(Q26778174)

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Isoform-specific antibodies reveal distinct subcellular localizations of C9orf72 in amyotrophic lateral sclerosis

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

A pan-European study of the C9orf72 repeat associated with FTLD: geographic prevalence, genomic instability, and intermediate repeats

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Altered distributions of nucleocytoplasmic transport-related proteins in the spinal cord of a mouse model of amyotrophic lateral sclerosis

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

p62 positive, TDP-43 negative, neuronal cytoplasmic and intranuclear inclusions in the cerebellum and hippocampus define the pathology of C9orf72-linked FTLD and MND/ALS

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

hnRNP A3 binds to GGGGCC repeats and is a constituent of p62-positive/TDP43-negative inclusions in the hippocampus of patients with C9orf72 mutations

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Modeling key pathological features of frontotemporal dementia with C9ORF72 repeat expansion in iPSC-derived human neurons

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Dipeptide repeat protein pathology in C9ORF72 mutation cases: clinico-pathological correlations

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Bidirectional transcripts of the expanded C9orf72 hexanucleotide repeat are translated into aggregating dipeptide repeat proteins

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Antisense transcripts of the expanded C9ORF72 hexanucleotide repeat form nuclear RNA foci and undergo repeat-associated non-ATG translation in c9FTD/ALS

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Early dipeptide repeat pathology in a frontotemporal dementia kindred with C9ORF72 mutation and intellectual disability

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

C9orf72 FTLD/ALS-associated Gly-Ala dipeptide repeat proteins cause neuronal toxicity and Unc119 sequestration

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Aggregation-prone c9FTD/ALS poly(GA) RAN-translated proteins cause neurotoxicity by inducing ER stress

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Hypermethylation of repeat expanded C9orf72 is a clinical and molecular disease modifier

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Frontotemporal lobar degeneration: defining phenotypic diversity through personalized medicine

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Antisense RNA foci in the motor neurons of C9ORF72-ALS patients are associated with TDP-43 proteinopathy.

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

FTD/ALS-associated poly(GR) protein impairs the Notch pathway and is recruited by poly(GA) into cytoplasmic inclusions

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Distribution of dipeptide repeat proteins in cellular models and C9orf72 mutation cases suggests link to transcriptional silencing

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

TDP-43 Proteinopathy and ALS: Insights into Disease Mechanisms and Therapeutic Targets

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Reduced C9orf72 protein levels in frontal cortex of amyotrophic lateral sclerosis and frontotemporal degeneration brain with the C9ORF72 hexanucleotide repeat expansion

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Dipeptide repeat protein toxicity in frontotemporal lobar degeneration and in motor neurone disease associated with expansions in C9ORF72-a cautionary note

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Unconventional translation of C9ORF72 GGGGCC expansion generates insoluble polypeptides specific to c9FTD/ALS

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

CGG repeat-associated translation mediates neurodegeneration in fragile X tremor ataxia syndrome

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

RNA toxicity from the ALS/FTD C9ORF72 expansion is mitigated by antisense intervention

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Discovery of a biomarker and lead small molecules to target r(GGGGCC)-associated defects in c9FTD/ALS.

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Antisense proline-arginine RAN dipeptides linked to C9ORF72-ALS/FTD form toxic nuclear aggregates that initiate in vitro and in vivo neuronal death

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Differential Toxicity of Nuclear RNA Foci versus Dipeptide Repeat Proteins in a Drosophila Model of C9ORF72 FTD/ALS.

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

TDP-43 and FUS: a nuclear affair

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

TARDBP mutations in amyotrophic lateral sclerosis with TDP-43 neuropathology: a genetic and histopathological analysis

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

A C9orf72 promoter repeat expansion in a Flanders-Belgian cohort with disorders of the frontotemporal lobar degeneration-amyotrophic lateral sclerosis spectrum: a gene identification study

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Frequency of the C9orf72 hexanucleotide repeat expansion in patients with amyotrophic lateral sclerosis and frontotemporal dementia: a cross-sectional study

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Presymptomatic cognitive and neuroanatomical changes in genetic frontotemporal dementia in the Genetic Frontotemporal dementia Initiative (GENFI) study: a cross-sectional analysis.

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

ALS-associated fused in sarcoma (FUS) mutations disrupt Transportin-mediated nuclear import

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

C9orf72 nucleotide repeat structures initiate molecular cascades of disease.

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

The C9orf72 repeat expansion disrupts nucleocytoplasmic transport.

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

GGGGCC repeat expansion in C9orf72 compromises nucleocytoplasmic transport

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Human iPSC-derived motoneurons harbouring TARDBP or C9ORF72 ALS mutations are dysfunctional despite maintaining viability

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

TARDBP mutations in individuals with sporadic and familial amyotrophic lateral sclerosis

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Three dimensions of the amyloid hypothesis: time, space and 'wingmen'

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Modifiers of C9orf72 dipeptide repeat toxicity connect nucleocytoplasmic transport defects to FTD/ALS.

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Advances in understanding the molecular basis of frontotemporal dementia

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Clinical and biomarker changes in dominantly inherited Alzheimer's disease

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Non-ATG-initiated translation directed by microsatellite expansions

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

RAN proteins and RNA foci from antisense transcripts in C9ORF72 ALS and frontotemporal dementia

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degeneration

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Deep proteomic evaluation of primary and cell line motoneuron disease models delineates major differences in neuronal characteristics

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

The product of C9orf72, a gene strongly implicated in neurodegeneration, is structurally related to DENN Rab-GEFs

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Sequestration of multiple RNA recognition motif-containing proteins by C9orf72 repeat expansions

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

C9ORF72, implicated in amytrophic lateral sclerosis and frontotemporal dementia, regulates endosomal trafficking

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Characterization of the dipeptide repeat protein in the molecular pathogenesis of c9FTD/ALS.

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Nucleolar stress and impaired stress granule formation contribute to C9orf72 RAN translation-induced cytotoxicity

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

The C9orf72 GGGGCC repeat is translated into aggregating dipeptide-repeat proteins in FTLD/ALS.

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Poly-dipeptides encoded by the C9orf72 repeats bind nucleoli, impede RNA biogenesis, and kill cells

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

C9orf72 repeat expansions cause neurodegeneration in Drosophila through arginine-rich proteins

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Alzheimer's disease: the amyloid cascade hypothesis

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Neurodegeneration. C9ORF72 repeat expansions in mice cause TDP-43 pathology, neuronal loss, and behavioral deficits

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Targeting RNA foci in iPSC-derived motor neurons from ALS patients with a C9ORF72 repeat expansion

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Brain distribution of dipeptide repeat proteins in frontotemporal lobar degeneration and motor neurone disease associated with expansions in C9ORF72

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021

Dipeptide repeat protein inclusions are rare in the spinal cord and almost absent from motor neurons in C9ORF72 mutant amyotrophic lateral sclerosis and are unlikely to cause their degeneration.

1 reference

https://api.crossref.org/works/10.1016%2FJ.CONB.2015.10.009

7 January 2021