Mechanisms of disease in frontotemporal lobar degeneration: gain of function versus loss of function effects
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FUS is sequestered in nuclear aggregates in ALS patient fibroblasts.Partial loss of TDP-43 function causes phenotypes of amyotrophic lateral sclerosis.Distinct partitioning of ALS associated TDP-43, FUS and SOD1 mutants into cellular inclusionsNeuropsychiatric symptom profile differs based on pathology in patients with clinically diagnosed behavioral variant frontotemporal dementia.RNA metabolism in neurodegenerative disease.Frontotemporal dementia and its subtypes: a genome-wide association study.Characterization of FUS mutations in amyotrophic lateral sclerosis using RNA-Seq.Targeting RNA binding proteins involved in neurodegeneration.Age-related incidence and family history in frontotemporal dementia: data from the Swedish Dementia RegistryPABPN1 suppresses TDP-43 toxicity in ALS disease models.The role of the innate immune system in Alzheimer's disease and frontotemporal lobar degeneration: an eye on microglia.Amyotrophic lateral sclerosis-linked FUS/TLS alters stress granule assembly and dynamics.RNA-mediated toxicity in neurodegenerative diseaseMolecular nexopathies: a new paradigm of neurodegenerative disease.The behavioral variant of frontotemporal dementia: linking neuropathology to social cognition.The neuropathology associated with repeat expansions in the C9ORF72 gene.Challenges of multimorbidity of the aging brain: a critical update.Predominance of spliceosomal complex formation over polyadenylation site selection in TDP-43 autoregulation.TDP-43-The key to understanding amyotrophic lateral sclerosis.Frontotemporal dementia: insights into the biological underpinnings of disease through gene co-expression network analysisQuantification of the Relative Contributions of Loss-of-function and Gain-of-function Mechanisms in TAR DNA-binding Protein 43 (TDP-43) ProteinopathiesPhysiological functions and pathobiology of TDP-43 and FUS/TLS proteins.Human TDP-43 and FUS selectively affect motor neuron maturation and survival in a murine cell model of ALS by non-cell-autonomous mechanisms.An autopsy case of frontotemporal lobar degeneration with the appearance of fused in sarcoma inclusions (basophilic inclusion body disease) clinically presenting corticobasal syndrome.Disease-associated mutations of TDP-43 promote turnover of the protein through the proteasomal pathway.Weighted Protein Interaction Network Analysis of Frontotemporal Dementia.Protein aggregation, misfolding and consequential human neurodegenerative diseases.The ALS-linked E102Q mutation in Sigma receptor-1 leads to ER stress-mediated defects in protein homeostasis and dysregulation of RNA-binding proteins.Temporal Expression of Mutant TDP-43 Correlates with Early Amyotrophic Lateral Sclerosis Phenotype and Motor Weakness.New advances in tau imaging in parkinsonism.Gene-based association studies report genetic links for clinical subtypes of frontotemporal dementia.Nuclear egress of TDP-43 and FUS occurs independently of Exportin-1/CRM1.
P2860
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P2860
Mechanisms of disease in frontotemporal lobar degeneration: gain of function versus loss of function effects
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
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2012年论文
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name
Mechanisms of disease in front ...... ersus loss of function effects
@ast
Mechanisms of disease in front ...... ersus loss of function effects
@en
type
label
Mechanisms of disease in front ...... ersus loss of function effects
@ast
Mechanisms of disease in front ...... ersus loss of function effects
@en
prefLabel
Mechanisms of disease in front ...... ersus loss of function effects
@ast
Mechanisms of disease in front ...... ersus loss of function effects
@en
P2093
P2860
P1476
Mechanisms of disease in front ...... ersus loss of function effects
@en
P2093
David M A Mann
Eileen H Bigio
Ian R A Mackenzie
Nigel J Cairns
P2860
P2888
P304
P356
10.1007/S00401-012-1030-4
P577
2012-08-10T00:00:00Z