Hofseth, Xiangli Cui, et al.. (2010). American Ginseng Suppresses Colitis through p53-Mediated Apoptosis of Inflammatory Cells. Cancer Prevention Research. 3(3). 339–347. 55 indexed citations
10.
Scacheri, Peter C., et al.. (2009). ITCH K63-Ubiquitinates the NOD2 Binding Protein, RIP2, to Influence Inflammatory Signaling Pathways. Current Biology. 19(15). 1255–1263. 119 indexed citations
11.
Yu, Jin, Venkata Subbaiah Kotakadi, Ying Lei, et al.. (2008). American ginseng suppresses inflammation and DNA damage associated with mouse colitis. Carcinogenesis. 29(12). 2351–2359. 68 indexed citations
12.
Matesic, Lydia E., Neal G. Copeland, & N.A. Jenkins. (2008). Itchy Mice: The Identification of a New Pathway for the Development of Autoimmunity. Current topics in microbiology and immunology. 321. 185–200. 29 indexed citations
13.
Kotakadi, Venkata Subbaiah, Jin Yu, Anne B. Hofseth, et al.. (2008). Ginkgo biloba extract EGb 761 has anti-inflammatory properties and ameliorates colitis in mice by driving effector T cell apoptosis. Carcinogenesis. 29(9). 1799–1806. 76 indexed citations
14.
Shembade, Noula, Nicole S. Harhaj, Michelle S. Parvatiyar, et al.. (2008). The E3 ligase Itch negatively regulates inflammatory signaling pathways by controlling the function of the ubiquitin-editing enzyme A20. Nature Immunology. 9(3). 254–262. 229 indexed citations
15.
Chen, Ceshi & Lydia E. Matesic. (2007). The Nedd4-like family of E3 ubiquitin ligases and cancer. Cancer and Metastasis Reviews. 26(3-4). 587–604. 189 indexed citations
16.
Wu, Xufeng, Kang Rao, Hong Zhang, et al.. (2002). Identification of an organelle receptor for myosin-Va. Nature Cell Biology. 4(4). 271–278. 384 indexed citations
17.
Matesic, Lydia E., Antonio De Maio, & Roger H. Reeves. (1999). Mapping Lipopolysaccharide Response Loci in Mice Using Recombinant Inbred and Congenic Strains. Genomics. 62(1). 34–41. 19 indexed citations
18.
Cabin, Deborah E., Jennifer W. McKee-Johnson, Lydia E. Matesic, et al.. (1998). Physical and Comparative Mapping of Distal Mouse Chromosome 16. Genome Research. 8(9). 940–950. 13 indexed citations
19.
Maio, Antonio De, et al.. (1998). GENETIC COMPONENT IN THE INFLAMMATORY RESPONSE INDUCED BY BACTERIAL LIPOPOLYSACCHARIDE. Shock. 10(5). 319–323. 71 indexed citations
20.
O’Malley, Janis P., Lydia E. Matesic, M. Christine Zink, et al.. (1998). Comparison of acute endotoxin-induced lesions in A/J and C57BL/6J mice. Journal of Heredity. 89(6). 525–530. 25 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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