Author

Claudia Rodríguez-López

Centro de Biología Molecular Severo OchoaORCID 0000-0001-6150-4702Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Neuroscience· 2 Pathology· 1

Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 2 Research Focus:differential expression· 2 Approach:experimental assay· 2 Research Focus:gene regulatory network inference· 2 Organism:human· 2 Organism:mouse· 2 Approach:statistical model· 2 Research Focus:cancer & tumor microenvironment· 1

Frequent Co-Authors

José J. LucasiD· 3 shared Claudio Toma AiD· 2 shared Ivó H. HernándeziD· 2 shared María Santos‐GalindoiD· 2 shared Sara PicóiD· 2 shared Ainara ElorzaiD· 1 shared Ainhoa Martínez‐Pizarro· 1 shared Alberto ParadelaiD· 1 shared

Activity by Year

2023-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 32 mutual co-author links

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3 shared papersNeuroscience

José J. LucasORCID

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3 papers

Recent·Most cited

NeurosciencebioRxivPreprintAug 23, 2024

TAF1-dependent transcriptional dysregulation underlies multiple sclerosis

Claudia Rodríguez-López, Ivó H. Hernández, José Terrón-Bautista…·José J. Lucas

This study identifies TAF1-dependent transcriptional dysregulation as a mechanism underlying multiple sclerosis progression and presents an in vivo model for therapeutic development.

DOI 10.1101/2024.08.23.609325

humanbulk RNA-seq

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PathologyHuman Molecular GeneticsPeer-reviewedMar 23, 2024

PAH DEFICIENT PATHOLOGY IN HUMANIZED c.1066-11G>A PHENYLKETONURIA MICE

Ainhoa Martínez‐Pizarro, Sara Picó, Arístides López‐Márquez…·Lourdes R. Desviat

This paper generates a partially humanized mouse model of PKU with the c.1066-11G>A PAH variant, showing splicing defects, metabolic imbalances, and neurological phenotypes.

6 citations

mouseexperimental assay

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NeuroscienceBiological PsychiatryPeer-reviewedMar 22, 2023

Pathogenic mis-splicing of CPEB4 in schizophrenia

Ivana Ollà, Antonio F. Pardiñas, Alberto Parras…·José J. Lucas

This study identifies aberrant CPEB4 splicing and downstream mis-expression of SCZ-risk genes as a novel etiological mechanism in schizophrenia.

24 citationstop 4%

humanmouse

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