(Q46737371)

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Reduced neuronal expression of synaptic transmission modulator HNK-1/neural cell adhesion molecule as a potential consequence of amyloid beta-mediated oxidative stress: a proteomic approach

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Europe PubMed Central

PubMed publication ID

24 December 2017

http://europepmc.org/abstract/MED/15686472

Reduced neuronal expression of synaptic transmission modulator HNK-1/neural cell adhesion molecule as a potential consequence of amyloid beta-mediated oxidative stress: a proteomic approach (English)

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Europe PubMed Central

PubMed publication ID

24 December 2017

http://europepmc.org/abstract/MED/15686472

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Stefani N Thomas

1

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Europe PubMed Central

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24 December 2017

http://europepmc.org/abstract/MED/15686472

Brian A Soreghan

2

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Europe PubMed Central

PubMed publication ID

24 December 2017

http://europepmc.org/abstract/MED/15686472

Mihaela Nistor

3

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Europe PubMed Central

PubMed publication ID

24 December 2017

http://europepmc.org/abstract/MED/15686472

Floyd Sarsoza

4

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Europe PubMed Central

PubMed publication ID

24 December 2017

http://europepmc.org/abstract/MED/15686472

Elizabeth Head

5

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Europe PubMed Central

PubMed publication ID

24 December 2017

http://europepmc.org/abstract/MED/15686472

Austin J Yang

6

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24 December 2017

http://europepmc.org/abstract/MED/15686472

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1 February 2005

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24 December 2017

http://europepmc.org/abstract/MED/15686472

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13

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Journal of Neurochemistry

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Europe PubMed Central

PubMed publication ID

24 December 2017

http://europepmc.org/abstract/MED/15686472

92

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Europe PubMed Central

PubMed publication ID

24 December 2017

http://europepmc.org/abstract/MED/15686472

4

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Europe PubMed Central

PubMed publication ID

24 December 2017

http://europepmc.org/abstract/MED/15686472

705-717

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Europe PubMed Central

PubMed publication ID

24 December 2017

http://europepmc.org/abstract/MED/15686472

Oxidation of cytosolic proteins and expression of creatine kinase BB in frontal lobe in different neurodegenerative disorders.

1 reference

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Protein oxidation in the brain in Alzheimer's disease

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Dramatic aggregation of Alzheimer abeta by Cu(II) is induced by conditions representing physiological acidosis.

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Cu(II) potentiation of alzheimer abeta neurotoxicity. Correlation with cell-free hydrogen peroxide production and metal reduction.

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cDNA cloning, genomic structure and chromosomal mapping of the mouse glucuronyltransferase-S involved in the biosynthesis of the HNK-1 carbohydrate epitope

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Amyloid-beta: an antioxidant that becomes a pro-oxidant and critically contributes to Alzheimer's disease

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Amyloid-beta is an antioxidant for lipoproteins in cerebrospinal fluid and plasma

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Proteomic analysis of protein oxidation in Alzheimer's disease brain

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Oxidative stress hypothesis in Alzheimer's disease

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Fibrillar beta-amyloid evokes oxidative damage in a transgenic mouse model of Alzheimer's disease

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Neuroplasticity failure in Alzheimer's disease: bridging the gap between plaques and tangles

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Rapid colorimetric assay for cellular growth and survival: Application to proliferation and cytotoxicity assays

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Proteomics: the move to mixtures

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Carbonyl toxicology and Alzheimer's disease

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In vitro aging of beta-amyloid protein causes peptide aggregation and neurotoxicity

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Physiological levels of beta-amyloid induce cerebral vessel dysfunction and reduce endothelial nitric oxide production

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Neural recognition molecules and synaptic plasticity

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Mice deficient for the HNK-1 sulfotransferase show alterations in synaptic efficacy and spatial learning and memory

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Quantification and significance of protein oxidation in biological samples

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Protein turnover by the proteasome in aging and disease.

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21 January 2018

Excess brain protein oxidation and enzyme dysfunction in normal aging and in Alzheimer disease

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Oxidative stress in Alzheimer's disease

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Aberrant sphingomyelin/ceramide metabolic-induced neuronal endosomal/lysosomal dysfunction: potential pathological consequences in age-related neurodegeneration.

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High-throughput proteomic-based identification of oxidatively induced protein carbonylation in mouse brain

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Intrahippocampal administration of an antibody against the HNK-1 carbohydrate impairs memory consolidation in an inhibitory learning task in mice.

1 reference

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Intraneuronal Alzheimer abeta42 accumulates in multivesicular bodies and is associated with synaptic pathology

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Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo

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High molecular weight neurofilament proteins are physiological substrates of adduction by the lipid peroxidation product hydroxynonenal

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Extracellular matrix molecules, long-term potentiation, memory consolidation and the brain angiotensin system

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Mice deficient in nervous system-specific carbohydrate epitope HNK-1 exhibit impaired synaptic plasticity and spatial learning

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Intracellular accumulation of insoluble, newly synthesized abetan-42 in amyloid precursor protein-transfected cells that have been treated with Abeta1-42.

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21 January 2018

Identifiers

10.1111/J.1471-4159.2004.02892.X

1 reference

Europe PubMed Central

PubMed publication ID

24 December 2017

http://europepmc.org/abstract/MED/15686472

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

24 December 2017

http://europepmc.org/abstract/MED/15686472

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