Glutamate carboxypeptidase II does not process amyloid‐β peptide

The accumulation of amyloid‐β (Aβ) peptide is thought to be a major causative mechanism of Alzheimer's disease. Aβ accumulation could be caused by dysregulated processing of amyloid precursor protein, yielding excessive amounts of Aβ, and/or by inefficient proteolytic degradation of the peptide...

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Veröffentlicht in:	The FASEB journal 2013-07, Vol.27 (7), p.2626-2632
Hauptverfasser:	Sedlák, František, Šácha, Pavel, Blechová, Miroslava, B&rnezinová, Anna, Šafařík, Martin, Šebestík, Jaroslav, Konvalinka, Jan
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer's disease Amyloid beta-Peptides - chemistry Amyloid beta-Peptides - metabolism Antigens, Surface - genetics Antigens, Surface - metabolism Biocatalysis - drug effects Catalytic Domain Chromatography, High Pressure Liquid depsipeptide Dipeptides - metabolism disaggregation exopeptidase Glutamate Carboxypeptidase II - antagonists & inhibitors Glutamate Carboxypeptidase II - genetics Glutamate Carboxypeptidase II - metabolism Humans Hydrolysis Mass Spectrometry Molecular Structure Neprilysin - genetics Neprilysin - metabolism Organophosphorus Compounds - pharmacology Peptide Fragments - chemistry Peptide Fragments - metabolism Proteolysis PSMA Recombinant Proteins - metabolism Substrate Specificity Tritium
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