Synaptic dysfunction and altered excitability in C9ORF72 ALS/FTD.

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Synaptic dysfunction and altered excitability in C9ORF72 ALS/FTD.

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2018 nî lūn-bûn

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2018年の論文

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2018年学术文章

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2018年学术文章

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2018年学术文章

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2018年学术文章

@zh-hans

2018年学术文章

@zh-my

2018年学术文章

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2018年學術文章

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2018年學術文章

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Synaptic dysfunction and altered excitability in C9ORF72 ALS/FTD.

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Synaptic dysfunction and altered excitability in C9ORF72 ALS/FTD.

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Synaptic dysfunction and altered excitability in C9ORF72 ALS/FTD.

@en

Synaptic dysfunction and altered excitability in C9ORF72 ALS/FTD.

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Synaptic dysfunction and altered excitability in C9ORF72 ALS/FTD.

@en

Synaptic dysfunction and altered excitability in C9ORF72 ALS/FTD.

@nl

P1476

Synaptic dysfunction and altered excitability in C9ORF72 ALS/FTD.

@en

P2093

Rita Sattler

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P2860

Adenosine deaminases acting on RNA (ADARs): RNA-editing enzymes

A mitochondrial origin for frontotemporal dementia and amyotrophic lateral sclerosis through CHCHD10 involvement

Ataxin-2 interacts with the DEAD/H-box RNA helicase DDX6 and interferes with P-bodies and stress granules

Ca2+ permeability of KA-AMPA--gated glutamate receptor channels depends on subunit composition

Molecular cloning of cDNA for double-stranded RNA adenosine deaminase, a candidate enzyme for nuclear RNA editing

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

Early presymptomatic cholinergic dysfunction in a murine model of amyotrophic lateral sclerosis

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

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

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

P304

98-108

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scholarly article

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10.1016/J.BRAINRES.2018.02.011

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P407

English

P433

Pt A

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P478

1693

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P50

Alexander Starr

P577

2018-02-14T00:00:00Z

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P698

29453960

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P921

amyotrophic lateral sclerosis

P932

5997509

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