Author

X. Hernandez-Alias

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 Evolutionary Biology· 1

Signature Assays, Organisms & Methods

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Organism:human· 3 Approach:statistical model· 3 Research Focus:chromatin & epigenetic regulation· 2 Assay:DNA methylation· 2 Research Focus:gene regulatory network inference· 2 Assay:whole-genome sequencing· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1

Frequent Co-Authors

L. Serrano· 3 shared M. H. Schaefer· 3 shared H. Benisty· 2 shared M. Irimia· 2 shared M. Weber· 2 shared A. Torres-Mendez· 1 shared D. Weghorn· 1 shared F. Mantica· 1 shared

Activity by Year

2019-2022 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 35 mutual co-author links

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Curved chords = mutual co-authorship

3 shared papersCancer Biology

L. Serrano

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Evolutionary conservation of A/T-ending codons reflects co-regulation of expression and complex formation.

H. Benisty, X. Hernandez-Alias, M. Weber, M. Anglada-Girotto, F. Mantica, L. Radusky, G. Senger, D. Weghorn, M. Irimia, M. H. Schaefer, L. Serrano

The paper shows that A/T-ending codons are conserved and co-regulated, enabling coordinated protein expression and complex formation across vertebrates.

bioRxiv · Jan 17, 2022Evolutionary Biology

Hypersilencing of SRRM4 suppresses basal microexon inclusion and promotes tumor growth across cancers

S. A. Head, X. Hernandez-Alias, J.-S. Yang, V. Beltran-Sastre, A. Torres-Mendez, M. Irimia, M. H. Schaefer, L. Serrano

This study shows that SRRM4 silencing in tumors suppresses microexon inclusion and promotes tumor growth by shifting cells toward differentiation.

PLOS Biology · Feb 23, 2021Peer-reviewedCancer Biology

Proliferation specific codon usage facilitates oncogene translation

H. Benisty, M. Weber, X. Hernandez-Alias, M. H. Schaefer, L. Serrano

The paper shows that oncogenes with codon usage adapted for efficient translation in proliferative cells are more frequently mutated in cancer.

bioRxiv · Jul 11, 2019Cancer Biology