Publicaciones en colaboración con investigadores/as de University of California, San Francisco (21)

2023

  1. Criteria for preclinical models of cholangiocarcinoma: scientific and medical relevance

    Nature Reviews Gastroenterology and Hepatology, Vol. 20, Núm. 7, pp. 462-480

  2. Oncolytic DNX-2401 virotherapy plus pembrolizumab in recurrent glioblastoma: a phase 1/2 trial

    Nature Medicine, Vol. 29, Núm. 6, pp. 1370-1378

  3. Signature-driven repurposing of Midostaurin for combination with MEK1/2 and KRASG12C inhibitors in lung cancer

    Nature Communications, Vol. 14, Núm. 1

  4. TIM-3 blockade in diffuse intrinsic pontine glioma models promotes tumor regression and antitumor immune memory

    Cancer Cell, Vol. 41, Núm. 11, pp. 1911-1926.e8

2020

  1. The Mir181ab1 cluster promotes KRAS-driven oncogenesis and progression in lung and pancreas

    Journal of Clinical Investigation, Vol. 130, Núm. 4, pp. 1879-1895

2019

  1. Antitumor activity of an engineered decoy receptor targeting CLCF1–CNTFR signaling in lung adenocarcinoma

    Nature Medicine, Vol. 25, Núm. 11, pp. 1783-1795

  2. Correction to: Methylthioadenosine promotes remyelination by inducing oligodendrocyte differentiation (Multiple Sclerosis and Demyelinating Disorders (2017) 2 (1) DOI: 10.1186/s40893-017-0020-8)

    Multiple Sclerosis and Demyelinating Disorders

2017

  1. Erratum: The disruption of mitochondrial axonal transport is an early event in neuroinflammation. [J Neuroinflammation., 12, 1, (2015)(152)] DOI: 10.1186/s12974-015-0375-8

    Journal of Neuroinflammation

2015

  1. Analysis of heritability and shared heritability based on genome-wide association studies for thirteen cancer types

    Journal of the National Cancer Institute, Vol. 107, Núm. 12

  2. The disruption of mitochondrial axonal transport is an early event in neuroinflammation

    Journal of Neuroinflammation, Vol. 12, Núm. 1

2014

  1. Imputation and subset-based association analysis across different cancer types identifies multiple independent risk loci in the TERT-CLPTM1L region on chromosome 5p15.33

    Human Molecular Genetics, Vol. 23, Núm. 24, pp. 6616-6633

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. 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