相关参考文献
注意：仅列出部分参考文献，下载原文获取全部文献信息。Nucleocytoplasmic transport defects in neurodegeneration - Cause or consequence?
Saskia Hutten et al.
SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY (2020)
Nucleocytoplasmic Proteomic Analysis Uncovers eRF1 and Nonsense-Mediated Decay as Modifiers of ALS/FTD C9orf72 Toxicity
Juan A. Ortega et al.
NEURON (2020)
G4C2 Repeat RNA Initiates a POM121-Mediated Reduction in Specific Nucleoporins in C9orf72 ALS/FTD
Alyssa N. Coyne et al.
NEURON (2020)
Quantitative proteomics identifies proteins that resist translational repression and become dysregulated in ALS-FUS
Desiree M. Baron et al.
HUMAN MOLECULAR GENETICS (2019)
RNA Binding Antagonizes Neurotoxic Phase Transitions of TDP-43
Jacob R. Mann et al.
NEURON (2019)
The RNA-binding protein FUS/TLS undergoes calcium-mediated nuclear egress during excitotoxic stress and is required for GRIA2 mRNA processing
Maeve Tischbein et al.
JOURNAL OF BIOLOGICAL CHEMISTRY (2019)
Improving homology-directed repair efficiency in human stem cells
William C. Skarnes et al.
METHODS (2019)
Physiological, Pathological, and Targetable Membraneless Organelles in Neurons
Veronica H. Ryan et al.
TRENDS IN NEUROSCIENCES (2019)
Modulation of actin polymerization affects nucleocytoplasmic transport in multiple forms of amyotrophic lateral sclerosis
Anthony Giampetruzzi et al.
NATURE COMMUNICATIONS (2019)
C9orf72-generated poly-GR and poly-PR do not directly interfere with nucleocytoplasmic transport
Joni Vanneste et al.
SCIENTIFIC REPORTS (2019)
ALS-linked FUS mutations confer loss and gain of function in the nucleus by promoting excessive formation of dysfunctional paraspeckles
Haiyan An et al.
ACTA NEUROPATHOLOGICA COMMUNICATIONS (2019)
Muscleblind acts as a modifier of FUS toxicity by modulating stress granule dynamics and SMN localization
Ian Casci et al.
NATURE COMMUNICATIONS (2019)
TDP-43 pathology disrupts nuclear pore complexes and nucleocytoplasmic transport in ALS/FTD
Ching-Chieh Chou et al.
NATURE NEUROSCIENCE (2018)
EasyFRAP-web: a web-based tool for the analysis of fluorescence recovery after photobleaching data
Grigorios Koulouras et al.
NUCLEIC ACIDS RESEARCH (2018)
RNA buffers the phase separation behavior of prion-like RNA binding proteins
Shovamayee Maharana et al.
SCIENCE (2018)
TDP43 nuclear export and neurodegeneration in models of amyotrophic lateral sclerosis and frontotemporal dementia
Hilary C. Archbold et al.
SCIENTIFIC REPORTS (2018)
Intrinsically Disordered Regions Can Contribute Promiscuous Interactions to RNP Granule Assembly
David S. W. Protter et al.
CELL REPORTS (2018)
Tau Protein Disrupts Nucleocytoplasmic Transport in Alzheimer's Disease
Bahareh Eftekharzadeh et al.
NEURON (2018)
Mutant FUS causes DNA ligation defects to inhibit oxidative damage repair in Amyotrophic Lateral Sclerosis
Haibo Wang et al.
NATURE COMMUNICATIONS (2018)
ALS mutations of FUS suppress protein translation and disrupt the regulation of nonsense-mediated decay
Marisa Kamelgarn et al.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2018)
Human SOD1 ALS Mutations in a Drosophila Knock-In Model Cause Severe Phenotypes and Reveal Dosage-Sensitive Gain- and Loss-of-Function Components
Asli Sahin et al.
GENETICS (2017)
The Ultrastructural Signature of Human Embryonic Stem Cells
Jean M. Underwood et al.
JOURNAL OF CELLULAR BIOCHEMISTRY (2017)
Human SOD1 ALS Mutations in a Drosophila Knock-In Model Cause Severe Phenotypes and Reveal Dosage-Sensitive Gain- and Loss-of-Function Components
Asli Sahin et al.
GENETICS (2017)
Calpain-Dependent Degradation of Nucleoporins Contributes to Motor Neuron Death in a Mouse Model of Chronic Excitotoxicity
Kaori Sugiyama et al.
JOURNAL OF NEUROSCIENCE (2017)
Toxic PRn poly-dipeptides encoded by the C9orf72 repeat expansion block nuclear import and export
Kevin Y. Shi et al.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2017)
ALS-linked FUS exerts a gain of toxic function involving aberrant p38 MAPK activation
Reddy Ranjith K. Sama et al.
SCIENTIFIC REPORTS (2017)
Calpain-dependent disruption of nucleo-cytoplasmic transport in ALS motor neurons
Takenari Yamashita et al.
SCIENTIFIC REPORTS (2017)
Phosphorylation of the FUS low-complexity domain disrupts phase separation, aggregation, and toxicity
Zachary Monahan et al.
EMBO JOURNAL (2017)
Expansion of the classification of FTLD-TDP: distinct pathology associated with rapidly progressive frontotemporal degeneration
Edward B. Lee et al.
ACTA NEUROPATHOLOGICA (2017)
Cytoplasmic protein aggregates interfere with nucleocytoplasmic transport of protein and RNA
Andreas C. Woerner et al.
SCIENCE (2016)
Proteomic analysis of FUS interacting proteins provides insights into FUS function and its role in ALS
Marisa Kamelgarn et al.
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE (2016)
Lamin Dysfunction Mediates Neurodegeneration in Tauopathies
Bess Frost et al.
CURRENT BIOLOGY (2016)
ALS/FTD-associated FUS activates GSK-3 to disrupt the VAPB-PTPIP51 interaction and ER-mitochondria associations
Radu Stoica et al.
EMBO REPORTS (2016)
Transport Selectivity of Nuclear Pores, Phase Separation, and Membraneless Organelles
H. Broder Schmidt et al.
TRENDS IN BIOCHEMICAL SCIENCES (2016)
Drosophila screen connects nuclear transport genes to DPR pathology in c9ALS/FTD
Steven Boeynaems et al.
SCIENTIFIC REPORTS (2016)
Genome-wide RNA-Seq of Human Motor Neurons Implicates Selective ER Stress Activation in Spinal Muscular Atrophy
Shi-Yan Ng et al.
CELL STEM CELL (2015)
Nuclear pore proteins and the control of genome functions
Arkaitz Ibarra et al.
GENES & DEVELOPMENT (2015)
Residue-by-Residue View of In Vitro FUS Granules that Bind the C-Terminal Domain of RNA Polymerase II
Kathleen A. Burke et al.
MOLECULAR CELL (2015)
The C9orf72 repeat expansion disrupts nucleocytoplasmic transport
Ke Zhang et al.
NATURE (2015)
GGGGCC repeat expansion in C9orf72 compromises nucleocytoplasmic transport
Brian D. Freibaum et al.
NATURE (2015)
Modifiers of C9orf72 dipeptide repeat toxicity connect nucleocytoplasmic transport defects to FTD/ALS
Ana Jovicic et al.
NATURE NEUROSCIENCE (2015)
ALS/FTD Mutation-Induced Phase Transition of FUS Liquid Droplets and Reversible Hydrogels into Irreversible Hydrogels Impairs RNP Granule Function
Tetsuro Murakami et al.
NEURON (2015)
Functions of FUS/TLS From DNA Repair to Stress Response: Implications for ALS
Reddy Ranjith Kumar Sama et al.
ASN NEURO (2014)
Identification of Long-Lived Proteins Reveals Exceptional Stability of Essential Cellular Structures
Brandon H. Toyama et al.
CELL (2013)
Amyotrophic lateral sclerosis-linked FUS/TLS alters stress granule assembly and dynamics
Desiree M. Baron et al.
MOLECULAR NEURODEGENERATION (2013)
A Drosophila model of FUS-related neurodegeneration reveals genetic interaction between FUS and TDP-43
Nicholas A. Lanson et al.
HUMAN MOLECULAR GENETICS (2011)
Expression of human FUS protein in Drosophila leads to progressive neurodegeneration
Yanbo Chen et al.
PROTEIN & CELL (2011)
ALS-associated fused in sarcoma (FUS) mutations disrupt Transportin-mediated nuclear import
Dorothee Dormann et al.
EMBO JOURNAL (2010)
Mutant FUS proteins that cause amyotrophic lateral sclerosis incorporate into stress granules
Daryl A. Bosco et al.
HUMAN MOLECULAR GENETICS (2010)
FUS GENE MUTATIONS IN FAMILIAL AND SPORADIC AMYOTROPHIC LATERAL SCLEROSIS
Rosa Rademakers et al.
MUSCLE & NERVE (2010)
Age-Dependent Deterioration of Nuclear Pore Complexes Causes a Loss of Nuclear Integrity in Postmitotic Cells
Maximiliano A. D'Angelo et al.
CELL (2009)
Analyzing real-time PCR data by the comparative C-T method
Thomas D. Schmittgen et al.
NATURE PROTOCOLS (2008)
HDAC6 rescues neurodegeneration and provides an essential link between autophagy and the UPS
Udai Bhan Pandey et al.
NATURE (2007)
FG-rich repeats of nuclear pore proteins form a three-dimensional meshwork with hydrogel-like properties
Steffen Frey et al.
SCIENCE (2006)
Multiple mechanisms promote the inhibition of classical nuclear import upon exposure to severe oxidative stress
M Kodiha et al.
CELL DEATH AND DIFFERENTIATION (2004)
Nuclear pore complexes form immobile networks and have a very low turnover in live mammalian cells
N Daigle et al.
JOURNAL OF CELL BIOLOGY (2001)
分享论文
