Reut Shalgi

2.7k total citations
24 papers, 1.9k citations indexed

About

Reut Shalgi is a scholar working on Molecular Biology, Cancer Research and Cellular and Molecular Neuroscience. According to data from OpenAlex, Reut Shalgi has authored 24 papers receiving a total of 1.9k indexed citations (citations by other indexed papers that have themselves been cited), including 20 papers in Molecular Biology, 7 papers in Cancer Research and 3 papers in Cellular and Molecular Neuroscience. Recurrent topics in Reut Shalgi's work include RNA Research and Splicing (12 papers), RNA modifications and cancer (7 papers) and MicroRNA in disease regulation (7 papers). Reut Shalgi is often cited by papers focused on RNA Research and Splicing (12 papers), RNA modifications and cancer (7 papers) and MicroRNA in disease regulation (7 papers). Reut Shalgi collaborates with scholars based in Israel, United States and Italy. Reut Shalgi's co-authors include Yitzhak Pilpel, Moshe Oren, Daniel S. Lieber, Christopher B. Burge, Susan Lindquist, Jessica A. Hurt, Niv Sabath, Mikko Taipale, Irina Krykbaeva and Jingfang Ju and has published in prestigious journals such as Proceedings of the National Academy of Sciences, Nature Communications and Molecular Cell.

In The Last Decade

Reut Shalgi

24 papers receiving 1.9k citations

Peers

Reut Shalgi

PHYSI

ONCOL

Gregor Rot Slovenia

Benjamin R. Nelson United States

Katlin B. Massirer Brazil

Kathi Zarnack Germany

Bertrand Chin‐Ming Tan Taiwan

Govindasamy Amuthan United States

Sergey Paushkin United States

Eric L. Van Nostrand United States

Roberta Benetti Italy

John E. Blume United States

Gregor Rot Slovenia

Reut Shalgi

2.7k ×1.6

527 ×0.6

176 ×1.2

139 ×1.1

PHYSI

33 ×0.3

ONCOL

Citations per year, relative to Reut Shalgi Reut Shalgi (= 1×) peers Gregor Rot

Countries citing papers authored by Reut Shalgi

Since Specialization

Citations

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

Fields of papers citing papers by Reut Shalgi

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Reut Shalgi

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

All Works

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20 of 20 papers shown

Levy‐Adam, Flonia, et al.. (2025). Regulation of physiological and pathological condensates by molecular chaperones. FEBS Journal. 292(13). 3271–3297. 4 indexed citations

Shalgi, Reut, et al.. (2022). Stress-induced transcriptional readthrough into neighboring genes is linked to intron retention. iScience. 25(12). 105543–105543. 9 indexed citations

Shalgi, Reut, et al.. (2022). Characterization of spontaneous seizures and EEG abnormalities in a mouse model of the human A350V IQSEC2 mutation and identification of a possible target for precision medicine based therapy. Epilepsy Research. 182. 106907–106907. 9 indexed citations

Heinrich, Ronit, et al.. (2022). Differential roles for DNAJ isoforms in HTT-polyQ and FUS aggregation modulation revealed by chaperone screens. Nature Communications. 13(1). 516–516. 19 indexed citations

Shalgi, Reut, et al.. (2021). The aging proteostasis decline: From nematode to human. Experimental Cell Research. 399(2). 112474–112474. 28 indexed citations

Sabath, Niv, et al.. (2020). Cellular proteostasis decline in human senescence. Proceedings of the National Academy of Sciences. 117(50). 31902–31913. 87 indexed citations

Sabath, Niv, et al.. (2019). Amino Acid Biosynthesis Regulation during Endoplasmic Reticulum Stress Is Coupled to Protein Expression Demands. iScience. 19. 204–213. 18 indexed citations

Levy, Nina S., Randall S. Walikonis, Raz Palty, et al.. (2019). An IQSEC2 Mutation Associated With Intellectual Disability and Autism Results in Decreased Surface AMPA Receptors. Frontiers in Molecular Neuroscience. 12. 43–43. 28 indexed citations

Sabath, Niv, et al.. (2019). Widespread PERK-dependent repression of ER targets in response to ER stress. Scientific Reports. 9(1). 4330–4330. 44 indexed citations

10.

Sabath, Niv, et al.. (2018). DoGFinder: a software for the discovery and quantification of readthrough transcripts from RNA-seq. BMC Genomics. 19(1). 597–597. 18 indexed citations

11.

Vilborg, Anna, Niv Sabath, Jenny F. Nathans, et al.. (2017). Comparative analysis reveals genomic features of stress-induced transcriptional readthrough. Proceedings of the National Academy of Sciences. 114(40). E8362–E8371. 85 indexed citations

12.

Shalgi, Reut, Jessica A. Hurt, Susan Lindquist, & Christopher B. Burge. (2014). Widespread Inhibition of Posttranscriptional Splicing Shapes the Cellular Transcriptome following Heat Shock. Cell Reports. 7(5). 1362–1370. 142 indexed citations

13.

Shalgi, Reut, Jessica A. Hurt, Irina Krykbaeva, et al.. (2013). Widespread Regulation of Translation by Elongation Pausing in Heat Shock. Molecular Cell. 49(3). 439–452. 253 indexed citations

14.

Shalgi, Reut, Yitzhak Pilpel, & Moshe Oren. (2010). Repression of transposable-elements – a microRNA anti-cancer defense mechanism?. Trends in Genetics. 26(6). 253–259. 31 indexed citations

15.

Dahary, Dvir, Reut Shalgi, & Yitzhak Pilpel. (2010). CpG Islands as a Putative Source for Animal miRNAs: Evolutionary and Functional Implications. Molecular Biology and Evolution. 28(5). 1545–1551. 4 indexed citations

16.

Christoffersen, Nanna R., Reut Shalgi, Lisa B. Frankel, et al.. (2009). p53-independent upregulation of miR-34a during oncogene-induced senescence represses MYC. Cell Death and Differentiation. 17(2). 236–245. 285 indexed citations

17.

Shalgi, Reut, Ran Brosh, Moshe Oren, Yitzhak Pilpel, & Varda Rotter. (2009). Coupling transcriptional and post-transcriptional miRNA regulation in the control of cell fate. Aging. 1(9). 762–770. 59 indexed citations

18.

Shalgi, Reut, Daniel S. Lieber, Moshe Oren, & Yitzhak Pilpel. (2007). Global and Local Architecture of the Mammalian microRNA–Transcription Factor Regulatory Network. PLoS Computational Biology. 3(7). e131–e131. 411 indexed citations

19.

Xi, Yaguang, Reut Shalgi, Øystein Fodstad, Yitzhak Pilpel, & Jingfang Ju. (2006). Differentially Regulated Micro-RNAs and Actively Translated Messenger RNA Transcripts by Tumor Suppressor p53 in Colon Cancer. Clinical Cancer Research. 12(7). 2014–2024. 182 indexed citations

20.

Shalgi, Reut, Michal Lapidot, Ron Shamir, & Yitzhak Pilpel. (2005). A catalog of stability-associated sequence elements in 3' UTRs of yeast mRNAs. Genome biology. 6(10). R86–R86. 53 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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