Compromised paraspeckle formation as a pathogenic factor in FUSopathies.
about
Inside out: the role of nucleocytoplasmic transport in ALS and FTLDImmunoprecipitation and mass spectrometry defines an extensive RBM45 protein-protein interaction networkEarly lethality and neuronal proteinopathy in mice expressing cytoplasm-targeted FUS that lacks the RNA recognition motif.Non-coding RNA in neural function, disease, and agingThe structure of human SFPQ reveals a coiled-coil mediated polymer essential for functional aggregation in gene regulationCharacterization of genetic loss-of-function of Fus in zebrafish.Self-assembled FUS binds active chromatin and regulates gene transcription.Gamma-synuclein pathology in amyotrophic lateral sclerosisA network of RNA and protein interactions in Fronto Temporal Dementia.Calcium-responsive transactivator (CREST) protein shares a set of structural and functional traits with other proteins associated with amyotrophic lateral sclerosis.Subcellular localization and RNAs determine FUS architecture in different cellular compartments.Proteins with Intrinsically Disordered Domains Are Preferentially Recruited to Polyglutamine Aggregates.Prion-like domains in RNA binding proteins are essential for building subnuclear paraspeckles.Depletion of NEAT1 lncRNA attenuates nucleolar stress by releasing sequestered P54nrb and PSF to facilitate c-Myc translation.TDP-43 and FUS en route from the nucleus to the cytoplasm.Directly converted patient-specific induced neurons mirror the neuropathology of FUS with disrupted nuclear localization in amyotrophic lateral sclerosis.Expression of microRNAs in human post-mortem amyotrophic lateral sclerosis spinal cords provides insight into disease mechanismsStructural, super-resolution microscopy analysis of paraspeckle nuclear body organization.FUS interacts with nuclear matrix-associated protein SAFB1 as well as Matrin3 to regulate splicing and ligand-mediated transcriptionRNA binding proteins: a common denominator of neuronal function and dysfunction.Physiological functions and pathobiology of TDP-43 and FUS/TLS proteins.Subnuclear re-localization of SOX10 and p54NRB correlates with a unique neurological phenotype associated with SOX10 missense mutations.Interaction and colocalization of HERMES/RBPMS with NonO, PSF, and G3BP1 in neuronal cytoplasmic RNP granules in mouse retinal line cells.Energy Homeostasis and Abnormal RNA Metabolism in Amyotrophic Lateral SclerosisPur-alpha functionally interacts with FUS carrying ALS-associated mutations.Paraspeckles: paragons of functional aggregation.Nucleic acid binding proteins affect the subcellular distribution of phosphorothioate antisense oligonucleotides.Humanized mutant FUS drives progressive motor neuron degeneration without aggregation in 'FUSDelta14' knockin mice.The roles of intrinsic disorder-based liquid-liquid phase transitions in the "Dr. Jekyll-Mr. Hyde" behavior of proteins involved in amyotrophic lateral sclerosis and frontotemporal lobar degeneration.Role of the visual experience-dependent nascent proteome in neuronal plasticity.Cerebral ischemia induces the aggregation of proteins linked to neurodegenerative diseases.The Hepatitis Delta Virus accumulation requires paraspeckle components and affects NEAT1 level and PSP1 localization.Protective paraspeckle hyper-assembly downstream of TDP-43 loss of function in amyotrophic lateral sclerosis.Nuclear egress of TDP-43 and FUS occurs independently of Exportin-1/CRM1.
P2860
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P2860
Compromised paraspeckle formation as a pathogenic factor in FUSopathies.
description
2013 nî lūn-bûn
@nan
2013 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2013 թվականի դեկտեմբերին հրատարակված գիտական հոդված
@hy
2013年の論文
@ja
2013年論文
@yue
2013年論文
@zh-hant
2013年論文
@zh-hk
2013年論文
@zh-mo
2013年論文
@zh-tw
2013年论文
@wuu
name
Compromised paraspeckle formation as a pathogenic factor in FUSopathies.
@ast
Compromised paraspeckle formation as a pathogenic factor in FUSopathies.
@en
type
label
Compromised paraspeckle formation as a pathogenic factor in FUSopathies.
@ast
Compromised paraspeckle formation as a pathogenic factor in FUSopathies.
@en
prefLabel
Compromised paraspeckle formation as a pathogenic factor in FUSopathies.
@ast
Compromised paraspeckle formation as a pathogenic factor in FUSopathies.
@en
P2860
P50
P356
P1476
Compromised paraspeckle formation as a pathogenic factor in FUSopathies.
@en
P2093
Hannah K Robinson
Natalia Ninkina
P2860
P304
P356
10.1093/HMG/DDT622
P577
2013-12-11T00:00:00Z