UB Paderborn / Katalog / Suche / in CDI

1 – 20 von 20

Sortiert nach

SOD1A4V aggregation alters ubiquitin homeostasis in a cell model of ALS

Journal of cell science, 2018-06, Vol.131 (11), p.jcs209122-jcs209122

2018

Volltextzugriff (PDF)

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

Volltextzugriff (PDF)

TDP-43 is a ubiquitylation substrate of the SCFcyclin F complex

Neurobiology of disease, 2022-06, Vol.167, p.105673-105673, Article 105673

2022

Volltextzugriff (PDF)

Alpha-2-Macroglobulin Is Acutely Sensitive to Freezing and Lyophilization: Implications for Structural and Functional Studies

PloS one, 2015-06, Vol.10 (6), p.e0130036-e0130036

2015

Volltextzugriff (PDF)

Ubiquitin homeostasis disruption, a common cause of proteostasis collapse in amyotrophic lateral sclerosis?

Neural regeneration research, 2022-10, Vol.17 (10), p.2218-2220

2022

Volltextzugriff (PDF)

Proteome Homeostasis Dysfunction: A Unifying Principle in ALS Pathogenesis

Trends in neurosciences (Regular ed.), 2020-05, Vol.43 (5), p.274-284

2020

Volltextzugriff (PDF)

Ubiquitin Homeostasis Is Disrupted in TDP-43 and FUS Cell Models of ALS

iScience, 2020-11, Vol.23 (11), p.101700-101700, Article 101700

2020

Volltextzugriff (PDF)

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

Volltextzugriff (PDF)

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

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

2017

Volltextzugriff (PDF)

Tryptophan 32-mediated SOD1 aggregation is attenuated by pyrimidine-like compounds in living cells

Scientific reports, 2018-10, Vol.8 (1), p.15590-12, Article 15590

2018

Volltextzugriff (PDF)

Distinct partitioning of ALS associated TDP-43, FUS and SOD1 mutants into cellular inclusions

Scientific reports, 2015-08, Vol.5 (1), p.13416-13416, Article 13416

2015

Volltextzugriff (PDF)

ALS-linked CCNF variant disrupts motor neuron ubiquitin homeostasis

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

2023

Volltextzugriff (PDF)

Cells Overexpressing ALS-Associated SOD1 Variants Are Differentially Susceptible to CuATSM-Associated Toxicity

ACS chemical neuroscience, 2022-08, Vol.13 (16), p.2371-2379

2022

Volltextzugriff (PDF)

CuATSM Protects Against the In Vitro Cytotoxicity of Wild-Type-Like Copper–Zinc Superoxide Dismutase Mutants but not Mutants That Disrupt Metal Binding

ACS chemical neuroscience, 2019-03, Vol.10 (3), p.1555-1564

2019

Volltextzugriff (PDF)

CuATSM improves motor function and extends survival but is not tolerated at a high dose in SOD1G93A mice with a C57BL/6 background

Scientific reports, 2021-09, Vol.11 (1), Article 19392

2021

Volltextzugriff (PDF)

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

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

2017

Volltextzugriff (PDF)

TDP-43 is a ubiquitylation substrate of the SCF cyclin F complex

Neurobiology of disease, 2022-06, Vol.167, p.105673

2022

Volltextzugriff (PDF)

CuATSM improves motor function and extends survival but is not tolerated at a high dose in SOD1 G93A mice with a C57BL/6 background

Scientific reports, 2021-09, Vol.11 (1), p.19392

2021

Volltextzugriff (PDF)

CuATSM improves motor function and extends survival but is not tolerated at a high dose in SOD1 G93A mice with a C57BL/6 background

Scientific reports, 2021-09, Vol.11 (1), p.1-12

2021

Volltextzugriff (PDF)

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

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

2018

Volltextzugriff (PDF)

1 – 20 von 20

Suche als RSS-Feed

Suchergebnisse filtern

Filter anzeigen

Nur zeigen

Geprüft (Peer-Review)
(20)
Mit Volltextzugriff
(20)

Publikationsform

Artikel
(20)

Sprache

Englisch
(20)
Japanisch
(3)

Erscheinungsjahr

n.n

Thema

Science & Technology
(16)
Life Sciences & Biomedicine
(11)
Amyotrophic Lateral Sclerosis
(9)
Humans
(9)
Neurosciences
(7)
Proteins
(7)
Amyotrophic Lateral Sclerosis - Metabolism
(6)
Animals
(6)
Mice
(6)
Mutation
(6)
Neurosciences & Neurology
(6)
Cell Biology
(5)
Multidisciplinary Sciences
(5)
Science & Technology - Other Topics
(5)
Superoxide Dismutase
(5)
Als
(4)
Biochemistry & Molecular Biology
(4)
Protein Aggregation
(4)
Protein Folding
(4)
Ubiquitin
(4)

15 weitere anzeigen...

Weniger anzeigen...

Zeitschrift / Serie

5 weitere anzeigen...

Weniger anzeigen...

Menü

Weitere Dienste

Einstellungen

SOD1A4V aggregation alters ubiquitin homeostasis in a cell model of ALS

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

TDP-43 is a ubiquitylation substrate of the SCFcyclin F complex

Alpha-2-Macroglobulin Is Acutely Sensitive to Freezing and Lyophilization: Implications for Structural and Functional Studies

Ubiquitin homeostasis disruption, a common cause of proteostasis collapse in amyotrophic lateral sclerosis?

Proteome Homeostasis Dysfunction: A Unifying Principle in ALS Pathogenesis

Ubiquitin Homeostasis Is Disrupted in TDP-43 and FUS Cell Models of ALS

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

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

Tryptophan 32-mediated SOD1 aggregation is attenuated by pyrimidine-like compounds in living cells

Distinct partitioning of ALS associated TDP-43, FUS and SOD1 mutants into cellular inclusions

ALS-linked CCNF variant disrupts motor neuron ubiquitin homeostasis

Cells Overexpressing ALS-Associated SOD1 Variants Are Differentially Susceptible to CuATSM-Associated Toxicity

CuATSM Protects Against the In Vitro Cytotoxicity of Wild-Type-Like Copper–Zinc Superoxide Dismutase Mutants but not Mutants That Disrupt Metal Binding

CuATSM improves motor function and extends survival but is not tolerated at a high dose in SOD1G93A mice with a C57BL/6 background

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

TDP-43 is a ubiquitylation substrate of the SCF cyclin F complex

CuATSM improves motor function and extends survival but is not tolerated at a high dose in SOD1 G93A mice with a C57BL/6 background

CuATSM improves motor function and extends survival but is not tolerated at a high dose in SOD1 G93A mice with a C57BL/6 background

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

Suchergebnisse filtern