UB Paderborn / Katalog / Suche / in CDI

Sortiert nach

Einfacher Volltextzugriff von (fast) überall

Installieren Sie die LibKey Nomad-Browsererweiterung und erhalten Sie von vielen Webseiten einfachen Zugriff auf lizenzierte Volltexte oder Open Access Publikationen. Mehr erfahren...

ALS-linked CCNF variant disrupts motor neuron ubiquitin homeostasis

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

2023

Volltextzugriff (PDF)

Amyloidogenic regions in beta-strands II and III modulate the aggregation and toxicity of SOD1 in living cells

Open biology, 2024-06, Vol.14 (6), p.230418-17

2024

Volltextzugriff (PDF)

Amyotrophic Lateral Sclerosis: Proteins, Proteostasis, Prions, and Promises

Frontiers in cellular neuroscience, 2020-11, Vol.14, p.581907-581907

2020

Volltextzugriff (PDF)

Assessment of protein inclusions in cultured cells using automated image analysis

STAR protocols, 2022-12, Vol.3 (4), p.101748-101748, Article 101748

2022

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)

Cerebrovascular amyloid angiopathy in bioengineered vessels is reduced by high‐density lipoprotein particles enriched in apolipoprotein E: Development of new models and analysis methods/amyloid/Abeta

Alzheimer's & dementia, 2020-12, Vol.16 (S2)

2020

Volltextzugriff (PDF)

Cerebrovascular amyloid angiopathy in bioengineered vessels is reduced by high‐density lipoprotein particles enriched in apolipoprotein E

Alzheimer's & dementia, 2020-12, Vol.16, p.n/a

2020

Volltextzugriff (PDF)

Cerebrovascular amyloid Angiopathy in bioengineered vessels is reduced by high-density lipoprotein particles enriched in Apolipoprotein E

Molecular neurodegeneration, 2020-03, Vol.15 (1), p.23-23, Article 23

2020

Volltextzugriff (PDF)

CNS-derived extracellular vesicles from superoxide dismutase 1 (SOD1)G93A ALS mice originate from astrocytes and neurons and carry misfolded SOD1

The Journal of biological chemistry, 2019-03, Vol.294 (10), p.3744-3759

2019

Volltextzugriff (PDF)

Corrigendum: Prion-Like Propagation of Protein Misfolding and Aggregation in Amyotrophic Lateral Sclerosis

Frontiers in molecular neuroscience, 2020-01, Vol.12, p.311-311

2020

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)

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)

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)

The cysteine-reactive small molecule ebselen facilitates effective SOD1 maturation

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

2018

Volltextzugriff (PDF)

Emerging Developments in Targeting Proteotoxicity in Neurodegenerative Diseases

CNS drugs, 2019-09, Vol.33 (9), p.883-904

2019

Volltextzugriff (PDF)

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, Article e3002462

2024

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)

Glutathionylation potentiates benign superoxide dismutase 1 variants to the toxic forms associated with amyotrophic lateral sclerosis

Scientific reports, 2013-11, Vol.3 (1), p.3275, Article 3275

2013

Volltextzugriff (PDF)

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

Volltextzugriff (PDF)

The microglial NLRP3 inflammasome is activated by amyotrophic lateral sclerosis proteins

Glia, 2020-02, Vol.68 (2), p.407-421

2020

Volltextzugriff (PDF)

Neurodegenerative disease-associated protein aggregates are poor inducers of the heat shock response in neuronal cells

Journal of cell science, 2020-08, Vol.133 (15)

2020

Volltextzugriff (PDF)

P4‐163: THE PATHOLOGICAL INTERACTOME OF TDP‐43 INCLUDES HUMAN WILDTYPE SOD1

Alzheimer's & dementia, 2019-07, Vol.15 (7S_Part_26), p.P1336-P1337

2019

Volltextzugriff (PDF)

THE PATHOLOGICAL INTERACTOME OF TDP-43 INCLUDES HUMAN WILDTYPE SOD1

Alzheimer's & dementia, 2019-07, Vol.15 (7), p.P1336-P1337

2019

Volltextzugriff (PDF)

Prion-Like Propagation of Protein Misfolding and Aggregation in Amyotrophic Lateral Sclerosis

Frontiers in molecular neuroscience, 2019-11, Vol.12, p.262-262

2019

Volltextzugriff (PDF)

1 – 25 von 41

Suche als RSS-Feed

Suchergebnisse filtern

Filter anzeigen

Nur zeigen

Geprüft (Peer-Review)
(40)
Mit Volltextzugriff
(39)

Publikationsform

Artikel
(40)
Buchkapitel
(1)

Sprache

Englisch
(41)

Erscheinungsjahr

n.n

Thema

Science & Technology
(28)
Life Sciences & Biomedicine
(20)
Amyotrophic Lateral Sclerosis
(16)
Humans
(15)
Proteins
(14)
Mutation
(13)
Superoxide Dismutase
(13)
Protein Aggregation
(12)
Neurosciences
(11)
Neurosciences & Neurology
(11)
Protein Folding
(11)
Amyotrophic Lateral Sclerosis - Genetics
(9)
Animals
(9)
Biochemistry & Molecular Biology
(9)
Mice
(9)
Superoxide Dismutase-1 - Genetics
(9)
Amyotrophic Lateral Sclerosis - Metabolism
(8)
Superoxide Dismutase-1 - Metabolism
(8)
Multidisciplinary Sciences
(7)
Neurodegeneration
(7)

15 weitere anzeigen...

Weniger anzeigen...

Menü

Weitere Dienste

Einstellungen

ALS-linked CCNF variant disrupts motor neuron ubiquitin homeostasis

Amyloidogenic regions in beta-strands II and III modulate the aggregation and toxicity of SOD1 in living cells

Amyotrophic Lateral Sclerosis: Proteins, Proteostasis, Prions, and Promises

Assessment of protein inclusions in cultured cells using automated image analysis

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

Cerebrovascular amyloid angiopathy in bioengineered vessels is reduced by high‐density lipoprotein particles enriched in apolipoprotein E: Development of new models and analysis methods/amyloid/Abeta

Cerebrovascular amyloid angiopathy in bioengineered vessels is reduced by high‐density lipoprotein particles enriched in apolipoprotein E

Cerebrovascular amyloid Angiopathy in bioengineered vessels is reduced by high-density lipoprotein particles enriched in Apolipoprotein E

CNS-derived extracellular vesicles from superoxide dismutase 1 (SOD1)G93A ALS mice originate from astrocytes and neurons and carry misfolded SOD1

Corrigendum: Prion-Like Propagation of Protein Misfolding and Aggregation in Amyotrophic Lateral Sclerosis

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

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

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

The cysteine-reactive small molecule ebselen facilitates effective SOD1 maturation

Emerging Developments in Targeting Proteotoxicity in Neurodegenerative Diseases

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

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

Glutathionylation potentiates benign superoxide dismutase 1 variants to the toxic forms associated with amyotrophic lateral sclerosis

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

The microglial NLRP3 inflammasome is activated by amyotrophic lateral sclerosis proteins

Neurodegenerative disease-associated protein aggregates are poor inducers of the heat shock response in neuronal cells

P4‐163: THE PATHOLOGICAL INTERACTOME OF TDP‐43 INCLUDES HUMAN WILDTYPE SOD1

THE PATHOLOGICAL INTERACTOME OF TDP-43 INCLUDES HUMAN WILDTYPE SOD1

Prion-Like Propagation of Protein Misfolding and Aggregation in Amyotrophic Lateral Sclerosis

Suchergebnisse filtern