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J Biol Chem, Vol. 274, Issue 27, 19011-19016, July 2, 1999
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From the Previous evidence by others has indicated that a
variety of cell cycle-related molecules are up-regulated in brains of
Alzheimer's disease patients. The significance of this increase,
however, is unclear. Accordingly, we examined the obligate nature of
cyclin-dependent kinases and select downstream targets of
these kinases in death of neurons evoked by B-amyloid (AB) protein. We
present pharmacological and molecular biological evidence that
cyclin-dependent kinases, in particular Cdk4/6, are
required for such neuronal death. In addition, we demonstrate that the
substrate of Cdk4/6, pRb/p107, is phosphorylated during AB treatment
and that one target of pRb/p107, the E2F·DP complex, is required for
AB-evoked neuronal death. These results provide evidence that cell
cycle elements play a required role in death of neurons evoked by AB
and suggest that these elements play an integral role in Alzheimer's
disease-related neuronal death.
Hoechst Marion Roussel, Neuroscience,
Bridgewater, New Jersey 08807 and the § Neuroscience
Research Institute, University of Ottawa,
Ottawa, Ontario K1H 8M5, Canada
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