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C9ORF72: What It Is, What It Does, and Why It Matters

Frontiers in cellular neuroscience, 2021-05, Vol.15

2021

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PhagoStat a scalable and interpretable end to end framework for efficient quantification of cell phagocytosis in neurodegenerative disease studies

Scientific reports, 2024-03, Vol.14 (1), p.6482-6482, Article 6482

2024

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Loss of function of C9orf72 causes motor deficits in a zebrafish model of amyotrophic lateral sclerosis

Annals of neurology, 2013-08, Vol.74 (2), p.180-187

2013

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c-Jun Reprograms Schwann Cells of Injured Nerves to Generate a Repair Cell Essential for Regeneration

Neuron (Cambridge, Mass.), 2012-08, Vol.75 (4), p.633-647

2012

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c-Jun in Schwann cells promotes axonal regeneration and motoneuron survival via paracrine signaling

The Journal of cell biology, 2012-07, Vol.198 (1), p.127-141

2012

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Novel VCP mutations expand the mutational spectrum of frontotemporal dementia

Neurobiology of aging, 2018-12, Vol.72, p.187.e11-187.e14

2018

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Interferon beta induces clearance of mutant ataxin 7 and improves locomotion in SCA7 knock-in mice

Brain (London, England : 1878), 2013-06, Vol.136 (Pt 6), p.1732-1745

2013

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C9ORF72 knockdown triggers FTD-like symptoms and cell pathology in mice

Frontiers in cellular neuroscience, 2023-04, Vol.17, p.1155929-1155929

2023

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MicroRNA signatures in genetic frontotemporal dementia and amyotrophic lateral sclerosis

Annals of clinical and translational neurology, 2022-11, Vol.9 (11), p.1778-1791

2022

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New Antibody-Free Mass Spectrometry-Based Quantification Reveals That C9ORF72 Long Protein Isoform Is Reduced in the Frontal Cortex of Hexanucleotide-Repeat Expansion Carriers

Frontiers in neuroscience, 2018-08, Vol.12, p.589-589

2018

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Mistargeting of SH3TC2 away from the recycling endosome causes Charcot–Marie–Tooth disease type 4C

Human molecular genetics, 2010-03, Vol.19 (6), p.1009-1018

2010

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Interrupted CAG expansions in ATXN2 gene expand the genetic spectrum of frontotemporal dementias

Acta neuropathologica communications, 2018-05, Vol.6 (1), p.41-41, Article 41

2018

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PML clastosomes prevent nuclear accumulation of mutant ataxin-7 and other polyglutamine proteins

The Journal of cell biology, 2006-07, Vol.174 (1), p.65-76

2006

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SQSTM1 mutations in French patients with frontotemporal dementia or frontotemporal dementia with amyotrophic lateral sclerosis

JAMA neurology, 2013-11, Vol.70 (11), p.1403

2013

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hnRNPA2B1 and hnRNPA1 mutations are rare in patients with “multisystem proteinopathy” and frontotemporal lobar degeneration phenotypes

Neurobiology of aging, 2014-04, Vol.35 (4), p.934.e5-934.e6

2014

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A Conditional Pan-Neuronal Drosophila Model of Spinocerebellar Ataxia 7 with a Reversible Adult Phenotype Suitable for Identifying Modifier Genes

The Journal of neuroscience, 2007-03, Vol.27 (10), p.2483-2492

2007

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Parkin mutations are frequent in patients with isolated early‐onset parkinsonism

Brain (London, England : 1878), 2003-06, Vol.126 (6), p.1271-1278

2003

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Polyglutamine and polyalanine expansions in ataxin7 result in different types of aggregation and levels of toxicity

Molecular and cellular neuroscience, 2006-03, Vol.31 (3), p.438-445

2006

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A Conditional Pan-Neuronal Drosophila Model of Spinocerebellar Ataxia 7 with a Reversible Adult Phenotype Suitable for Identifying Modifier Genes

The Journal of neuroscience, 2007-03, Vol.27 (10), p.2483-2492

2007

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The Gastric Myoelectrical Activity Response To Emotional Stimuli

2018 IX International Seminar of Biomedical Engineering (SIB), 2018, p.1-5

2018

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C9ORF72: What It Is, What It Does, and Why It Matters

PhagoStat a scalable and interpretable end to end framework for efficient quantification of cell phagocytosis in neurodegenerative disease studies

Loss of function of C9orf72 causes motor deficits in a zebrafish model of amyotrophic lateral sclerosis

c-Jun Reprograms Schwann Cells of Injured Nerves to Generate a Repair Cell Essential for Regeneration

c-Jun in Schwann cells promotes axonal regeneration and motoneuron survival via paracrine signaling

Novel VCP mutations expand the mutational spectrum of frontotemporal dementia

Interferon beta induces clearance of mutant ataxin 7 and improves locomotion in SCA7 knock-in mice

C9ORF72 knockdown triggers FTD-like symptoms and cell pathology in mice

MicroRNA signatures in genetic frontotemporal dementia and amyotrophic lateral sclerosis

New Antibody-Free Mass Spectrometry-Based Quantification Reveals That C9ORF72 Long Protein Isoform Is Reduced in the Frontal Cortex of Hexanucleotide-Repeat Expansion Carriers

Mistargeting of SH3TC2 away from the recycling endosome causes Charcot–Marie–Tooth disease type 4C

Interrupted CAG expansions in ATXN2 gene expand the genetic spectrum of frontotemporal dementias

PML clastosomes prevent nuclear accumulation of mutant ataxin-7 and other polyglutamine proteins

SQSTM1 mutations in French patients with frontotemporal dementia or frontotemporal dementia with amyotrophic lateral sclerosis

hnRNPA2B1 and hnRNPA1 mutations are rare in patients with “multisystem proteinopathy” and frontotemporal lobar degeneration phenotypes

A Conditional Pan-Neuronal Drosophila Model of Spinocerebellar Ataxia 7 with a Reversible Adult Phenotype Suitable for Identifying Modifier Genes

Parkin mutations are frequent in patients with isolated early‐onset parkinsonism

Polyglutamine and polyalanine expansions in ataxin7 result in different types of aggregation and levels of toxicity

A Conditional Pan-Neuronal Drosophila Model of Spinocerebellar Ataxia 7 with a Reversible Adult Phenotype Suitable for Identifying Modifier Genes

The Gastric Myoelectrical Activity Response To Emotional Stimuli

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