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Protein folding alterations in amyotrophic lateral sclerosis

Brain research, 2016-10, Vol.1648 (Pt B), p.633-649

2016

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Redox dysregulation as a driver for DNA damage and its relationship to neurodegenerative diseases

Translational neurodegeneration, 2023-04, Vol.12 (1), p.18-18, Article 18

2023

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Emerging Evidence Highlighting the Importance of Redox Dysregulation in the Pathogenesis of Amyotrophic Lateral Sclerosis (ALS)

Frontiers in cellular neuroscience, 2021-02, Vol.14, p.581950-581950

2021

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Prescribing Cold: The Science and Practice of Cryotherapy in Dental Medicine

Journal of pharmacy & bioallied science, 2024-07, Vol.16 (Suppl 3), p.S1935-S1937

2024

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Editorial: Restoring endoplasmic reticulum proteostasis to treat neurological disorders

Frontiers in pharmacology, 2023-03, Vol.14, p.1176805-1176805

2023

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ALS-associated TDP-43 induces endoplasmic reticulum stress, which drives cytoplasmic TDP-43 accumulation and stress granule formation

PloS one, 2013-11, Vol.8 (11), p.e81170-e81170

2013

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The Cysteine (Cys) Residues Cys-6 and Cys-111 in Mutant Superoxide Dismutase 1 (SOD1) A4V Are Required for Induction of Endoplasmic Reticulum Stress in Amyotrophic Lateral Sclerosis

Journal of molecular neuroscience, 2020-09, Vol.70 (9), p.1357-1368

2020

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Impaired NHEJ repair in amyotrophic lateral sclerosis is associated with TDP-43 mutations

Molecular neurodegeneration, 2020-09, Vol.15 (1), p.1-51, Article 51

2020

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ALS/FTD-associated mutation in cyclin F inhibits ER-Golgi trafficking, inducing ER stress, ERAD and Golgi fragmentation

Scientific reports, 2023-11, Vol.13 (1), p.20467-20467, Article 20467

2023

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ERp57 is protective against mutant SOD1-induced cellular pathology in amyotrophic lateral sclerosis

Human molecular genetics, 2018-04, Vol.27 (8), p.1311-1331

2018

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Correction to: the Cysteine (Cys) Residues Cys-6 and Cys-111 in Mutant Superoxide Dismutase 1 (SOD1) A4V Are Required for Induction of Endoplasmic Reticulum Stress in Amyotrophic Lateral Sclerosis

Journal of molecular neuroscience, 2020-09, Vol.70 (9), p.1369-1369

2020

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Redox Regulation in Amyotrophic Lateral Sclerosis

Oxidative medicine and cellular longevity, 2013-01, Vol.2013 (2013), p.1-12

2013

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The Redox Activity of Protein Disulfide Isomerase Inhibits ALS Phenotypes in Cellular and Zebrafish Models

iScience, 2020-05, Vol.23 (5), p.101097-101097, Article 101097

2020

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The Mitochondrial-associated ER membrane (MAM) compartment and its dysregulation in Amyotrophic Lateral Sclerosis (ALS)

Seminars in cell & developmental biology, 2021-04, Vol.112, p.105-113

2021

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Protein Disulphide Isomerases: emerging roles of PDI and ERp57 in the nervous system and as therapeutic targets for ALS

Expert opinion on therapeutic targets, 2017-01, Vol.21 (1), p.37-49

2017

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Novel roles for protein disulphide isomerase in disease states: a double edged sword?

Frontiers in cell and developmental biology, 2015-05, Vol.3, p.30-30

2015

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Rab1-dependent ER–Golgi transport dysfunction is a common pathogenic mechanism in SOD1, TDP-43 and FUS-associated ALS

Acta neuropathologica, 2015-11, Vol.130 (5), p.679-697

2015

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Amyotrophic lateral sclerosis-linked UBQLN2 mutants inhibit endoplasmic reticulum to Golgi transport, leading to Golgi fragmentation and ER stress

Cellular and molecular life sciences : CMLS, 2020-10, Vol.77 (19), p.3859-3873

2020

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The Unfolded Protein Response and the Role of Protein Disulfide Isomerase in Neurodegeneration

Frontiers in cell and developmental biology, 2016-01, Vol.3, p.80-80

2016

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C9orf72-Associated Dipeptide Repeat Expansions Perturb ER-Golgi Vesicular Trafficking, Inducing Golgi Fragmentation and ER Stress, in ALS/FTD

Molecular neurobiology, 2024-05

2024

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Protein disulphide isomerase is associated with mutant SOD1 in canine degenerative myelopathy

Neuroreport, 2019-01, Vol.30 (1), p.8-13

2019

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Protein Disulfide Isomerase Endoplasmic Reticulum Protein 57 (ERp57) is Protective Against ALS-Associated Mutant TDP-43 in Neuronal Cells

Neuromolecular medicine, 2024-06, Vol.26 (1), p.23

2024

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Efficacy of peptide nucleic acid and selected conjugates against specific cellular pathologies of amyotrophic lateral sclerosis

Bioorganic & medicinal chemistry, 2016-04, Vol.24 (7), p.1520-1527

2016

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Protein folding alterations in amyotrophic lateral sclerosis

Redox dysregulation as a driver for DNA damage and its relationship to neurodegenerative diseases

Emerging Evidence Highlighting the Importance of Redox Dysregulation in the Pathogenesis of Amyotrophic Lateral Sclerosis (ALS)

Prescribing Cold: The Science and Practice of Cryotherapy in Dental Medicine

Editorial: Restoring endoplasmic reticulum proteostasis to treat neurological disorders

ALS-associated TDP-43 induces endoplasmic reticulum stress, which drives cytoplasmic TDP-43 accumulation and stress granule formation

The Cysteine (Cys) Residues Cys-6 and Cys-111 in Mutant Superoxide Dismutase 1 (SOD1) A4V Are Required for Induction of Endoplasmic Reticulum Stress in Amyotrophic Lateral Sclerosis

Impaired NHEJ repair in amyotrophic lateral sclerosis is associated with TDP-43 mutations

ALS/FTD-associated mutation in cyclin F inhibits ER-Golgi trafficking, inducing ER stress, ERAD and Golgi fragmentation

ERp57 is protective against mutant SOD1-induced cellular pathology in amyotrophic lateral sclerosis

Correction to: the Cysteine (Cys) Residues Cys-6 and Cys-111 in Mutant Superoxide Dismutase 1 (SOD1) A4V Are Required for Induction of Endoplasmic Reticulum Stress in Amyotrophic Lateral Sclerosis

Redox Regulation in Amyotrophic Lateral Sclerosis

The Redox Activity of Protein Disulfide Isomerase Inhibits ALS Phenotypes in Cellular and Zebrafish Models

The Mitochondrial-associated ER membrane (MAM) compartment and its dysregulation in Amyotrophic Lateral Sclerosis (ALS)

Protein Disulphide Isomerases: emerging roles of PDI and ERp57 in the nervous system and as therapeutic targets for ALS

Novel roles for protein disulphide isomerase in disease states: a double edged sword?

Rab1-dependent ER–Golgi transport dysfunction is a common pathogenic mechanism in SOD1, TDP-43 and FUS-associated ALS

Amyotrophic lateral sclerosis-linked UBQLN2 mutants inhibit endoplasmic reticulum to Golgi transport, leading to Golgi fragmentation and ER stress

The Unfolded Protein Response and the Role of Protein Disulfide Isomerase in Neurodegeneration

C9orf72-Associated Dipeptide Repeat Expansions Perturb ER-Golgi Vesicular Trafficking, Inducing Golgi Fragmentation and ER Stress, in ALS/FTD

Protein disulphide isomerase is associated with mutant SOD1 in canine degenerative myelopathy

Protein Disulfide Isomerase Endoplasmic Reticulum Protein 57 (ERp57) is Protective Against ALS-Associated Mutant TDP-43 in Neuronal Cells

Efficacy of peptide nucleic acid and selected conjugates against specific cellular pathologies of amyotrophic lateral sclerosis

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