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

Anti-sense DNA d(GGCCCC)n expansions in C9ORF72 form i-motifs and protonated hairpins

3 Dec 2015

Abstract excerpt

The G4C2 hexanucleotide repeat expansion mutation (HREM) in C9ORF72, represents the most common mutation associated with amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). Three main disease mechanisms have been proposed to date: C9ORF72 haploinsufficiency, RNA toxicity, and accumulation of dipeptide repeat proteins. Pure GC content of the HREM potentially enables the formation of...

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 DNA and Nucleic Acid Chemistry
Share to Neurogenetic and Muscular Disorders Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 26632347
DOI: 10.1038/srep17944

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

Anti-sense DNA d(GGCCCC)n expansions in C9ORF72 form i-motifs and protonated hairpinsPMID 26632347Read ↗

Emerging role of RNA•DNA hybrids inC9orf72-linked neurodegenerationSemantic proximity Read ↗

The Emerging Role of DNA Damage in the Pathogenesis of the C9orf72 Repeat Expansion in Amyotrophic Lateral SclerosisSemantic proximity Read ↗

C9orf72 hexanucleotide repeat associated with amyotrophic lateral sclerosis and frontotemporal dementia forms RNA G-quadruplexes.Semantic proximity Read ↗

Pathogenic C9ORF72 Antisense Repeat RNA Forms a Double Helix with Tandem C:C MismatchesSemantic proximity Read ↗

Role of C9orf72 hexanucleotide repeat expansions in ALS/FTD pathogenesisSemantic proximity Read ↗

Characterization of DNA G-quadruplex species forming from C9ORF72 G4C2-expanded repeats associated with amyotrophic lateral sclerosis and frontotemporal lobar degenerationSemantic proximity Read ↗

ALS and FTD linked GGGGCC-repeat containing DNA oligonucleotide folds into two distinct G-quadruplexes.Semantic proximity Read ↗

Antisense oligonucleotide targeting pathogenic sense repeat RNA in <i>C9ORF72</i> suppresses production of antisense-dependent dipeptide repeat proteins implicated in ALS/FTDSemantic proximity Read ↗

The Role of Dipeptide Repeats in C9ORF72-Related ALS-FTDSemantic proximity Read ↗

Fast MAS NMR Spectroscopy Can Identify G-Quartets and Double-Stranded Structures in Aggregates Formed by GGGGCC RNA RepeatsSemantic proximity Read ↗

CRISPR/Cas9-Mediated Excision of ALS/FTD-Causing Hexanucleotide Repeat Expansion in <i>C9ORF72</i> rescues major disease mechanisms <i>in vivo</i> and <i>in vitro</i>Semantic proximity Read ↗

Bidirectional transcripts of the expanded C9orf72 hexanucleotide repeat are translated into aggregating dipeptide repeat proteinsSemantic proximity Read ↗

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