Carboxy‐terminal truncation of long‐tailed amyloid β‐peptide is inhibited by serine protease inhibitor and peptide aldehyde
- 13 March 1998
- journal article
- Published by Wiley in FEBS Letters
- Vol. 424 (3) , 136-138
- https://doi.org/10.1016/s0014-5793(98)00157-4
Abstract
The 42/43-residue amyloid β-peptide (Aβ) is widely believed to play a major role in Alzheimer's disease. The present study shows that the rat brain contains a carboxypeptidase that efficiently deletes three amino acids from Aβ1–43. The carboxypeptidase activity in the brain was completely inhibited by 1 mM phenylmethylsulfonyl fluoride, suggesting the protease is a serine carboxypeptidase. The carboxy-terminal truncation of Aβ1–43 was moderately inhibited by carbobenzoxy-Leu-leucinal, carbobenzoxy-Leu-Leu-leucinal, and carbobenzoxy-Leu-Leu-norvalinal, and weakly by antipain. The present data suggest that the serine carboxypeptidase contributes to the generation of short-tailed Aβ peptides and is important in the intracellular clearance of Aβ1–42/43 in brains.Keywords
This publication has 23 references indexed in Scilit:
- Secreted amyloid β–protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's diseaseNature Medicine, 1996
- Long Amyloid .beta.-Protein Secreted from Wild-Type Human Neuroblastoma IMR-32 CellsBiochemistry, 1995
- Cell Biology of the Amyloid beta-Protein Precursor and the Mechanism of Alzheimer's DiseaseAnnual Review of Cell Biology, 1994
- Visualization of Aβ42(43) and Aβ40 in senile plaques with end-specific Aβ monoclonals: Evidence that an initially deposited species is Aβ42(43)Neuron, 1994
- An Increased Percentage of Long Amyloid β Protein Secreted by Familial Amyloid β Protein Precursor (βApp 717 ) MutantsScience, 1994
- Rapid Communication: Characterization of β‐Amyloid Peptide from Human Cerebrospinal FluidJournal of Neurochemistry, 1993
- Cells with a familial Alzheimerʼs disease mutation produce authentic β-peptideNeuroReport, 1993
- Structural alterations in the peptide backbone of beta-amyloid core protein may account for its deposition and stability in Alzheimer's disease.Journal of Biological Chemistry, 1993
- Amyloid plaque core protein in Alzheimer disease and Down syndrome.Proceedings of the National Academy of Sciences, 1985
- Alzheimer's disease: Initial report of the purification and characterization of a novel cerebrovascular amyloid proteinBiochemical and Biophysical Research Communications, 1984