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

C9orf72 frontotemporal lobar degeneration is characterised by frequent neuronal sense and antisense RNA foci

29 Oct 2013

Abstract excerpt

An expanded GGGGCC repeat in a non-coding region of the C9orf72 gene is a common cause of frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis. Non-coding repeat expansions may cause disease by reducing the expression level of the gene they reside in, by producing toxic aggregates of repeat RNA termed RNA foci, or by producing toxic proteins generated by repeat-associated non-ATG...

Read the complete abstract on PubMed

Topics

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

Share to Alzheimer's disease research and treatments
Share to Amyotrophic Lateral Sclerosis Research
Share to Parkinson's Disease Mechanisms and Treatments

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 24170096
DOI: 10.1007/s00401-013-1200-z

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

C9orf72 frontotemporal lobar degeneration is characterised by frequent neuronal sense and antisense RNA fociPMID 24170096Read ↗

In-depth clinico-pathological examination of RNA foci in a large cohort of C9ORF72 expansion carriersSemantic proximity Read ↗

Antisense RNA foci in the motor neurons of C9ORF72-ALS patients are associated with TDP-43 proteinopathySemantic proximity Read ↗

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

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

RAN proteins and RNA foci from antisense transcripts in <i>C9ORF72</i> ALS and frontotemporal dementiaSemantic proximity Read ↗

Unraveling the Role of RNA Mediated Toxicity of C9orf72 Repeats in C9-FTD/ALSSemantic proximity Read ↗

C9orf72 amyotrophic lateral sclerosis and frontotemporal dementia: gain or loss of function?Semantic proximity Read ↗

Modeling key pathological features of frontotemporal dementia with C9ORF72 repeat expansion in iPSC-derived human neurons.Semantic proximity Read ↗

Insights into the pathogenic mechanisms of Chromosome 9 open reading frame 72 (C9orf72) repeat expansionsSemantic proximity Read ↗

The neuropathology associated with repeat expansions in the C9ORF72 gene.Semantic proximity Read ↗

c9orf72 Disease-Related Foci Are Each Composed of One Mutant Expanded Repeat RNA.Semantic proximity Read ↗

There has been an awakening: Emerging mechanisms of C9orf72 mutations in FTD/ALS.Semantic proximity Read ↗

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