Author

René L. Vidal

Universidad MayorORCID 0000-0002-4305-7387Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Neuroscience· 3 Genomics· 1

Signature Assays, Organisms & Methods

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Organism:mouse· 4 Approach:experimental assay· 3 Research Focus:differential expression· 2 Research Focus:drug response / drug discovery· 2 Organism:human· 2 Assay:proteomics· 2 Approach:statistical model· 2 Assay:bulk RNA-seq· 1

Frequent Co-Authors

Claudio A. HetziD· 3 shared Lars PlateiD· 3 shared Marisol Cisternas-OlmedoiD· 3 shared S. Pablo SardiiD· 3 shared Alberto J. M. MartíniD· 2 shared Paula García-Huerta· 2 shared Paulina Troncoso-EscuderoiD· 2 shared R. Luke WisemaniD· 2 shared

Activity by Year

2020-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 39 mutual co-author links

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3 shared papersNeuroscience

Claudio A. HetzORCID

Mutual co-authors in cluster

Author profile →

4 papers

Recent·Most cited

GenomicsInternational Journal of Molecular SciencesPeer-reviewedJun 29, 2023

Transcriptional and Histone acetylation changes associated with CRE elements expose key factors governing the regulatory circuit in early stage of Huntington's disease models.

Sandra Arancibia-Opazo, Sebastián Contreras-Riquelme, Mario Sánchez…·Mauricio Sáez

10 citations

mousebulk RNA-seq

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NeuroscienceThe EMBO JournalPeer-reviewedOct 31, 2022

Control of mammalian brain aging by the unfolded protein response (UPR)

Felipe Cabral‐Miranda, Giovanni Tamburini, Gabriela Martínez…·Claudio A. Hetz

The paper shows that manipulating the UPR pathway can restore brain function and reduce aging-related deficits.

97 citationstop 1%

mouseexperimental assay

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NeuroscienceMolecular TherapyPeer-reviewedFeb 5, 2021

Enforced dimerization between XBP1s and ATF6f enhances the protective effects of the unfolded protein response (UPR) in models of neurodegeneration

René L. Vidal, Denisse Sepúlveda, Paulina Troncoso-Escudero…·Claudio A. Hetz

This study shows that forcing dimerization between ATF6f and XBP1s enhances UPR activity, reducing protein aggregation in neurodegenerative disease models.

42 citations

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NeuroscienceActa NeuropathologicaPeer-reviewedJul 8, 2020

Insulin-like growth factor 2 (IGF2) protects against Huntington's disease through the extracellular disposal of protein aggregates

Paula García-Huerta, Paulina Troncoso-Escudero, Di Wu…·Claudio A. Hetz

This study identifies IGF2 as a disease modifier that reduces intracellular protein aggregates by promoting their extracellular disposal in Huntington's disease models.

70 citationstop 3%

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