2. Academic Validation
  3. beta -Amyloid peptide-induced apoptosis regulated by a novel protein containing a g protein activation module

beta -Amyloid peptide-induced apoptosis regulated by a novel protein containing a g protein activation module

  • J Biol Chem. 2001 Jun 1;276(22):18748-56. doi: 10.1074/jbc.M011161200.
E M Kajkowski 1,  C F Lo,  X Ning,  S Walker,  H J Sofia,  W Wang,  W Edris,  P Chanda,  E Wagner,  S Vile,  K Ryan,  B McHendry-Rinde,  S C Smith,  A Wood,  K J Rhodes,  J D Kennedy,  J Bard,  J S Jacobsen,  B A Ozenberger
Affiliations

Affiliation

  • 1 Wyeth Neuroscience, Wyeth-Ayerst Research, CN 8000, Princeton, New Jersey 08543-8000, USA.
PMID: 11278849 DOI: 10.1074/jbc.M011161200
Abstract

Degeneration of neurons in Alzheimer's disease is mediated by beta-amyloid peptide by diverse mechanisms, which include a putative apoptotic component stimulated by unidentified signaling events. This report describes a novel beta-amyloid peptide-binding protein (denoted BBP) containing a G protein-coupling module. BBP is one member of a family of three proteins containing this conserved structure. The BBP subtype bound human beta-amyloid peptide in vitro with high affinity and specificity. Expression of BBP in Cell Culture induced caspase-dependent vulnerability to beta-amyloid peptide toxicity. Expression of a signaling-deficient dominant negative BBP mutant suppressed sensitivity of human Ntera-2 neurons to beta-amyloid peptide mediated toxicity. These findings suggest that BBP is a target of neurotoxic beta-amyloid peptide and provide new insight into the molecular pathophysiology of Alzheimer's disease.

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