[HTML][HTML] C9orf72 dipeptide repeats impair the assembly, dynamics, and function of membrane-less organelles

KH Lee, P Zhang, HJ Kim, DM Mitrea, M Sarkar… - Cell, 2016 - cell.com
Expansion of a hexanucleotide repeat GGGGCC (G 4 C 2) in C9ORF72 is the most common
cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Transcripts …

[HTML][HTML] Cell-to-cell transmission of dipeptide repeat proteins linked to C9orf72-ALS/FTD

T Westergard, BK Jensen, X Wen, J Cai, E Kropf… - Cell reports, 2016 - cell.com
Aberrant hexanucleotide repeat expansions in C9orf72 are the most common genetic
change underlying amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) …

Reduced autophagy upon C9ORF72 loss synergizes with dipeptide repeat protein toxicity in G4C2 repeat expansion disorders

M Boivin, V Pfister, A Gaucherot, F Ruffenach… - The EMBO …, 2020 - embopress.org
Expansion of G4C2 repeats within the C9ORF72 gene is the most common cause of
amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Such repeats lead …

[HTML][HTML] Glycine-alanine dipeptide repeat protein contributes to toxicity in a zebrafish model of C9orf72 associated neurodegeneration

Y Ohki, A Wenninger-Weinzierl, A Hruscha… - Molecular …, 2017 - Springer
Background The most frequent genetic cause of frontotemporal lobar degeneration (FTLD)
and amyotrophic lateral sclerosis (ALS) is the expansion of a GGGGCC hexanucleotide …

[HTML][HTML] C9orf72 arginine-rich dipeptide proteins interact with ribosomal proteins in vivo to induce a toxic translational arrest that is rescued by eIF1A

TG Moens, T Niccoli, KM Wilson, ML Atilano… - Acta …, 2019 - Springer
A GGGGCC hexanucleotide repeat expansion within the C9orf72 gene is the most common
genetic cause of both amyotrophic lateral sclerosis and frontotemporal dementia. Sense and …

[HTML][HTML] Unraveling the Role of RNA Mediated Toxicity of C9orf72 Repeats in C9-FTD/ALS

V Kumar, GM Hasan, MI Hassan - Frontiers in neuroscience, 2017 - frontiersin.org
The most frequent genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal
dementia (FTD) is intronic hexanucleotide (G4C2) repeat expansions (HRE) in the C9orf72 …

[HTML][HTML] Emerging perspectives on dipeptide repeat proteins in C9ORF72 ALS/FTD

A Schmitz, J Pinheiro Marques, I Oertig… - Frontiers in cellular …, 2021 - frontiersin.org
The most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal
dementia (FTD) is a hexanucleotide expansion in the chromosome 9 open reading frame 72 …

[HTML][HTML] Chimeric peptide species contribute to divergent dipeptide repeat pathology in c9ALS/FTD and SCA36

ZT McEachin, TF Gendron, N Raj, M García-Murias… - Neuron, 2020 - cell.com
GGGGCC hexanucleotide repeat expansions (HREs) in C9orf72 cause amyotrophic lateral
sclerosis (ALS) and frontotemporal dementia (FTD) and lead to the production of …

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

S May, D Hornburg, MH Schludi, T Arzberger… - Acta …, 2014 - Springer
Hexanucleotide repeat expansion in C9orf72 is the most common pathogenic mutation in
patients with amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration …

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

A Jovičić, J Mertens, S Boeynaems, E Bogaert… - Nature …, 2015 - nature.com
C9orf72 mutations are the most common cause of amyotrophic lateral sclerosis (ALS) and
frontotemporal dementia (FTD). Dipeptide repeat proteins (DPRs) produced by …