PS2 mutation increases neuronal cell vulnerability to neurotoxicants through activation of caspase-3 by enhancing of ryanodine receptor-mediated calcium release

FASEB J. 2006 Jan;20(1):151-3. doi: 10.1096/fj.05-4017fje;1.
No abstract available

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyloid beta-Peptides / pharmacology
  • Animals
  • Apoptosis / drug effects
  • Calcium / metabolism*
  • Caspase 3
  • Caspases / metabolism*
  • Dantrolene / pharmacology
  • Endoplasmic Reticulum / drug effects
  • Endoplasmic Reticulum / metabolism
  • Enzyme Activation / drug effects
  • Gene Expression Regulation
  • Genes, Transgenic, Suicide
  • Glutamic Acid / pharmacology
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • Mice
  • Mutation / genetics*
  • Neurons / drug effects*
  • Neurons / enzymology
  • Neurons / metabolism
  • Neurotoxins / pharmacology
  • Neurotoxins / toxicity*
  • PC12 Cells
  • Presenilin-2
  • Protein Transport
  • Rats
  • Ryanodine Receptor Calcium Release Channel / metabolism*

Substances

  • Amyloid beta-Peptides
  • Membrane Proteins
  • Neurotoxins
  • Presenilin-2
  • Ryanodine Receptor Calcium Release Channel
  • Glutamic Acid
  • Casp3 protein, mouse
  • Casp3 protein, rat
  • Caspase 3
  • Caspases
  • Dantrolene
  • Calcium