Regulation of apoptosis by presenilin 1

Neurobiol Aging. Jan-Feb 1998;19(1 Suppl):S23-7. doi: 10.1016/s0197-4580(98)00041-4.

Abstract

Familial Alzheimer's disease is transmitted as an autosomal dominant disorder and, in 5-10% of the cases, is caused by mutations in the coding regions of two homologous genes, Presenilin 1 and 2 (PS1 and PS2). Previously, we have shown that PS2, a homolog of PS1. regulates apoptosis induced in neurons by trophic withdrawal or Abeta, and in T-cells by Fas ligand. We now report that PS1 also regulates apoptosis. Both wild-type and the H115Y mutant form of PS1 enhance Fas-mediated apoptosis in Jurkat cells. We also observed that wild-type and the H115Y mutant form of PS1 differentially regulate Jun Kinase, an important enzyme regulating apoptosis.

MeSH terms

  • Aging / metabolism
  • Apoptosis / genetics
  • Apoptosis / physiology*
  • Blotting, Western
  • Calcium-Calmodulin-Dependent Protein Kinases / metabolism
  • Cell Line
  • DNA, Neoplasm / biosynthesis
  • DNA, Neoplasm / genetics
  • Humans
  • JNK Mitogen-Activated Protein Kinases
  • Jurkat Cells
  • Membrane Proteins / genetics
  • Membrane Proteins / physiology*
  • Mitogen-Activated Protein Kinases*
  • Mutation
  • Oxidation-Reduction
  • Presenilin-1
  • Transfection
  • fas Receptor / metabolism

Substances

  • DNA, Neoplasm
  • Membrane Proteins
  • PSEN1 protein, human
  • Presenilin-1
  • fas Receptor
  • Calcium-Calmodulin-Dependent Protein Kinases
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases