C9orf72 ablation in mice does not cause motor neuron degeneration or motor deficits

C9ORF72 repeat expansions in mice cause TDP-43 pathology, neuronal loss, and behavioral deficits

(2015) J. Chew et al.   SCIENCE

C9orf72 amyotrophic lateral sclerosis and frontotemporal dementia

(2014) Sarah Mizielinska et al.   CURRENT OPINION IN NEUROLOGY

C9ORF72, implicated in amytrophic lateral sclerosis and frontotemporal dementia, regulates endosomal trafficking

(2014) Manal A. Farg et al.   HUMAN MOLECULAR GENETICS

C9orf72 nucleotide repeat structures initiate molecular cascades of disease

(2014) Aaron R. Haeusler et al.   NATURE

Reduced C9orf72 protein levels in frontal cortex of amyotrophic lateral sclerosis and frontotemporal degeneration brain with the C9ORF72 hexanucleotide repeat expansion

(2014) Adrian J. Waite et al.   NEUROBIOLOGY OF AGING

Subdomain-Mediated Axon-Axon Signaling and Chemoattraction Cooperate to Regulate Afferent Innervation of the Lateral Habenula

(2014) Ewoud Roberto Eduard Schmidt et al.   NEURON

C9orf72 repeat expansions cause neurodegeneration in Drosophila through arginine-rich proteins

(2014) S. Mizielinska et al.   SCIENCE

RETRACTED ARTICLE: A new inducible transgenic mouse model for C9orf72-associated GGGGCC repeat expansion supports a gain-of-function mechanism in C9orf72-associated ALS and FTD

(2014) Renate K Hukema et al.   Acta Neuropathologica Communications

The product of C9orf72, a gene strongly implicated in neurodegeneration, is structurally related to DENN Rab-GEFs

(2013) Timothy P. Levine et al.   BIOINFORMATICS

Highly Efficient Targeted Mutagenesis in Mice Using TALENs

(2013) Sudeepta Kumar Panda et al.   GENETICS

ALS-associated mutations in FUS disrupt the axonal distribution and function of SMN

(2013) Ewout J.N. Groen et al.   HUMAN MOLECULAR GENETICS

The mouse C9ORF72 ortholog is enriched in neurons known to degenerate in ALS and FTD

(2013) Naoki Suzuki et al.   NATURE NEUROSCIENCE

Unconventional Translation of C9ORF72 GGGGCC Expansion Generates Insoluble Polypeptides Specific to c9FTD/ALS

(2013) Peter E.A. Ash et al.   NEURON

RNA Toxicity from the ALS/FTD C9ORF72 Expansion Is Mitigated by Antisense Intervention

(2013) Christopher J. Donnelly et al.   NEURON

Deletion of C9ORF72 Results in Motor Neuron Degeneration and Stress Sensitivity in C. elegans

(2013) Martine Therrien et al.   PLoS One

Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degeneration

(2013) C. Lagier-Tourenne et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

The C9orf72 GGGGCC Repeat Is Translated into Aggregating Dipeptide-Repeat Proteins in FTLD/ALS

(2013) K. Mori et al.   SCIENCE

A fast and sensitive alternative for  -galactosidase detection in mouse embryos

(2012) S. Sundararajan et al.   DEVELOPMENT

Frequency of the C9orf72 hexanucleotide repeat expansion in patients with amyotrophic lateral sclerosis and frontotemporal dementia: a cross-sectional study

(2012) Elisa Majounie et al.   LANCET NEUROLOGY

Expanded GGGGCC Hexanucleotide Repeat in Noncoding Region of C9ORF72 Causes Chromosome 9p-Linked FTD and ALS

(2011) Mariely DeJesus-Hernandez et al.   NEURON

A Hexanucleotide Repeat Expansion in C9ORF72 Is the Cause of Chromosome 9p21-Linked ALS-FTD

(2011) Alan E. Renton et al.   NEURON

Combined Neural Inactivation of Suppressor of Cytokine Signaling-3 and Protein-Tyrosine Phosphatase-1B Reveals Additive, Synergistic, and Factor-Specific Roles in the Regulation of Body Energy Balance

(2010) N. Briancon et al.   DIABETES

Semaphorin 3F Is a Bifunctional Guidance Cue for Dopaminergic Axons and Controls Their Fasciculation, Channeling, Rostral Growth, and Intracortical Targeting

(2009) S. M. Kolk et al.   JOURNAL OF NEUROSCIENCE