Chachin M, Shimohama S, Kunugi Y U, Taniguchi T
Department of Neurobiology, Kyoto Pharmaceutical University, Japan.
Jpn J Pharmacol. 1996 Jun;71(2):175-7. doi: 10.1254/jjp.71.175.
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.
我们之前已经证明，与对照组相比，β型蛋白激酶C（PKC）的蛋白水平在阿尔茨海默病（AD）大脑中显著降低。为了阐明这是否是由于PKC合成减少和/或降解增加所致，本研究进行了对照和AD大脑中PKC同工酶mRNA水平的检测。本研究表明，α、β和γ型PKC的mRNA水平在对照和AD大脑中没有显著变化。因此，AD大脑中β型PKC蛋白含量的降低可能是由降解增加引起的。
