Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

SRSF1-dependent nuclear export inhibition of C9ORF72 repeat transcripts prevents neurodegeneration and associated motor deficits

5 Jul 2017

Abstract excerpt

Hexanucleotide repeat expansions in the C9ORF72 gene are the commonest known genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia. Expression of repeat transcripts and dipeptide repeat proteins trigger multiple mechanisms of neurotoxicity. How repeat transcripts get exported from the nucleus is unknown. Here, we show that depletion of the nuclear export adaptor SRSF1 prevents...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Amyotrophic Lateral Sclerosis Research
Share to Neurogenetic and Muscular Disorders Research
Share to RNA Research and Splicing

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 28677678
DOI: 10.1038/ncomms16063

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

SRSF1-dependent nuclear export inhibition of C9ORF72 repeat transcripts prevents neurodegeneration and associated motor deficitsPMID 28677678Read ↗

SRSF1-dependent inhibition of C9ORF72-repeat RNA nuclear export: genome-wide mechanisms for neuroprotection in amyotrophic lateral sclerosisSemantic proximity Read ↗

A cell-penetrant peptide blocking <i>C9ORF72</i> -repeat RNA nuclear export suppresses neurodegenerationSemantic proximity Read ↗

Safety and efficacy of <i>C9ORF72</i> -repeat RNA nuclear export inhibition in amyotrophic lateral sclerosisSemantic proximity Read ↗

High-throughput screen of 100 000 small molecules in C9ORF72 ALS neurons identifies spliceosome modulators that mobilize G4C2 repeat RNA into nuclear export and repeat associated non-canonical translationSemantic proximity Read ↗

<i>In vivo</i> CGG repeat RNA binding protein capture identifies RAN translation modifiers and suppressors of repeat toxicitySemantic proximity Read ↗

Sequestration of multiple RNA recognition motif-containing proteins by C9orf72 repeat expansionsSemantic proximity Read ↗

Molecular mechanisms underlying nucleotide repeat expansion disorders.Semantic proximity Read ↗

GGGGCC repeat expansion in C9orf72 compromises nucleocytoplasmic transport.Semantic proximity Read ↗

Reactivation of nonsense-mediated mRNA decay protects against C9orf72 dipeptide-repeat neurotoxicitySemantic proximity Read ↗

Invited Review: Decoding the pathophysiological mechanisms that underlie RNA dysregulation in neurodegenerative disorders: a review of the current state of the artSemantic proximity Read ↗

A behavioral screen for mediators of age-dependent TDP-43 neurodegeneration identifies SF2/SRSF1 among a group of potent suppressors in both neurons and gliaSemantic proximity Read ↗

RNA toxicity in non-coding repeat expansion disorders.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.