Author

Paula García-Huerta

Instituto de Neurociencia Biomédica

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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Neuroscience· 2

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Research Focus:differential expression· 2 Research Focus:drug response / drug discovery· 2 Approach:experimental assay· 2 Organism:human· 2 Organism:mouse· 2 Assay:proteomics· 2 Research Focus:cell type annotation· 1 Research Focus:protein structure prediction· 1

Frequent Co-Authors

Claudio A. HetziD· 2 shared Lars PlateiD· 2 shared Marisol Cisternas-OlmedoiD· 2 shared Paulina Troncoso-EscuderoiD· 2 shared R. Luke WisemaniD· 2 shared René L. VidaliD· 2 shared S. Pablo SardiiD· 2 shared Alberto J. M. MartíniD· 1 shared

Activity by Year

2020-2021 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 43 mutual co-author links

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2 shared papersNeuroscience

Claudio A. HetzORCID

Mutual co-authors in cluster

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2 papers

Recent·Most cited

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, Paula García-Huerta, Constanza González, Lars Plate, Carolina Jerez, José Cánovas, Claudia A. Rivera, Valentina Castillo, Marisol Cisternas-Olmedo, Sirley Leal, Alexis N. Martinez, Julia M. D. Grandjean, Sonia Donzelli, , Claudio A. Hetz

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

Molecular Therapy · Feb 5, 2021Peer-reviewedNeuroscience

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, Arun Thiruvalluvan, Marisol Cisternas-Olmedo, Daniel R. Henríquez, Lars Plate, Pedro Chaná‐Cuevas, Cristian Saquel, Peter Thielen, Kenneth A. Longo, Brad J. Geddes, Gerardo Zelmar Lederkremer, Neeraj Sharma, Marina Shenkman, , 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.

Acta Neuropathologica · Jul 8, 2020Peer-reviewedNeuroscience