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Article

The Biological and Pathological Function of the Presenilin-1 ΔExon 9 Mutation Is Independent of Its Defect to Undergo Proteolytic Processing

1 Mar 1999

Abstract excerpt

The two homologous presenilins are key factors for the generation of amyloid beta-peptide (Abeta), since Alzheimer's disease (AD)-associated mutations enhance the production of the pathologically relevant 42-amino acid Abeta (Abeta42), and a gene knockout of presenilin-1 (PS1) significantly inhibits total Abeta production. Presenilins undergo proteolytic processing within the domain encoded by exon 9, a process...

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PMID: 10075646
DOI: 10.1074/jbc.274.12.7615

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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The Biological and Pathological Function of the Presenilin-1 ΔExon 9 Mutation Is Independent of Its Defect to Undergo Proteolytic ProcessingPMID 10075646Read ↗

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