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Oxidative damage of 14-3-3 zeta and gamma isoforms in Alzheimer's disease and cerebral amyloid angiopathy

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Oxidative damage of 14-3-3 zeta and gamma isoforms in Alzheimer's disease and cerebral amyloid angiopathy. / Santpere, G; Puig, B; Ferrer, I; Puig Martorell, Berta.

in: NEUROSCIENCE, Jahrgang 146, Nr. 4, 08.06.2007, S. 1640-51.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Santpere, G, Puig, B, Ferrer, I & Puig Martorell, B 2007, 'Oxidative damage of 14-3-3 zeta and gamma isoforms in Alzheimer's disease and cerebral amyloid angiopathy', NEUROSCIENCE, Jg. 146, Nr. 4, S. 1640-51. https://doi.org/10.1016/j.neuroscience.2007.03.013

APA

Santpere, G., Puig, B., Ferrer, I., & Puig Martorell, B. (2007). Oxidative damage of 14-3-3 zeta and gamma isoforms in Alzheimer's disease and cerebral amyloid angiopathy. NEUROSCIENCE, 146(4), 1640-51. https://doi.org/10.1016/j.neuroscience.2007.03.013

Vancouver

Santpere G, Puig B, Ferrer I, Puig Martorell B. Oxidative damage of 14-3-3 zeta and gamma isoforms in Alzheimer's disease and cerebral amyloid angiopathy. NEUROSCIENCE. 2007 Jun 8;146(4):1640-51. https://doi.org/10.1016/j.neuroscience.2007.03.013

Bibtex

@article{76525c450c484552b04df6ac53749965,
title = "Oxidative damage of 14-3-3 zeta and gamma isoforms in Alzheimer's disease and cerebral amyloid angiopathy",
abstract = "Previous studies have shown oxidative damage resulting from amyloid Abeta exposure to cultured cells and in murine models. A target of oxidation is 14-3-3 which comprises a group of proteins involved in kinase activation and chaperone activity. The present study shows glycoxidative damage, as revealed with mono and bi-dimensional gel electrophoresis and Western blotting, followed by in-gel digestion and mass spectrometry, in the frontal cortex in Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA), a neurodegenerative disease with deposition of Abeta in cerebral blood vessels and in diffuse plaques unaccompanied by intraneuronal hyper-phosphorylated tau deposition. malondialdehyde-lysine (MDA-Lys)-, but not 4-hydroxy-2-nonenal (HNE)-immunoreactive adducts, and N-carboxyethyl-lysine (CEL), but not N-carboxymethyl-lysine (CML)-products, were present in 14-3-3 involving zeta and gamma isoforms in both AD and CAA. These findings demonstrate that 14-3-3 glyco- and lipoxidation occurs in AD and CAA, probably as a direct consequence of Abeta deposition.",
keywords = "14-3-3 Proteins, Aged, Aged, 80 and over, Alzheimer Disease, Amyloid beta-Peptides, Blotting, Western, Cerebral Amyloid Angiopathy, Electrophoresis, Female, Frontal Lobe, Humans, Male, Mass Spectrometry, Middle Aged",
author = "G Santpere and B Puig and I Ferrer and {Puig Martorell}, Berta",
year = "2007",
month = jun,
day = "8",
doi = "10.1016/j.neuroscience.2007.03.013",
language = "English",
volume = "146",
pages = "1640--51",
journal = "NEUROSCIENCE",
issn = "0306-4522",
publisher = "Elsevier Limited",
number = "4",

}

RIS

TY - JOUR

T1 - Oxidative damage of 14-3-3 zeta and gamma isoforms in Alzheimer's disease and cerebral amyloid angiopathy

AU - Santpere, G

AU - Puig, B

AU - Ferrer, I

AU - Puig Martorell, Berta

PY - 2007/6/8

Y1 - 2007/6/8

N2 - Previous studies have shown oxidative damage resulting from amyloid Abeta exposure to cultured cells and in murine models. A target of oxidation is 14-3-3 which comprises a group of proteins involved in kinase activation and chaperone activity. The present study shows glycoxidative damage, as revealed with mono and bi-dimensional gel electrophoresis and Western blotting, followed by in-gel digestion and mass spectrometry, in the frontal cortex in Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA), a neurodegenerative disease with deposition of Abeta in cerebral blood vessels and in diffuse plaques unaccompanied by intraneuronal hyper-phosphorylated tau deposition. malondialdehyde-lysine (MDA-Lys)-, but not 4-hydroxy-2-nonenal (HNE)-immunoreactive adducts, and N-carboxyethyl-lysine (CEL), but not N-carboxymethyl-lysine (CML)-products, were present in 14-3-3 involving zeta and gamma isoforms in both AD and CAA. These findings demonstrate that 14-3-3 glyco- and lipoxidation occurs in AD and CAA, probably as a direct consequence of Abeta deposition.

AB - Previous studies have shown oxidative damage resulting from amyloid Abeta exposure to cultured cells and in murine models. A target of oxidation is 14-3-3 which comprises a group of proteins involved in kinase activation and chaperone activity. The present study shows glycoxidative damage, as revealed with mono and bi-dimensional gel electrophoresis and Western blotting, followed by in-gel digestion and mass spectrometry, in the frontal cortex in Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA), a neurodegenerative disease with deposition of Abeta in cerebral blood vessels and in diffuse plaques unaccompanied by intraneuronal hyper-phosphorylated tau deposition. malondialdehyde-lysine (MDA-Lys)-, but not 4-hydroxy-2-nonenal (HNE)-immunoreactive adducts, and N-carboxyethyl-lysine (CEL), but not N-carboxymethyl-lysine (CML)-products, were present in 14-3-3 involving zeta and gamma isoforms in both AD and CAA. These findings demonstrate that 14-3-3 glyco- and lipoxidation occurs in AD and CAA, probably as a direct consequence of Abeta deposition.

KW - 14-3-3 Proteins

KW - Aged

KW - Aged, 80 and over

KW - Alzheimer Disease

KW - Amyloid beta-Peptides

KW - Blotting, Western

KW - Cerebral Amyloid Angiopathy

KW - Electrophoresis

KW - Female

KW - Frontal Lobe

KW - Humans

KW - Male

KW - Mass Spectrometry

KW - Middle Aged

U2 - 10.1016/j.neuroscience.2007.03.013

DO - 10.1016/j.neuroscience.2007.03.013

M3 - SCORING: Journal article

C2 - 17445990

VL - 146

SP - 1640

EP - 1651

JO - NEUROSCIENCE

JF - NEUROSCIENCE

SN - 0306-4522

IS - 4

ER -