Wolozin B, Alexander P, Palacino J
Department of Pharmacology, Loyola University Medical Center, Maywood, IL 60153, USA.
Neurobiol Aging. 1998 Jan-Feb;19(1 Suppl):S23-7. doi: 10.1016/s0197-4580(98)00041-4.
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.
