Motohiko Chachin (1), Shun Shimohama (2), Yukiko U. Kunugi (1) and Takashi Taniguchi (1,*)
(1) Department of Neurobiology, Kyoto Pharmaceutical University, Yamashina-ku, Kyoto 607, Japan (2) Department of Neurology, Faculty of Medicine, Kyoto University, Sakyo-ku, Kyoto 606, Japan (*) To whom correspondence should be addressed.
Abstract: We have previously demonstrated that the protein level of type beta protein kinase C (PKC)was significantly reduced in Alzheimer's disease (AD) brains compared to controls. To clarify whether this is due to decreased synthesis and/or increased degradation of PKC, the present study was performed to examine mRNA levels of PKC isozymes in control and AD brains. The present study indicated that mRNA levels of types alpha, beta and gamma PKC were not significantly changed in the control and AD brains. Thus, the reduction of type beta PKC protein content in AD brains might be caused by increased degradation.
Alzheimer's disease, Protein kinase C, mRNA
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