Publicacións en colaboración con investigadores/as de Centro de Investigación Médica Aplicada (14)

2024

  1. GCN2 inhibition reduces mutant SOD1 clustering and toxicity and delays disease progression in an amyotrophic lateral sclerosis mouse model

    Translational Neurodegeneration

  2. Pharmacological inhibition of the integrated stress response accelerates disease progression in an amyotrophic lateral sclerosis mouse model

    British Journal of Pharmacology, Vol. 181, Núm. 3, pp. 495-508

2023

  1. Microglia and astrocyte activation is region-dependent in the α-synuclein mouse model of Parkinson's disease

    GLIA, Vol. 71, Núm. 3, pp. 571-587

  2. Stabilization of 14-3-3 protein-protein interactions with Fusicoccin-A decreases alpha-synuclein dependent cell-autonomous death in neuronal and mouse models

    Neurobiology of Disease, Vol. 183

2022

  1. The Role and Therapeutic Potential of the Integrated Stress Response in Amyotrophic Lateral Sclerosis

    International Journal of Molecular Sciences, Vol. 23, Núm. 14

2020

  1. Cb2 receptors and neuron–glia interactions modulate neurotoxicity generated by magl inhibition

    Biomolecules, Vol. 10, Núm. 8, pp. 1-15

  2. Fine tuning of the unfolded protein response by ISRIB improves neuronal survival in a model of amyotrophic lateral sclerosis

    Cell Death and Disease, Vol. 11, Núm. 5

  3. N-terminal acetylation mutants affect alpha-synuclein stability, protein levels and neuronal toxicity

    Neurobiology of Disease, Vol. 137

2017

  1. E46K α-synuclein pathological mutation causes cell-autonomous toxicity without altering protein turnover or aggregation

    Proceedings of the National Academy of Sciences of the United States of America, Vol. 114, Núm. 39, pp. E8274-E8283

2013

  1. Proteostasis of polyglutamine varies among neurons and predicts neurodegeneration

    Nature Chemical Biology, Vol. 9, Núm. 9, pp. 586-594

2012

  1. Protein aggregates in Huntington's disease

    Experimental Neurology, Vol. 238, Núm. 1, pp. 1-11

2011

  1. Identifying polyglutamine protein species in situ that best predict neurodegeneration

    Nature Chemical Biology, Vol. 7, Núm. 12, pp. 925-934

2010

  1. Quantitative relationships between huntingtin levels, polyglutamine length, inclusion body formation, and neuronal death provide novel insight into huntington's disease molecular pathogenesis

    Journal of Neuroscience, Vol. 30, Núm. 31, pp. 10541-10550

2009

  1. IKK phosphorylates Huntingtin and targets it for degradation by the proteasome and lysosome

    Journal of Cell Biology, Vol. 187, Núm. 7, pp. 1083-1099