Decreased number of Gemini of coiled bodies and U12 snRNA level in amyotrophic lateral sclerosis.
about
Altered ribostasis: RNA-protein granules in degenerative disordersInside out: the role of nucleocytoplasmic transport in ALS and FTLDCopy Number Variations in the Survival Motor Neuron Genes: Implications for Spinal Muscular Atrophy and Other Neurodegenerative DiseasesConverging mechanisms in ALS and FTD: disrupted RNA and protein homeostasisNeuronal RNA-binding proteins in health and diseaseALS-causative mutations in FUS/TLS confer gain and loss of function by altered association with SMN and U1-snRNP.Loss of nuclear TDP-43 in amyotrophic lateral sclerosis (ALS) causes altered expression of splicing machinery and widespread dysregulation of RNA splicing in motor neurones.Nuclear localization of SMN and FUS is not altered in fibroblasts from patients with sporadic ALSLinking RNA Dysfunction and Neurodegeneration in Amyotrophic Lateral Sclerosis.The pathogenicity of splicing defects: mechanistic insights into pre-mRNA processing inform novel therapeutic approaches.Minor intron splicing is regulated by FUS and affected by ALS-associated FUS mutantsMinor splicing pathway is not minor any more: implications for the pathogenesis of motor neuron diseases.RNA metabolism in ALS: when normal processes become pathological.Gem depletion: amyotrophic lateral sclerosis and spinal muscular atrophy crossover.Targeting TDP-43 in neurodegenerative diseases.Developing therapies for spinal muscular atrophy.Old versus New Mechanisms in the Pathogenesis of ALS.Cajal bodies in neuronsDistinct pathways leading to TDP-43-induced cellular dysfunctions.Linking amyotrophic lateral sclerosis and spinal muscular atrophy through RNA-transcriptome homeostasis: a genomics perspective.Faulty RNA splicing: consequences and therapeutic opportunities in brain and muscle disorders.Gain-of-function profilin 1 mutations linked to familial amyotrophic lateral sclerosis cause seed-dependent intracellular TDP-43 aggregation.U6 snRNA expression prevents toxicity in TDP-43-knockdown cells.Motor Neuron Gene Therapy: Lessons from Spinal Muscular Atrophy for Amyotrophic Lateral Sclerosis.De novo design of RNA-binding proteins with a prion-like domain related to ALS/FTD proteinopathies.Mislocated FUS is sufficient for gain-of-toxic-function amyotrophic lateral sclerosis phenotypes in mice.Variant snRNPs: New players within the spliceosome system.Unexpected similarities between C9ORF72 and sporadic forms of ALS/FTD suggest a common disease mechanismAberrant activation of non-coding RNA targets of transcriptional elongation complexes contributes to TDP-43 toxicity
P2860
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P2860
Decreased number of Gemini of coiled bodies and U12 snRNA level in amyotrophic lateral sclerosis.
description
2013 nî lūn-bûn
@nan
2013年の論文
@ja
2013年学术文章
@wuu
2013年学术文章
@zh
2013年学术文章
@zh-cn
2013年学术文章
@zh-hans
2013年学术文章
@zh-my
2013年学术文章
@zh-sg
2013年學術文章
@yue
2013年學術文章
@zh-hant
name
Decreased number of Gemini of ...... amyotrophic lateral sclerosis.
@en
Decreased number of Gemini of ...... amyotrophic lateral sclerosis.
@nl
type
label
Decreased number of Gemini of ...... amyotrophic lateral sclerosis.
@en
Decreased number of Gemini of ...... amyotrophic lateral sclerosis.
@nl
prefLabel
Decreased number of Gemini of ...... amyotrophic lateral sclerosis.
@en
Decreased number of Gemini of ...... amyotrophic lateral sclerosis.
@nl
P2093
P2860
P356
P1476
Decreased number of Gemini of ...... amyotrophic lateral sclerosis
@en
P2093
Akihide Koyama
Akio Yokoseki
Akiyoshi Kakita
Atsushi Shiga
Chun-Feng Tan
Hitoshi Takahashi
Mariko Yokoo
Masatoyo Nishizawa
Taisuke Kato
Takeshi Fujino
P2860
P304
P356
10.1093/HMG/DDT262
P577
2013-06-04T00:00:00Z