Publicaciones (27) Publicaciones de Montse Arrasate Iragui

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. Disease-associated polyglutamine stretches in monomeric huntingtin adopt a compact structure

    Journal of Molecular Biology, Vol. 421, Núm. 4-5, pp. 587-600

  2. Erratum: Identifying polyglutamine protein species in situ that best predict neurodegeneration (Nature Chemical Biology (2011) 7 (925-934))

    Nature Chemical Biology

  3. 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. A small-molecule scaffold induces autophagy in primary neurons and protects against toxicity in a Huntington disease model

    Proceedings of the National Academy of Sciences of the United States of America, Vol. 107, Núm. 39, pp. 16982-16987

  2. 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

2005

  1. Automated microscope system for determining factors that predict neuronal fate

    Proceedings of the National Academy of Sciences of the United States of America, Vol. 102, Núm. 10, pp. 3840-3845

2004

  1. Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death

    Nature, Vol. 431, Núm. 7010, pp. 805-810

  2. Using antibodies to analyze polyglutamine stretches.

    Methods in molecular biology (Clifton, N.J.), Vol. 277, pp. 103-128