Luis Toledo

3.6k total citations · 1 hit paper
18 papers, 2.7k citations indexed

About

Luis Toledo is a scholar working on Molecular Biology, Oncology and Cell Biology. According to data from OpenAlex, Luis Toledo has authored 18 papers receiving a total of 2.7k indexed citations (citations by other indexed papers that have themselves been cited), including 18 papers in Molecular Biology, 8 papers in Oncology and 2 papers in Cell Biology. Recurrent topics in Luis Toledo's work include DNA Repair Mechanisms (18 papers), Cancer-related Molecular Pathways (6 papers) and CRISPR and Genetic Engineering (5 papers). Luis Toledo is often cited by papers focused on DNA Repair Mechanisms (18 papers), Cancer-related Molecular Pathways (6 papers) and CRISPR and Genetic Engineering (5 papers). Luis Toledo collaborates with scholars based in Denmark, Spain and Germany. Luis Toledo's co-authors include Óscar Fernández-Capetillo, Matilde Murga, Simon Bekker‐Jensen, Niels Mailand, Matthias Altmeyer, Claudia Lukas, Jiří Bártek, R. Soria-Ruiz, Maj‐Britt Rask and Dorthe Helena Larsen and has published in prestigious journals such as Cell, Nature Communications and The Journal of Experimental Medicine.

In The Last Decade

Luis Toledo

17 papers receiving 2.7k citations

Hit Papers

ATR Prohibits Replication Catastrophe by Preventing Globa... 2013 2026 2017 2021 2013 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
Luis Toledo Denmark 14 2.5k 1.2k 454 358 182 18 2.7k
Zhongsheng You United States 25 2.6k 1.0× 976 0.8× 449 1.0× 501 1.4× 180 1.0× 49 2.8k
Gloria G. Glick United States 16 2.1k 0.8× 799 0.6× 454 1.0× 347 1.0× 220 1.2× 18 2.2k
Katherine Minter‐Dykhouse United States 14 1.7k 0.7× 707 0.6× 419 0.9× 348 1.0× 160 0.9× 15 2.0k
Andrea Krempler Germany 12 1.8k 0.7× 914 0.7× 283 0.6× 520 1.5× 136 0.7× 19 2.2k
Andrea Cocito Italy 9 2.0k 0.8× 683 0.6× 274 0.6× 332 0.9× 184 1.0× 11 2.3k
Apolinar Maya‐Mendoza Denmark 23 1.8k 0.7× 631 0.5× 331 0.7× 282 0.8× 181 1.0× 45 2.2k
Lili Yamasaki United States 19 1.8k 0.7× 1.3k 1.1× 380 0.8× 254 0.7× 211 1.2× 23 2.3k
Larisa Litovchick United States 24 1.4k 0.5× 669 0.5× 293 0.6× 245 0.7× 151 0.8× 54 1.8k
Richard A. DiTullio United States 9 2.8k 1.1× 1.4k 1.1× 408 0.9× 604 1.7× 260 1.4× 9 3.1k
Julie M. Bailis United States 21 1.5k 0.6× 788 0.6× 299 0.7× 273 0.8× 122 0.7× 55 2.0k

Countries citing papers authored by Luis Toledo

Since Specialization
Citations

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

Fields of papers citing papers by Luis Toledo

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Luis Toledo

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

All Works

18 of 18 papers shown
1.
Rodríguez‐Acebes, Sara, et al.. (2025). DNA polymerase α/primase extraction from chromatin by VCP/p97 restricts ATR activation during unperturbed DNA replication. Nature Communications. 16(1). 5706–5706.
2.
Coscia, Fabian, Andreas Mund, Mads Lerdrup, et al.. (2022). The TRESLIN-MTBP complex couples completion of DNA replication with S/G2 transition. Molecular Cell. 82(18). 3350–3365.e7. 16 indexed citations
3.
Benada, Jan, G. Baldi, Kumar Somyajit, et al.. (2020). Physiological Tolerance to ssDNA Enables Strand Uncoupling during DNA Replication. Cell Reports. 30(7). 2416–2429.e7. 50 indexed citations
4.
Aranda, Sergi, et al.. (2019). Acute hydroxyurea-induced replication blockade results in replisome components disengagement from nascent DNA without causing fork collapse. Cellular and Molecular Life Sciences. 77(4). 735–749. 13 indexed citations
6.
Toledo, Luis, et al.. (2017). Replication Catastrophe: When a Checkpoint Fails because of Exhaustion. Molecular Cell. 66(6). 735–749. 162 indexed citations
7.
Haahr, Peter, Saskia Hoffmann, Maxim A. X. Tollenaere, et al.. (2016). Activation of the ATR kinase by the RPA-binding protein ETAA1. Nature Cell Biology. 18(11). 1196–1207. 191 indexed citations
8.
Toledo, Luis, Matthias Altmeyer, Maj‐Britt Rask, et al.. (2014). ATR Prohibits Replication Catastrophe by Preventing Global Exhaustion of RPA. Cell. 156(1-2). 374–374. 16 indexed citations
9.
Larsen, Dorthe Helena, Julie A. Clapperton, Myriam Gwerder, et al.. (2014). The NBS1–Treacle complex controls ribosomal RNA transcription in response to DNA damage. Nature Cell Biology. 16(8). 792–803. 125 indexed citations
10.
Altmeyer, Matthias, Luis Toledo, Þorkell Guðjόnsson, et al.. (2013). The Chromatin Scaffold Protein SAFB1 Renders Chromatin Permissive for DNA Damage Signaling. Molecular Cell. 52(2). 206–220. 57 indexed citations
11.
Toledo, Luis, Matthias Altmeyer, Maj‐Britt Rask, et al.. (2013). ATR Prohibits Replication Catastrophe by Preventing Global Exhaustion of RPA. Cell. 155(5). 1088–1103. 661 indexed citations breakdown →
12.
Guðjόnsson, Þorkell, Matthias Altmeyer, Velibor Savic, et al.. (2012). TRIP12 and UBR5 Suppress Spreading of Chromatin Ubiquitylation at Damaged Chromosomes. Cell. 150(4). 697–709. 262 indexed citations
13.
Murga, Matilde, Stefano Campaner, Andrés J. López‐Contreras, et al.. (2011). Exploiting oncogene-induced replicative stress for the selective killing of Myc-driven tumors. Nature Structural & Molecular Biology. 18(12). 1331–1335. 295 indexed citations
14.
Toledo, Luis, Matilde Murga, & Óscar Fernández-Capetillo. (2011). Targeting ATR and Chk1 kinases for cancer treatment: A new model for new (and old) drugs. Molecular Oncology. 5(4). 368–373. 140 indexed citations
15.
Toledo, Luis, Matilde Murga, Rafal Zur, et al.. (2011). A cell-based screen identifies ATR inhibitors with synthetic lethal properties for cancer-associated mutations. Nature Structural & Molecular Biology. 18(6). 721–727. 365 indexed citations
16.
Toledo, Luis, Matilde Murga, Paula Gutierrez‐Martinez, R. Soria-Ruiz, & Óscar Fernández-Capetillo. (2008). ATR signaling can drive cells into senescence in the absence of DNA breaks. Genes & Development. 22(3). 297–302. 136 indexed citations
17.
Cuadrado, Myriam, Bárbara Martínez-Pastor, Matilde Murga, et al.. (2006). ATM regulates ATR chromatin loading in response to DNA double-strand breaks. The Journal of Experimental Medicine. 203(2). 297–303. 185 indexed citations
18.
Cuadrado, Myriam, Bárbara Martínez-Pastor, Matilde Murga, et al.. (2006). ATM regulates ATR chromatin loading in response to DNA double-strand breaks. The Journal of Cell Biology. 172(5). i9–i9. 4 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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