Renata C. Matos

972 total citations
12 papers, 541 citations indexed

About

Renata C. Matos is a scholar working on Molecular Biology, Insect Science and Infectious Diseases. According to data from OpenAlex, Renata C. Matos has authored 12 papers receiving a total of 541 indexed citations (citations by other indexed papers that have themselves been cited), including 5 papers in Molecular Biology, 5 papers in Insect Science and 4 papers in Infectious Diseases. Recurrent topics in Renata C. Matos's work include Insect symbiosis and bacterial influences (4 papers), Invertebrate Immune Response Mechanisms (4 papers) and Antimicrobial Resistance in Staphylococcus (4 papers). Renata C. Matos is often cited by papers focused on Insect symbiosis and bacterial influences (4 papers), Invertebrate Immune Response Mechanisms (4 papers) and Antimicrobial Resistance in Staphylococcus (4 papers). Renata C. Matos collaborates with scholars based in France, Portugal and Japan. Renata C. Matos's co-authors include François Leulier, Pascale Serror, Lionel Rigottier‐Gois, Maria de Fátima Silva Lopes, Francis Repoila, Martin Schwarzer, Bruno González‐Zorn, Nicolas Lapaque, Thierry Meylheuc and Laurent Debarbieux and has published in prestigious journals such as Cell Metabolism, Scientific Reports and The Journal of Infectious Diseases.

In The Last Decade

Renata C. Matos

12 papers receiving 537 citations

Peers

Renata C. Matos
J.M. Wells United Kingdom
Renata C. Matos
Citations per year, relative to Renata C. Matos Renata C. Matos (= 1×) peers J.M. Wells

Countries citing papers authored by Renata C. Matos

Since Specialization
Citations

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

Fields of papers citing papers by Renata C. Matos

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Renata C. Matos. 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 Renata C. Matos. The network helps show where Renata C. Matos may publish in the future.

Co-authorship network of co-authors of Renata C. Matos

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

All Works

12 of 12 papers shown
1.
Grenier, Théodore, Jessika Consuegra, Mariana Galvão Ferrarini, et al.. (2023). Intestinal GCN2 controls Drosophila systemic growth in response to Lactiplantibacillus plantarum symbiotic cues encoded by r/tRNA operons. eLife. 12. 7 indexed citations
3.
Matos, Renata C., Pascal Courtin, Isabel Ayala, et al.. (2022). DltC acts as an interaction hub for AcpS, DltA and DltB in the teichoic acid d-alanylation pathway of Lactiplantibacillus plantarum. Scientific Reports. 12(1). 13133–13133. 10 indexed citations
5.
Matos, Renata C., Martin Schwarzer, Hugo Gervais, et al.. (2017). D-Alanylation of teichoic acids contributes to Lactobacillus plantarum-mediated Drosophila growth during chronic undernutrition. Nature Microbiology. 2(12). 1635–1647. 75 indexed citations
6.
Storelli, Gilles, Maura Strigini, Théodore Grenier, et al.. (2017). Drosophila Perpetuates Nutritional Mutualism by Promoting the Fitness of Its Intestinal Symbiont Lactobacillus plantarum. Cell Metabolism. 27(2). 362–377.e8. 110 indexed citations
7.
Wessner, Françoise, Caroline Lacoux, Nathalie Goeders, et al.. (2015). Regulatory crosstalk between type I and type II toxin-antitoxin systems in the human pathogen Enterococcus faecalis. RNA Biology. 12(10). 1099–1108. 25 indexed citations
8.
Rigottier‐Gois, Lionel, et al.. (2014). The Surface Rhamnopolysaccharide Epa ofEnterococcus faecalisIs a Key Determinant of Intestinal Colonization. The Journal of Infectious Diseases. 211(1). 62–71. 67 indexed citations
9.
Matos, Renata C. & François Leulier. (2014). Lactobacilli-Host mutualism: "learning on the fly". Microbial Cell Factories. 13(Suppl 1). S6–S6. 39 indexed citations
10.
Matos, Renata C., Nicolas Lapaque, Lionel Rigottier‐Gois, et al.. (2013). Enterococcus faecalis Prophage Dynamics and Contributions to Pathogenic Traits. PLoS Genetics. 9(6). e1003539–e1003539. 157 indexed citations
11.
Gaspar, Frédéric Bustos, Natalia Montero, Renata C. Matos, et al.. (2012). Incongruence between the cps type 2 genotype and host-related phenotypes of an Enterococcus faecalis food isolate. International Journal of Food Microbiology. 158(2). 120–125. 4 indexed citations
12.
Matos, Renata C., et al.. (2009). Study on the dissemination of the bcrABDR cluster in Enterococcus spp. reveals that the BcrAB transporter is sufficient to confer high-level bacitracin resistance. International Journal of Antimicrobial Agents. 34(2). 142–147. 29 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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