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
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Aging / metabolism
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Apoptosis / genetics
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Apoptosis / physiology*
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Blotting, Western
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Calcium-Calmodulin-Dependent Protein Kinases / metabolism
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Cell Line
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DNA, Neoplasm / biosynthesis
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DNA, Neoplasm / genetics
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Humans
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JNK Mitogen-Activated Protein Kinases
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Jurkat Cells
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Membrane Proteins / genetics
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Membrane Proteins / physiology*
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Mitogen-Activated Protein Kinases*
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Mutation
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Oxidation-Reduction
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Presenilin-1
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Transfection
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fas Receptor / metabolism
Substances
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DNA, Neoplasm
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Membrane Proteins
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PSEN1 protein, human
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Presenilin-1
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fas Receptor
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Calcium-Calmodulin-Dependent Protein Kinases
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JNK Mitogen-Activated Protein Kinases
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Mitogen-Activated Protein Kinases