Journal of Biological Chemistry · 1998 · 916 citations · 33 references
Life SciencesBiochemistryMolecular BiologyEnzymologyMolecular NeuroscienceNeurodegenerationAlzheimer DiseaseAmyloid FormationEnzyme FunctionNeurodegenerative DiseasesProteolytic EnzymesProteolytic ProcessingAmyloid Beta PeptidesAmyloid FibrilsAmyloidogenic ProteinsGene DisruptionProtease Cleavage SitesProteolytic Enzyme ActivationProteolytic Enzyme ActivityTargeted Gene Disruption
Amyloid β peptide accumulates in Alzheimer disease brains and is produced by proteolytic processing of APP at β, α, and γ sites, but the responsible enzymes remain unclear. Knockout studies show that TACE is the key α‑secretase for APP, and its inhibition reduces APP secretion and alters Aβ production in cultured cells.
The amyloid protein, Aβ, which accumulates in the brains of Alzheimer patients, is derived by proteolysis of the amyloid protein precursor (APP). APP can undergo endoproteolytic processing at three sites, one at the amino terminus of the Aβ domain (β-cleavage), one within the Aβ domain (α-cleavage), and one at the carboxyl terminus of the Aβ domain (γ-cleavage). The enzymes responsible for these activities have not been unambiguously identified. By the use of gene disruption (knockout), we now demonstrate that TACE (tumor necrosis factor α converting enzyme), a member of the ADAM family (adisintegrinand metalloprotease-family) of proteases, plays a central role in regulated α-cleavage of APP. Our data suggest that TACE may be the α-secretase responsible for the majority of regulated α-cleavage in cultured cells. Furthermore, we show that inhibiting this enzyme affects both APP secretion and Aβ formation in cultured cells.
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A metalloproteinase disintegrin that releases tumour-necrosis factor-α from cells
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