Regulation of Apoptosis by Presenilin 1
作者： B Wolozin , P Alexander , J Palacino
DOI: 10.1016/S0197-4580(98)00041-4
关键词: Neurodegeneration 、 Fas ligand 、 Cancer research 、 Apoptosis 、 Jurkat cells 、 Mutation 、 Inhibitor of apoptosis domain 、 Cell biology 、 Presenilin 、 JUN kinase 、 Biology
摘要: Familial Alzheimer's disease is transmitted as an autosomal dominant disorder and, in 5-10% of the cases, caused by mutations coding regions two homologous genes, Presenilin 1 and 2 (PS1 PS2). Previously, we have shown that PS2, a homolog PS1. regulates apoptosis induced neurons trophic withdrawal or Abeta, T-cells Fas ligand. We now report PS1 also apoptosis. Both wild-type H115Y mutant form enhance Fas-mediated Jurkat cells. observed differentially regulate Jun Kinase, important enzyme regulating
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