DCTN1 Binds to TDP-43 and Regulates TDP-43 Aggregation
暂无分享,去创建一个
H. Okano | Y. Uehara | S. Hirose | Y. Tsuboi | Fumiyoshi Ishidate | Mitsuru Ishikawa | S. Fujioka | K. Iwasaki | Takuya Watanabe | S. Hirano | Takayasu Mishima | Kaori Kubota | Manami Deshimaru | Mariko Kinoshita-Kawada | J. Yuasa-Kawada | Yasuyoshi Tanaka | M. Hiramoto
[1] F. Hirth,et al. Triad of TDP43 control in neurodegeneration: autoregulation, localization and aggregation , 2021, Nature Reviews Neuroscience.
[2] Michael S. Fernandopulle,et al. RNA transport and local translation in neurodevelopmental and neurodegenerative disease , 2021, Nature Neuroscience.
[3] J. Veldink,et al. Genetic analysis of ALS cases in the isolated island population of Malta , 2021, European journal of human genetics : EJHG.
[4] J. Twiss,et al. The functional organization of axonal mRNA transport and translation , 2020, Nature Reviews Neuroscience.
[5] Nikita R. Dsouza,et al. Novel destabilizing Dynactin variant (DCTN1 p.Tyr78His) in patient with Perry syndrome. , 2020, Parkinsonism & related disorders.
[6] A. Yildiz,et al. Activation and Regulation of Cytoplasmic Dynein. , 2020, Trends in biochemical sciences.
[7] P. Fratta,et al. Cytoplasmic functions of TDP-43 and FUS and their role in ALS. , 2020, Seminars in cell & developmental biology.
[8] Takahiro A. Kato,et al. In Vitro Modeling of the Bipolar Disorder and Schizophrenia Using Patient-Derived Induced Pluripotent Stem Cells with Copy Number Variations of PCDH15 and RELN , 2019, eNeuro.
[9] Lin Guo,et al. Cytoplasmic TDP-43 De-mixing Independent of Stress Granules Drives Inhibition of Nuclear Import, Loss of Nuclear TDP-43, and Cell Death , 2019, Neuron.
[10] E. Holzbaur,et al. Dynein activators and adaptors at a glance , 2019, Journal of Cell Science.
[11] Y. Rao,et al. A crucial role for Arf6 in the response of commissural axons to Slit , 2019, Development.
[12] J. Fukae,et al. Modeling Parkinson’s Disease and Atypical Parkinsonian Syndromes Using Induced Pluripotent Stem Cells , 2018, International journal of molecular sciences.
[13] H. Okano,et al. The pathogenesis linked to coenzyme Q10 insufficiency in iPSC-derived neurons from patients with multiple-system atrophy , 2018, Scientific Reports.
[14] Nicolas L. Fawzi,et al. Protein Phase Separation: A New Phase in Cell Biology. , 2018, Trends in cell biology.
[15] Samara L. Reck-Peterson,et al. The cytoplasmic dynein transport machinery and its many cargoes , 2018, Nature Reviews Molecular Cell Biology.
[16] C. Holt,et al. FUS Phase Separation Is Modulated by a Molecular Chaperone and Methylation of Arginine Cation-π Interactions , 2018, Cell.
[17] Seung Joong Kim,et al. Nuclear Import Receptor Inhibits Phase Separation of FUS through Binding to Multiple Sites , 2018, Cell.
[18] M. Simons,et al. Phase Separation of FUS Is Suppressed by Its Nuclear Import Receptor and Arginine Methylation , 2018, Cell.
[19] Julie C. Sung,et al. Nuclear-Import Receptors Reverse Aberrant Phase Transitions of RNA-Binding Proteins with Prion-like Domains , 2018, Cell.
[20] M. Farrer,et al. Establishing diagnostic criteria for Perry syndrome , 2017, Journal of Neurology, Neurosurgery, and Psychiatry.
[21] J. Taylor,et al. Lost in Transportation: Nucleocytoplasmic Transport Defects in ALS and Other Neurodegenerative Diseases , 2017, Neuron.
[22] A. Carter,et al. Cryo-EM shows how dynactin recruits two dyneins for faster movement , 2017, Nature.
[23] M. Ko,et al. Neural differentiation of human embryonic stem cells induced by the transgene-mediated overexpression of single transcription factors. , 2017, Biochemical and biophysical research communications.
[24] M. Goldberg. Nuclear pore complex tethers to the cytoskeleton. , 2017, Seminars in cell & developmental biology.
[25] D. Dickson,et al. Perry Syndrome: A Distinctive Type of TDP-43 Proteinopathy , 2017, Journal of neuropathology and experimental neurology.
[26] Chadwick M. Hales,et al. TDP-43 pathology disrupts nuclear pore complexes and nucleocytoplasmic transport in ALS/FTD , 2017, Alzheimer's & Dementia.
[27] A. Bird,et al. Cryo-EM Reveals How Human Cytoplasmic Dynein Is Auto-inhibited and Activated , 2017, Cell.
[28] N. Hattori,et al. Reduced TDP-43 Expression Improves Neuronal Activities in a Drosophila Model of Perry Syndrome , 2017, EBioMedicine.
[29] Rohit V Pappu,et al. CIDER: Resources to Analyze Sequence-Ensemble Relationships of Intrinsically Disordered Proteins , 2017, Biophysical journal.
[30] Dennis W Dickson,et al. Pathology of Neurodegenerative Diseases. , 2017, Cold Spring Harbor perspectives in biology.
[31] Robert H. Brown,et al. Decoding ALS: from genes to mechanism , 2016, Nature.
[32] R. Takahashi,et al. Cytoplasmic aggregates of dynactin in iPSC-derived tyrosine hydroxylase-positive neurons from a patient with Perry syndrome. , 2016, Parkinsonism & related disorders.
[33] E. Buratti,et al. Physiological functions and pathobiology of TDP‐43 and FUS/TLS proteins , 2016, Journal of neurochemistry.
[34] Brian Raught,et al. A Dynamic Protein Interaction Landscape of the Human Centrosome-Cilium Interface , 2015, Cell.
[35] Kai Zhang,et al. The structure of the dynactin complex and its interaction with dynein , 2015, Science.
[36] Takayuki Oka,et al. A Novel DCTN1 mutation with late‐onset parkinsonism and frontotemporal atrophy , 2014, Movement disorders : official journal of the Movement Disorder Society.
[37] N. Hattori,et al. p150glued-Associated Disorders Are Caused by Activation of Intrinsic Apoptotic Pathway , 2014, PloS one.
[38] K. Eggan,et al. Axonal Transport of TDP-43 mRNA Granules Is Impaired by ALS-Causing Mutations , 2014, Neuron.
[39] E. Holzbaur,et al. The Regulation of Autophagosome Dynamics by Huntingtin and HAP1 Is Disrupted by Expression of Mutant Huntingtin, Leading to Defective Cargo Degradation , 2014, The Journal of Neuroscience.
[40] L. Greensmith,et al. Cytoplasmic dynein heavy chain: the servant of many masters , 2013, Trends in Neurosciences.
[41] D. Cleveland,et al. Converging Mechanisms in ALS and FTD: Disrupted RNA and Protein Homeostasis , 2013, Neuron.
[42] E. Holzbaur,et al. Dynactin Subunit p150Glued Is a Neuron-Specific Anti-Catastrophe Factor , 2013, PLoS biology.
[43] T. Südhof,et al. Rapid Single-Step Induction of Functional Neurons from Human Pluripotent Stem Cells , 2013, Neuron.
[44] G. Sobue,et al. dnc-1/dynactin 1 Knockdown Disrupts Transport of Autophagosomes and Induces Motor Neuron Degeneration , 2013, PloS one.
[45] K. Yamanaka,et al. Accelerated Disease Onset with Stabilized Familial Amyotrophic Lateral Sclerosis (ALS)-linked Mutant TDP-43 Proteins , 2012, The Journal of Biological Chemistry.
[46] E. Holzbaur,et al. Dynactin Is Required for Transport Initiation from the Distal Axon , 2012, Neuron.
[47] Ji Han Kim,et al. The p150Glued CAP-Gly Domain Regulates Initiation of Retrograde Transport at Synaptic Termini , 2012, Neuron.
[48] B. Berger,et al. Multicoil2: Predicting Coiled Coils and Their Oligomerization States from Sequence in the Twilight Zone , 2011, PloS one.
[49] Gene W. Yeo,et al. Long pre-mRNA depletion and RNA missplicing contribute to neuronal vulnerability from loss of TDP-43 , 2011, Nature Neuroscience.
[50] I. Zaliapin,et al. CLIP-170-dependent capture of membrane organelles by microtubules initiates minus-end directed transport. , 2009, Developmental cell.
[51] S. Bullock,et al. Egalitarian is a selective RNA-binding protein linking mRNA localization signals to the dynein motor. , 2009, Genes & development.
[52] A. Gitler,et al. TDP-43 Is Intrinsically Aggregation-prone, and Amyotrophic Lateral Sclerosis-linked Mutations Accelerate Aggregation and Increase Toxicity* , 2009, The Journal of Biological Chemistry.
[53] M. Farrer,et al. Pallidonigral TDP-43 pathology in Perry syndrome. , 2009, Parkinsonism & related disorders.
[54] J. Caviston,et al. Huntingtin as an essential integrator of intracellular vesicular trafficking. , 2009, Trends in cell biology.
[55] J. Trojanowski,et al. Expression of TDP-43 C-terminal Fragments in Vitro Recapitulates Pathological Features of TDP-43 Proteinopathies* , 2009, Journal of Biological Chemistry.
[56] M. Farrer,et al. DCTN1 mutations in Perry syndrome , 2009, Nature Genetics.
[57] Andrea D'Ambrogio,et al. Structural determinants of the cellular localization and shuttling of TDP-43 , 2008, Journal of Cell Science.
[58] Y. Itoyama,et al. Development of a high-throughput microarray-based resequencing system for neurological disorders and its application to molecular genetics of amyotrophic lateral sclerosis. , 2008, Archives of neurology.
[59] J. Trojanowski,et al. Disturbance of Nuclear and Cytoplasmic TAR DNA-binding Protein (TDP-43) Induces Disease-like Redistribution, Sequestration, and Aggregate Formation* , 2008, Journal of Biological Chemistry.
[60] B. McConkey,et al. TARDBP mutations in individuals with sporadic and familial amyotrophic lateral sclerosis , 2008, Nature Genetics.
[61] Anna Akhmanova,et al. Tracking the ends: a dynamic protein network controls the fate of microtubule tips , 2008, Nature Reviews Molecular Cell Biology.
[62] Xun Hu,et al. TDP-43 Mutations in Familial and Sporadic Amyotrophic Lateral Sclerosis , 2008, Science.
[63] H. Cai,et al. The G59S Mutation in p150glued Causes Dysfunction of Dynactin in Mice , 2007, The Journal of Neuroscience.
[64] T. Ichisaka,et al. Induction of Pluripotent Stem Cells from Adult Human Fibroblasts by Defined Factors , 2007, Cell.
[65] T. Graf. Faculty Opinions recommendation of Induction of pluripotent stem cells from adult human fibroblasts by defined factors. , 2007 .
[66] C. Kaltschmidt,et al. Transcription Factor NF-κB Is Transported to the Nucleus via Cytoplasmic Dynein/Dynactin Motor Complex in Hippocampal Neurons , 2007, PloS one.
[67] J. Caviston,et al. Huntingtin facilitates dynein/dynactin-mediated vesicle transport , 2007, Proceedings of the National Academy of Sciences.
[68] J. Trojanowski,et al. TDP-43 proteinopathy: the neuropathology underlying major forms of sporadic and familial frontotemporal lobar degeneration and motor neuron disease , 2007, Acta Neuropathologica.
[69] H. Akiyama,et al. TDP-43 is a component of ubiquitin-positive tau-negative inclusions in frontotemporal lobar degeneration and amyotrophic lateral sclerosis. , 2006, Biochemical and biophysical research communications.
[70] Bruce L. Miller,et al. Ubiquitinated TDP-43 in Frontotemporal Lobar Degeneration and Amyotrophic Lateral Sclerosis , 2006, Science.
[71] Andrew D. Stephens,et al. A microtubule-binding domain in dynactin increases dynein processivity by skating along microtubules , 2006, Nature Cell Biology.
[72] A. Ludolph,et al. Point mutations of the p150 subunit of dynactin (DCTN1) gene in ALS , 2004, Neurology.
[73] M. Koltzenburg,et al. Axoplasmic Importins Enable Retrograde Injury Signaling in Lesioned Nerve , 2003, Neuron.
[74] T. Schroer,et al. Analysis of the dynein-dynactin interaction in vitro and in vivo. , 2003, Molecular biology of the cell.
[75] T. Schroer,et al. CLIP-170 interacts with dynactin complex and the APC-binding protein EB1 by different mechanisms. , 2003, Cell motility and the cytoskeleton.
[76] Shin J. Oh,et al. Mutant dynactin in motor neuron disease , 2003, Nature Genetics.
[77] I. Vernos,et al. Dynactin is required for bidirectional organelle transport , 2003, The Journal of cell biology.
[78] Z. Wszolek,et al. Japanese family with parkinsonism, depression, weight loss, and central hypoventilation , 2002, Neurology.
[79] Dan L. Sackett,et al. p53 is associated with cellular microtubules and is transported to the nucleus by dynein , 2000, Nature Cell Biology.
[80] V. Allan,et al. Dynactin , 2000, Current Biology.
[81] C. Echeverri,et al. Colocalization of cytoplasmic dynein with dynactin and CLIP-170 at microtubule distal ends. , 1999, Journal of cell science.
[82] J Schultz,et al. SMART, a simple modular architecture research tool: identification of signaling domains. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[83] S. Hersch,et al. Interaction of Huntingtin-Associated Protein with Dynactin P150Glued , 1998, The Journal of Neuroscience.
[84] P. Worley,et al. Huntingtin-associated protein 1 (HAP1) interacts with the p150Glued subunit of dynactin. , 1997, Human molecular genetics.
[85] R. Vallee,et al. Cytoplasmic dynein binds dynactin through a direct interaction between the intermediate chains and p150Glued , 1995, The Journal of cell biology.
[86] S. Karki,et al. Affinity Chromatography Demonstrates a Direct Binding between Cytoplasmic Dynein and the Dynactin Complex * , 1995, The Journal of Biological Chemistry.
[87] C. Waterman-Storer,et al. The p150Glued component of the dynactin complex binds to both microtubules and the actin-related protein centractin (Arp-1). , 1995, Proceedings of the National Academy of Sciences of the United States of America.
[88] M. Sheetz,et al. Dynactin, a conserved, ubiquitously expressed component of an activator of vesicle motility mediated by cytoplasmic dynein , 1991, The Journal of cell biology.
[89] R. Vallee,et al. Homology of a 150K cytoplasmic dynein-associated polypeptide with the Drosophila gene Glued , 1991, Nature.
[90] P. Bratty,et al. Hereditary mental depression and Parkinsonism with taurine deficiency. , 1975, Archives of neurology.
[91] Norman E. Davey,et al. Proteome-wide analysis of human disease mutations in short linear motifs: neglected players in cancer? , 2014, Molecular bioSystems.
[92] Debasis Dash,et al. Location of disorder in coiled coil proteins is influenced by its biological role and subcellular localization: a GO-based study on human proteome. , 2012, Molecular bioSystems.
[93] E. Holzbaur,et al. Cytoplasmic Dynein Dysfunction and Neurodegenerative Disease , 2012 .
[94] Obradovic,et al. Predicting Protein Disorder for N-, C-, and Internal Regions. , 1999, Genome informatics. Workshop on Genome Informatics.