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Intercellular propagated misfolding of wild-type Cu/Zn superoxide dismutase occurs via exosome-dependent and -independent mechanisms

Proceedings of the National Academy of Sciences - PNAS, 2014-03, Vol.111 (9), p.3620-3625

2014

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The cysteine-reactive small molecule ebselen facilitates effective SOD1 maturation

Nature communications, 2018-04, Vol.9 (1), p.1693-9, Article 1693

2018

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Strategies to promote the maturation of ALS-associated SOD1 mutants: small molecules return to the fold

Neural regeneration research, 2019-09, Vol.14 (9), p.1511-1512

2019

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Mutant Cu/Zn Superoxide Dismutase (A4V) Turnover Is Altered in Cells Containing Inclusions

Frontiers in molecular neuroscience, 2021-11, Vol.14, p.771911-771911

2021

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High-content analysis of proteostasis capacity in cellular models of amyotrophic lateral sclerosis (ALS)

Scientific reports, 2024-06, Vol.14 (1), p.13844-11

2024

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Misfolding at the synapse: A role in amyotrophic lateral sclerosis pathogenesis?

Frontiers in molecular neuroscience, 2022-09, Vol.15, p.997661-997661

2022

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Pathogenic mutation in the ALS/FTD gene, CCNF, causes elevated Lys48-linked ubiquitylation and defective autophagy

Cellular and molecular life sciences : CMLS, 2018-01, Vol.75 (2), p.335-354

2018

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Improving the Delivery of SOD1 Antisense Oligonucleotides to Motor Neurons Using Calcium Phosphate-Lipid Nanoparticles

Frontiers in neuroscience, 2017-08, Vol.11, p.476-476

2017

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The Ubiquitin Proteasome System Is a Key Regulator of Pluripotent Stem Cell Survival and Motor Neuron Differentiation

Cells (Basel, Switzerland), 2019-06, Vol.8 (6), p.581

2019

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Unbiased Label-Free Quantitative Proteomics of Cells Expressing Amyotrophic Lateral Sclerosis (ALS) Mutations in CCNF Reveals Activation of the Apoptosis Pathway: A Workflow to Screen Pathogenic Gene Mutations

Frontiers in molecular neuroscience, 2021-04, Vol.14, p.627740-627740

2021

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Flow cytometric measurement of the cellular propagation of TDP-43 aggregation

Prion, 2017-05, Vol.11 (3), p.195-204

2017

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Susceptibility of Mutant SOD1 to Form a Destabilized Monomer Predicts Cellular Aggregation and Toxicity but Not In vitro Aggregation Propensity

Frontiers in neuroscience, 2016-11, Vol.10, p.499-499

2016

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Spinal motor neuron protein supersaturation patterns are associated with inclusion body formation in ALS

Proceedings of the National Academy of Sciences - PNAS, 2017-05, Vol.114 (20), p.E3935-E3943

2017

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P2X7 antagonism using Brilliant Blue G reduces body weight loss and prolongs survival in female SOD1G93A amyotrophic lateral sclerosis mice

PeerJ (San Francisco, CA), 2017-03, Vol.5, p.e3064-e3064

2017

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ALS-linked CCNF variant disrupts motor neuron ubiquitin homeostasis

Human molecular genetics, 2023-07, Vol.32 (14), p.2386-2398

2023

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Addition of exogenous SOD1 aggregates causes TDP-43 mislocalisation and aggregation

Cell stress & chaperones, 2017-11, Vol.22 (6), p.893-902

2017

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Evaluating protein cross-linking as a therapeutic strategy to stabilize SOD1 variants in a mouse model of familial ALS

PLoS biology, 2024-01, Vol.22 (1), p.e3002462-e3002462, Article e3002462

2024

Volltextzugriff (PDF)

Misfolded Polyglutamine, Polyalanine, and Superoxide Dismutase 1 Aggregate via Distinct Pathways in the Cell

The Journal of biological chemistry, 2014-03, Vol.289 (10), p.6669-6680

2014

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Longitudinal assessment of metal concentrations and copper isotope ratios in the G93A SOD1 mouse model of amyotrophic lateral sclerosis

Metallomics, 2017-02, Vol.9 (2), p.161

2017

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Evaluation of Skin Fibroblasts from Amyotrophic Lateral Sclerosis Patients for the Rapid Study of Pathological Features

Neurotoxicity research, 2015-08, Vol.28 (2), p.138-146

2015

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CCNF mutations in amyotrophic lateral sclerosis and frontotemporal dementia

Nature communications, 2016-04, Vol.7 (1), p.11253-11253, Article 11253

2016

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SOD1 A4V aggregation alters ubiquitin homeostasis in a cell model of ALS

Journal of cell science, 2018-06, Vol.131 (11)

2018

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Intercellular propagated misfolding of wild-type Cu/Zn superoxide dismutase occurs via exosome-dependent and -independent mechanisms

The cysteine-reactive small molecule ebselen facilitates effective SOD1 maturation

Strategies to promote the maturation of ALS-associated SOD1 mutants: small molecules return to the fold

Mutant Cu/Zn Superoxide Dismutase (A4V) Turnover Is Altered in Cells Containing Inclusions

High-content analysis of proteostasis capacity in cellular models of amyotrophic lateral sclerosis (ALS)

Misfolding at the synapse: A role in amyotrophic lateral sclerosis pathogenesis?

Pathogenic mutation in the ALS/FTD gene, CCNF, causes elevated Lys48-linked ubiquitylation and defective autophagy

Improving the Delivery of SOD1 Antisense Oligonucleotides to Motor Neurons Using Calcium Phosphate-Lipid Nanoparticles

The Ubiquitin Proteasome System Is a Key Regulator of Pluripotent Stem Cell Survival and Motor Neuron Differentiation

Unbiased Label-Free Quantitative Proteomics of Cells Expressing Amyotrophic Lateral Sclerosis (ALS) Mutations in CCNF Reveals Activation of the Apoptosis Pathway: A Workflow to Screen Pathogenic Gene Mutations

Flow cytometric measurement of the cellular propagation of TDP-43 aggregation

Susceptibility of Mutant SOD1 to Form a Destabilized Monomer Predicts Cellular Aggregation and Toxicity but Not In vitro Aggregation Propensity

Spinal motor neuron protein supersaturation patterns are associated with inclusion body formation in ALS

P2X7 antagonism using Brilliant Blue G reduces body weight loss and prolongs survival in female SOD1G93A amyotrophic lateral sclerosis mice

ALS-linked CCNF variant disrupts motor neuron ubiquitin homeostasis

Addition of exogenous SOD1 aggregates causes TDP-43 mislocalisation and aggregation

Evaluating protein cross-linking as a therapeutic strategy to stabilize SOD1 variants in a mouse model of familial ALS

Misfolded Polyglutamine, Polyalanine, and Superoxide Dismutase 1 Aggregate via Distinct Pathways in the Cell

Longitudinal assessment of metal concentrations and copper isotope ratios in the G93A SOD1 mouse model of amyotrophic lateral sclerosis

Evaluation of Skin Fibroblasts from Amyotrophic Lateral Sclerosis Patients for the Rapid Study of Pathological Features

CCNF mutations in amyotrophic lateral sclerosis and frontotemporal dementia

SOD1 A4V aggregation alters ubiquitin homeostasis in a cell model of ALS

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