Ruth E. Thomas

3.0k total citations · 1 hit paper
17 papers, 2.2k citations indexed

About

Ruth E. Thomas is a scholar working on Cell Biology, Molecular Biology and Physiology. According to data from OpenAlex, Ruth E. Thomas has authored 17 papers receiving a total of 2.2k indexed citations (citations by other indexed papers that have themselves been cited), including 8 papers in Cell Biology, 7 papers in Molecular Biology and 7 papers in Physiology. Recurrent topics in Ruth E. Thomas's work include Autophagy in Disease and Therapy (6 papers), Lysosomal Storage Disorders Research (5 papers) and Parkinson's Disease Mechanisms and Treatments (4 papers). Ruth E. Thomas is often cited by papers focused on Autophagy in Disease and Therapy (6 papers), Lysosomal Storage Disorders Research (5 papers) and Parkinson's Disease Mechanisms and Treatments (4 papers). Ruth E. Thomas collaborates with scholars based in United States, United Kingdom and Canada. Ruth E. Thomas's co-authors include Leo J. Pallanck, Angela C. Poole, Evelyn S. Vincow, Heidi M. McBride, Alexander J. Whitworth, Selina Yu, Roger D. Cone, Michele A. Kelly, Ximena Opitz-Araya and Malcolm J. Low and has published in prestigious journals such as Cell, Proceedings of the National Academy of Sciences and PLoS ONE.

In The Last Decade

Ruth E. Thomas

17 papers receiving 2.2k citations

Hit Papers

The PINK1/Parkin pathway regulates mitochondrial morphology 2008 2026 2014 2020 2008 200 400 600

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
Ruth E. Thomas United States 12 1.2k 855 757 448 422 17 2.2k
Oleg S. Gorbatyuk United States 24 1.4k 1.1× 317 0.4× 550 0.7× 576 1.3× 304 0.7× 41 2.6k
J. Alex Parker Canada 25 1.3k 1.1× 290 0.3× 670 0.9× 287 0.6× 494 1.2× 51 2.5k
M. Galbiati Italy 30 1.1k 0.9× 529 0.6× 708 0.9× 508 1.1× 342 0.8× 66 2.6k
Tiemo J. Klisch United States 21 1.1k 0.9× 757 0.9× 155 0.2× 291 0.6× 272 0.6× 35 2.2k
Janne M. Toivonen Spain 19 1.2k 1.0× 246 0.3× 308 0.4× 96 0.2× 338 0.8× 41 2.1k
Elio Messi Italy 23 723 0.6× 371 0.4× 349 0.5× 281 0.6× 205 0.5× 45 1.7k
Nicholas Verity United Kingdom 11 1.2k 1.0× 388 0.5× 256 0.3× 932 2.1× 521 1.2× 12 2.0k
Jacqueline C. Mitchell United Kingdom 21 1.3k 1.1× 254 0.3× 1.2k 1.5× 443 1.0× 430 1.0× 41 2.4k
Helois Radford United Kingdom 11 1.3k 1.1× 379 0.4× 248 0.3× 921 2.1× 489 1.2× 12 2.1k

Countries citing papers authored by Ruth E. Thomas

Since Specialization
Citations

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

Fields of papers citing papers by Ruth E. Thomas

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Ruth E. Thomas

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

All Works

17 of 17 papers shown
1.
Vincow, Evelyn S., et al.. (2024). Glucocerebrosidase deficiency leads to neuropathology via cellular immune activation. PLoS Genetics. 20(11). e1011105–e1011105. 1 indexed citations
2.
Thomas, Ruth E., et al.. (2024). A Drosophila model for mechanistic investigation of tau protein spread. Disease Models & Mechanisms. 17(9). 2 indexed citations
3.
Jewett, Kathryn A., Ruth E. Thomas, Chi Q. Phan, et al.. (2021). Glucocerebrosidase reduces the spread of protein aggregation in a Drosophila melanogaster model of neurodegeneration by regulating proteins trafficked by extracellular vesicles. PLoS Genetics. 17(2). e1008859–e1008859. 23 indexed citations
4.
Vincow, Evelyn S., Ruth E. Thomas, Gennifer E. Merrihew, Michael J. MacCoss, & Leo J. Pallanck. (2021). Slowed Protein Turnover in Aging Drosophila Reflects a Shift in Cellular Priorities. The Journals of Gerontology Series A. 76(10). 1734–1739. 9 indexed citations
5.
Vincow, Evelyn S., Ruth E. Thomas, Gennifer E. Merrihew, et al.. (2019). Autophagy accounts for approximately one-third of mitochondrial protein turnover and is protein selective. Autophagy. 15(9). 1592–1605. 34 indexed citations
6.
Thomas, Ruth E., et al.. (2018). Lon protease inactivation in Drosophila causes unfolded protein stress and inhibition of mitochondrial translation. Cell Death Discovery. 4(1). 51–51. 26 indexed citations
7.
Thomas, Ruth E., Evelyn S. Vincow, Gennifer E. Merrihew, et al.. (2018). Glucocerebrosidase deficiency promotes protein aggregation through dysregulation of extracellular vesicles. PLoS Genetics. 14(9). e1007694–e1007694. 34 indexed citations
9.
Davis, Marie Y., Kien Trinh, Ruth E. Thomas, et al.. (2016). Glucocerebrosidase Deficiency in Drosophila Results in α-Synuclein-Independent Protein Aggregation and Neurodegeneration. PLoS Genetics. 12(3). e1005944–e1005944. 78 indexed citations
10.
Davis, Marie Y., et al.. (2015). Using a Drosophila GBA deficiency model to understand the role of GBA in Parkinson’s disease (P2.146). Neurology. 84(14_supplement). 1 indexed citations
11.
Thomas, Ruth E., et al.. (2014). PINK1-Parkin Pathway Activity Is Regulated by Degradation of PINK1 in the Mitochondrial Matrix. PLoS Genetics. 10(5). e1004279–e1004279. 98 indexed citations
12.
Vincow, Evelyn S., Gennifer E. Merrihew, Ruth E. Thomas, et al.. (2013). The PINK1–Parkin pathway promotes both mitophagy and selective respiratory chain turnover in vivo. Proceedings of the National Academy of Sciences. 110(16). 6400–6405. 358 indexed citations
13.
Poole, Angela C., Ruth E. Thomas, Selina Yu, Evelyn S. Vincow, & Leo J. Pallanck. (2010). The Mitochondrial Fusion-Promoting Factor Mitofusin Is a Substrate of the PINK1/Parkin Pathway. PLoS ONE. 5(4). e10054–e10054. 361 indexed citations
14.
Poole, Angela C., et al.. (2008). The PINK1/Parkin pathway regulates mitochondrial morphology. Proceedings of the National Academy of Sciences. 105(5). 1638–1643. 709 indexed citations breakdown →
15.
Morgan, Caurnel, Ruth E. Thomas, & Roger D. Cone. (2003). Melanocortin-5 receptor deficiency promotes defensive behavior in male mice. Hormones and Behavior. 45(1). 58–63. 33 indexed citations
16.
Chen, Wenbiao, Michele A. Kelly, Ximena Opitz-Araya, et al.. (1997). Exocrine Gland Dysfunction in MC5-R-Deficient Mice: Evidence for Coordinated Regulation of Exocrine Gland Function by Melanocortin Peptides. Cell. 91(6). 789–798. 389 indexed citations
17.
Thomas, Ruth E. & Paul Roberts. (1966). COMPARATIVE FREQUENCY OF X-RAY INDUCED CROSSOVER-SUPPRESSING ABERRATIONS RECOVERED FROM OOCYTES AND SPERM OF DROSOPHILA MELANOGASTER . Genetics. 53(5). 855–862. 6 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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