Yoav D. Shaul

8.3k total citations · 3 hit papers
40 papers, 4.6k citations indexed

About

Yoav D. Shaul is a scholar working on Molecular Biology, Cell Biology and Immunology. According to data from OpenAlex, Yoav D. Shaul has authored 40 papers receiving a total of 4.6k indexed citations (citations by other indexed papers that have themselves been cited), including 29 papers in Molecular Biology, 9 papers in Cell Biology and 7 papers in Immunology. Recurrent topics in Yoav D. Shaul's work include Melanoma and MAPK Pathways (6 papers), Protein Kinase Regulation and GTPase Signaling (5 papers) and Cancer Cells and Metastasis (4 papers). Yoav D. Shaul is often cited by papers focused on Melanoma and MAPK Pathways (6 papers), Protein Kinase Regulation and GTPase Signaling (5 papers) and Cancer Cells and Metastasis (4 papers). Yoav D. Shaul collaborates with scholars based in Israel, United States and Germany. Yoav D. Shaul's co-authors include Rony Seger, David M. Sabatini, Robert A. Lindquist, Carson C. Thoreen, Yasemin Sancak, Liron Bar‐Peled, Timothy R. Peterson, Sima Lev, Vladimir Litvak and Prathapan Thiru and has published in prestigious journals such as Science, Cell and Proceedings of the National Academy of Sciences.

In The Last Decade

Yoav D. Shaul

39 papers receiving 4.5k citations

Hit Papers

The Rag GTPases Bind Raptor and Mediate Amino Acid Signal... 2006 2026 2012 2019 2008 2006 2019 500 1000 1.5k 2.0k

Peers

Yoav D. Shaul
Rachel Toth United Kingdom
Peter Adamson United Kingdom
Jung Min Han South Korea
Thomas Grewal Australia
Ho Lee South Korea
Sandeep Gurbuxani United States
Christoph Reinhard United States
Yoav D. Shaul
Citations per year, relative to Yoav D. Shaul Yoav D. Shaul (= 1×) peers Johannes Graumann

Countries citing papers authored by Yoav D. Shaul

Since Specialization
Citations

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

Fields of papers citing papers by Yoav D. Shaul

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Yoav D. Shaul. 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 Yoav D. Shaul. The network helps show where Yoav D. Shaul may publish in the future.

Co-authorship network of co-authors of Yoav D. Shaul

This figure shows the co-authorship network connecting the top 25 collaborators of Yoav D. Shaul. A scholar is included among the top collaborators of Yoav D. Shaul 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 Yoav D. Shaul. Yoav D. Shaul 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.
Navrátil, Jiří, et al.. (2025). Orchestrating movement: the role of Caveolin-1 in migration and metastasis. Molecular Cancer. 24(1). 267–267.
2.
Solaimuthu, Balakrishnan, et al.. (2024). The exostosin glycosyltransferase 1/STAT3 axis is a driver of breast cancer aggressiveness. Proceedings of the National Academy of Sciences. 121(3). e2316733121–e2316733121. 5 indexed citations
3.
Solaimuthu, Balakrishnan, et al.. (2022). DPYSL2 interacts with JAK1 to mediate breast cancer cell migration. The Journal of Cell Biology. 221(7). 11 indexed citations
4.
Solaimuthu, Balakrishnan, et al.. (2021). Monitoring Breast Cancer Growth and Metastatic Colony Formation in Mice using Bioluminescence. Journal of Visualized Experiments. 4 indexed citations
5.
Shilo, Asaf, Shaya Lev, Maxim Mogilevsky, et al.. (2019). 2-APB and CBD-Mediated Targeting of Charged Cytotoxic Compounds Into Tumor Cells Suggests the Involvement of TRPV2 Channels. Frontiers in Pharmacology. 10. 1198–1198. 19 indexed citations
6.
Gershkovitz, Maya, Tanya Fainsod-Levi, Saleh Khawaled, et al.. (2018). Microenvironmental Cues Determine Tumor Cell Susceptibility to Neutrophil Cytotoxicity. Cancer Research. 78(17). 5050–5059. 30 indexed citations
7.
Gershkovitz, Maya, Yaki Caspi, Tanya Fainsod-Levi, et al.. (2018). TRPM2 Mediates Neutrophil Killing of Disseminated Tumor Cells. Cancer Research. 78(10). 2680–2690. 165 indexed citations
8.
Shaul, Yoav D., Bingbing Yuan, Prathapan Thiru, et al.. (2015). MERAV: a tool for comparing gene expression across human tissues and cell types. Nucleic Acids Research. 44(D1). D560–D566. 100 indexed citations
9.
Reuven, Nina, et al.. (2013). The Hippo pathway kinase Lats2 prevents DNA damage-induced apoptosis through inhibition of the tyrosine kinase c-Abl. Cell Death and Differentiation. 20(10). 1330–1340. 54 indexed citations
10.
McNeill, Helen, Marius Sudol, Georg Halder, et al.. (2011). The Hippo tumor suppressor pathway: a report on ‘the second workshop on the Hippo tumor suppressor pathway’. Cell Death and Differentiation. 18(8). 1388–1390. 2 indexed citations
11.
Lindquist, Robert A., Kathleen Ottina, Douglas B. Wheeler, et al.. (2011). Genome-scale RNAi on living-cell microarrays identifies novel regulators ofDrosophila melanogasterTORC1–S6K pathway signaling. Genome Research. 21(3). 433–446. 26 indexed citations
12.
Shaul, Yoav D., et al.. (2009). Specific phosphorylation and activation of ERK1c by MEK1b: a unique route in the ERK cascade. Genes & Development. 23(15). 1779–1790. 31 indexed citations
13.
Sancak, Yasemin, Timothy R. Peterson, Yoav D. Shaul, et al.. (2008). The Rag GTPases Bind Raptor and Mediate Amino Acid Signaling to mTORC1. Science. 320(5882). 1496–1501. 2092 indexed citations breakdown →
14.
Shaul, Yoav D. & Rony Seger. (2006). The MEK/ERK cascade: From signaling specificity to diverse functions. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research. 1773(8). 1213–1226. 761 indexed citations breakdown →
15.
Aebersold, Daniel M., Yoav D. Shaul, Yuval Yung, et al.. (2004). Extracellular Signal-Regulated Kinase 1c (ERK1c), a Novel 42-Kilodalton ERK, Demonstrates Unique Modes of Regulation, Localization, and Function. Molecular and Cellular Biology. 24(22). 10000–10015. 53 indexed citations
16.
Shaul, Yoav D. & Rony Seger. (2004). Use of Inhibitors in the Study of MAPK Signaling. Humana Press eBooks. 250. 113–126. 3 indexed citations
17.
Litvak, Vladimir, et al.. (2002). Targeting of Nir2 to Lipid Droplets Is Regulated by a Specific Threonine Residue within Its PI-Transfer Domain. Current Biology. 12(17). 1513–1518. 48 indexed citations
18.
Litvak, Vladimir, Donghua Tian, Yoav D. Shaul, & Sima Lev. (2000). Targeting of PYK2 to Focal Adhesions as a Cellular Mechanism for Convergence between Integrins and G Protein-coupled Receptor Signaling Cascades. Journal of Biological Chemistry. 275(42). 32736–32746. 74 indexed citations
19.
Haviv, I., et al.. (1998). pX, the HBV-encoded coactivator, suppresses the phenotypes of TBP and TAFII250 mutants. Genes & Development. 12(8). 1217–1226. 29 indexed citations
20.
Agami, Reuven, et al.. (1997). The transcriptional activation and repression domains of RFX1, a context-dependent regulator, can mutually neutralize their activities. Nucleic Acids Research. 25(18). 3621–3628. 51 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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