| First Author | Kajkowski EM | Year | 2001 |
| Journal | J Biol Chem | Volume | 276 |
| Issue | 22 | Pages | 18748-56 |
| PubMed ID | 11278849 | Mgi Jnum | J:69767 |
| Mgi Id | MGI:2135414 | Doi | 10.1074/jbc.M011161200 |
| Citation | Kajkowski EM, et al. (2001) beta -Amyloid peptide-induced apoptosis regulated by a novel protein containing a g protein activation module. J Biol Chem 276(22):18748-56 |
| abstractText | 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. |
