Author

A. J. Lopez-Contreras

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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Cell Biology· 2 Cancer Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:chromatin & epigenetic regulation· 1 Assay:DNA methylation· 1

Frequent Co-Authors

E. Albers· 2 shared O. Fernandez-Capetillo· 2 shared A. Avram· 1 shared A. Bachi· 1 shared A. Gnocchi· 1 shared A. Romero-Franco· 1 shared A. Wals· 1 shared C. Checa-Rodriguez· 1 shared

Activity by Year

2020-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 20 mutual co-author links

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Curved chords = mutual co-authorship

2 shared papersCancer Biology

E. Albers

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Circadian regulation of Homologous Recombination by Cryptochrome1-mediated dampening of DNA end resection

A. Romero-Franco, C. Checa-Rodriguez, S. Jimeno, M. Castellano-Pozo, P. Aguilera, H. Miras, A. Wals, S. Jimeno-Gonzalez, A. J. Lopez-Contreras, P. Huertas

The paper shows circadian regulation of DNA resection through CRY1 and CCAR2, impacting cancer progression and radiation response.

bioRxiv · Jan 22, 2023Cell Biology

Supraphysiological protection from replication stress does not extend mammalian lifespan

E. Albers, A. Avram, M. Sbroggio, O. Fernandez-Capetillo, A. J. Lopez-Contreras

This study shows that enhancing replication stress protection in mice does not increase lifespan, suggesting replication stress is not a major driver of normal aging.

bioRxiv · Jan 17, 2020Cancer Biology

ATR expands embryonic stem cell fate potential in response to replication stress

S. Atashpaz, S. Samadi Shams, J. M. Gonzalez, E. Sebestyen, N. Arghavanifard, A. Gnocchi, E. Albers, S. Minardi, G. Faga, P. Soffientini, E. Allievi, V. Cancila, A. Bachi, O. Fernandez-Capetillo, C. Tripodo, , V. Costanzo

This study identifies an ATR-CHK1 pathway in ESCs that enhances fate potential by inducing 2C-like gene expression in response to replication stress.

bioRxiv · Jan 1, 2020Cell Biology