TRIM28 regulates the nuclear accumulation and toxicity of both alpha-synuclein and tau
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Maxime W. C. Rousseaux | H. Zoghbi | J. Botas | J. Troncoso | T. Westbrook | P. Jafar-Nejad | María de Haro | I. Al-Ramahi | M. Rousseaux | C. Lasagna-Reeves | Tiemo J. Klisch | Thomas F. Westbrook | Jeehye Park | A. de Maio | L. Vilanova-Vélez | Lauren See | Ajay Sharma | Nan Lu | Luis Vilanova-Velez | P. Jafar‐nejad
[1] Maxime W. C. Rousseaux,et al. Ataxin-1 oligomers induce local spread of pathology and decreasing them by passive immunization slows Spinocerebellar ataxia type 1 phenotypes , 2015, eLife.
[2] U. Sengupta,et al. Pathological Interface Between Oligomeric Alpha-Synuclein and Tau in Synucleinopathies , 2015, Biological Psychiatry.
[3] Maxime W. C. Rousseaux,et al. A native interactor scaffolds and stabilizes toxic ATAXIN-1 oligomers in SCA1 , 2015, eLife.
[4] R. Barker,et al. The role of tau in the pathological process and clinical expression of Huntington’s disease , 2015, Brain : a journal of neurology.
[5] E. Masliah,et al. Parkinson’s Disease Genes VPS35 and EIF4G1 Interact Genetically and Converge on α-Synuclein , 2015, Neuron.
[6] E. Masliah,et al. Parkinson’s Disease Genes VPS35 and EIF4G1 Interact Genetically and Converge on α-Synuclein , 2015, Neuron.
[7] Elisabeth L. Moussaud-Lamodière,et al. Alpha-synuclein and tau: teammates in neurodegeneration? , 2014, Molecular Neurodegeneration.
[8] A. Gitler,et al. The novel Parkinson's disease linked mutation G51D attenuates in vitro aggregation and membrane binding of α-synuclein, and enhances its secretion and nuclear localization in cells. , 2014, Human molecular genetics.
[9] D. Ann,et al. KAPtain in charge of multiple missions: Emerging roles of KAP1. , 2014, World journal of biological chemistry.
[10] I. Ferrer,et al. Huntington's disease is a four-repeat tauopathy with tau nuclear rods , 2014, Nature Medicine.
[11] Bidisha Roy,et al. Interactions between Tau and α-synuclein augment neurotoxicity in a Drosophila model of Parkinson's disease. , 2014, Human molecular genetics.
[12] A. Buisson,et al. Activity-Dependent Tau Protein Translocation to Excitatory Synapse Is Disrupted by Exposure to Amyloid-Beta Oligomers , 2014, The Journal of Neuroscience.
[13] J. Clarimón,et al. Confluence of α-synuclein, tau, and β-amyloid pathologies in dementia with Lewy bodies. , 2013, Journal of neuropathology and experimental neurology.
[14] A. Saykin,et al. Pathways to neurodegeneration: mechanistic insights from GWAS in Alzheimer's disease, Parkinson's disease, and related disorders. , 2013, American journal of neurodegenerative disease.
[15] Bin Zhang,et al. Distinct α-Synuclein Strains Differentially Promote Tau Inclusions in Neurons , 2013, Cell.
[16] Michel Goedert,et al. Tau pathology and neurodegeneration , 2013, The Lancet Neurology.
[17] Hyojin Kang,et al. RAS–MAPK–MSK1 pathway modulates ataxin 1 protein levels and toxicity in SCA1 , 2013, Nature.
[18] Thomas C. Südhof,et al. Systematic Mutagenesis of α-Synuclein Reveals Distinct Sequence Requirements for Physiological and Pathological Activities , 2012, The Journal of Neuroscience.
[19] David S. Park,et al. Progressive dopaminergic cell loss with unilateral-to-bilateral progression in a genetic model of Parkinson disease , 2012, Proceedings of the National Academy of Sciences.
[20] J. Lancia,et al. Tau oligomers and tau toxicity in neurodegenerative disease. , 2012, Biochemical Society transactions.
[21] D. Dinsdale,et al. Sustained translational repression by eIF2α-P mediates prion neurodegeneration , 2012, Nature.
[22] M. Chesselet,et al. A Progressive Mouse Model of Parkinson’s Disease: The Thy1-aSyn (“Line 61”) Mice , 2012, Neurotherapeutics.
[23] Jason I. Herschkowitz,et al. The pINDUCER lentiviral toolkit for inducible RNA interference in vitro and in vivo , 2011, Proceedings of the National Academy of Sciences.
[24] L. Buée,et al. Nuclear Tau, a Key Player in Neuronal DNA Protection* , 2010, The Journal of Biological Chemistry.
[25] Dan Liu,et al. Genome-wide YFP Fluorescence Complementation Screen Identifies New Regulators for Telomere Signaling in Human Cells* , 2010, Molecular & Cellular Proteomics.
[26] R. Kayed,et al. Preparation and characterization of neurotoxic tau oligomers. , 2010, Biochemistry.
[27] T. Südhof,et al. α-Synuclein Promotes SNARE-Complex Assembly in Vivo and in Vitro , 2010, Science.
[28] Maojun Yang,et al. MAGE-RING protein complexes comprise a family of E3 ubiquitin ligases. , 2010, Molecular cell.
[29] E. Yaksi,et al. Acetylation of Tau Inhibits Its Degradation and Contributes to Tauopathy , 2010, Neuron.
[30] J. Trojanowski,et al. Synergistic Interactions between Aβ, Tau, and α-Synuclein: Acceleration of Neuropathology and Cognitive Decline , 2010, The Journal of Neuroscience.
[31] Sonja W. Scholz,et al. Genome-Wide Association Study reveals genetic risk underlying Parkinson’s disease , 2009, Nature Genetics.
[32] Aideen Long,et al. Statistical methods for analysis of high-throughput RNA interference screens , 2009, Nature Methods.
[33] Yang Shi,et al. SCFβ-TRCP controls oncogenic transformation and neural differentiation through REST degradation , 2008, Nature.
[34] M. Cookson,et al. Cell systems and the toxic mechanism(s) of α-synuclein , 2008, Experimental Neurology.
[35] David S. Park,et al. The Parkinson's disease gene DJ-1 is also a key regulator of stroke-induced damage , 2007, Proceedings of the National Academy of Sciences.
[36] Bin Zhang,et al. Synapse Loss and Microglial Activation Precede Tangles in a P301S Tauopathy Mouse Model , 2007, Neuron.
[37] J. Parvin,et al. Alpha-synuclein acts in the nucleus to inhibit histone acetylation and promote neurotoxicity. , 2006, Human molecular genetics.
[38] A. Lang,et al. Interface between tauopathies and synucleinopathies: A tale of two proteins , 2006, Annals of neurology.
[39] Philippe Amouyel,et al. α-synuclein locus duplication as a cause of familial Parkinson's disease , 2004, The Lancet.
[40] A Dürr,et al. Causal relation between α-synuclein locus duplication as a cause of familial Parkinson's disease , 2004, The Lancet.
[41] D. Price,et al. Stabilization of α-Synuclein Protein with Aging and Familial Parkinson's Disease-Linked A53T Mutation , 2004, The Journal of Neuroscience.
[42] Christina A. Wilson,et al. Degradative organelles containing mislocalized α- and β-synuclein proliferate in presenilin-1 null neurons , 2004, The Journal of cell biology.
[43] Janel O. Johnson,et al. α-Synuclein Locus Triplication Causes Parkinson's Disease , 2003, Science.
[44] D. Dickson,et al. Colocalization of Tau and Alpha‐Synuclein Epitopes in Lewy Bodies , 2003, Journal of neuropathology and experimental neurology.
[45] Robert Burke,et al. Resistance of α-synuclein null mice to the parkinsonian neurotoxin MPTP , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[46] Makoto Hashimoto,et al. Differential neuropathological alterations in transgenic mice expressing α‐synuclein from the platelet‐derived growth factor and Thy‐1 promoters , 2002, Journal of neuroscience research.
[47] D. Geschwind,et al. Human Wild-Type Tau Interacts with wingless Pathway Components and Produces Neurofibrillary Pathology in Drosophila , 2002, Neuron.
[48] M. Vitek,et al. Tau is essential to β-amyloid-induced neurotoxicity , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[49] K. Kosaka,et al. Relationship in the formation process between neurofibrillary tangles and Lewy bodies in the hippocampus of dementia with Lewy bodies brains , 2002, Journal of the Neurological Sciences.
[50] Joshua M. Shulman,et al. Tauopathy in Drosophila: Neurodegeneration Without Neurofibrillary Tangles , 2001, Science.
[51] M. Pfaffl,et al. A new mathematical model for relative quantification in real-time RT-PCR. , 2001, Nucleic acids research.
[52] P. Chambon,et al. Bonus, a Drosophila homolog of TIF1 proteins, interacts with nuclear receptors and can inhibit betaFTZ-F1-dependent transcription. , 2001, Molecular cell.
[53] P. Chambon,et al. Mice lacking the transcriptional corepressor TIF1beta are defective in early postimplantation development. , 2000, Development.
[54] Bin Zhang,et al. Age-Dependent Emergence and Progression of a Tauopathy in Transgenic Mice Overexpressing the Shortest Human Tau Isoform , 1999, Neuron.
[55] Kazuko Aoto,et al. Cellular co-localization of phosphorylated tau- and NACP/α-synuclein-epitopes in Lewy bodies in sporadic Parkinson's disease and in dementia with Lewy bodies , 1999, Brain Research.
[56] M. Cookson,et al. Cell systems and the toxic mechanism(s) of alpha-synuclein. , 2008, Experimental neurology.
[57] A Dürr,et al. Causal relation between alpha-synuclein gene duplication and familial Parkinson's disease. , 2004, Lancet.
[58] A. Singleton,et al. alpha-Synuclein locus triplication causes Parkinson's disease. , 2003, Science.
[59] M G Spillantini,et al. Alpha-synuclein in Lewy bodies. , 1997, Nature.
[60] K. Rajewsky,et al. A cre-transgenic mouse strain for the ubiquitous deletion of loxP-flanked gene segments including deletion in germ cells. , 1995, Nucleic acids research.