Author

R. Blanco

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cancer Biology· 2 Immunology· 1

Signature Assays, Organisms & Methods

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Organism:mouse· 3 Assay:bulk RNA-seq· 2 Research Focus:cell signaling & trafficking· 2 Approach:experimental assay· 2 Organism:human· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:development & morphogenesis· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

E. Molina· 2 shared J. Leon· 2 shared L. Garcia-Gutierrez· 2 shared A. Fernandez· 1 shared A. Martin· 1 shared A. Ramiro· 1 shared A. Ruiz· 1 shared A. V. Marin· 1 shared

Activity by Year

2018-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 19 mutual co-author links

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2 shared papersCancer Biology

E. Molina

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

MYC directly transactivates CR2/CD21, the receptor of the Epstein-Barr virus, and enhances the viral infection of Burkitt lymphoma cells

E. Molina, L. Garcia-Gutierrez, V. Junco, M. Perez-Olivares, V. G de Yebenes, R. Blanco, L. Quevedo, J. C. Acosta, A. V. Marin, D. Ulgiati, R. Merino, I. Varela, J. R. Regueiro, I. Moreno de Alboran, A. Ramiro, J. Leon

This paper identifies CR2/CD21 as a direct target of MYC and shows that MYC enhances EBV infection in Burkitt lymphoma cells.

bioRxiv · Dec 28, 2022 · PreprintCancer Biology

CCR5 deficiency impairs CD4+ T cell memory responses and antigenic sensitivity through increased ceramide synthesis

A. Martin, R. Blanco, J. Casas, M. E. Saez, E. Rodriguez-Bovolenta, I. E. de Rojas, C. Drechsler, L. M. Real, G. Fabrias, A. Ruiz, M. Castro, W. W. A. Schamel, B. Alarcon, H. M. van Santen, S. Manes

This study shows that CCR5 deficiency in CD4+ T cells increases ceramide synthesis, reduces TCR nanoclustering, and impairs memory responses and antigenic sensitivity.

bioRxiv · Feb 14, 2020Immunology

Myc stimulates cell cycle progression through the activation of Cdk1 and phosphorylation of p27

J. Leon, L. Garcia-Gutierrez, G. Bretones, E. Molina, I. Arechaga, J. C. R. Acosta, R. Blanco, A. Fernandez, L. Alonso, P. Sicinski, M. Barbacid, D. Santamaria

The paper shows Myc activates Cdk1 to phosphorylate p27 at Thr187, promoting its degradation and cell cycle progression, with Cdk1 inhibition causing synthetic lethality with Myc.

bioRxiv · Dec 16, 2018Cancer Biology