初步探讨蛋白激酶C（PKC）在脑低氧预适应发生机制中的作用，以我室建立的小鼠低氧预适应模型，结合SDS2聚丙烯酰胺凝胶电泳（SDS2PAGE）、蛋白印迹（Western bolt）等生化技术，观察了低氧预适应对小鼠大脑皮层及海马组织内PKC膜转位的影响。结果表明，1在小鼠大脑皮层和海马组织内的PKC膜转位均随着低氧次数（小鼠低氧耐受时间) 的增加而增高。特别是低氧3次的海马组织和低氧4次的大脑皮层和海马组织内，PKC膜转位的增加有统计学显著意义。结果提示，PKC的激活可能在脑低氧预适应发生机制中具有重要的作用。

NeurograninyRC3 is a neural-specific Ca21-sensitive calmodulin CaM)-binding protein whose CaM-binding affinity is modulated by phosphorylation and oxidation. Here we show that deletion of the Ng gene in mice did not result in obvious developmental or neuroanatomical abnormalities but caused an impairment of spatial learning and changes in hippocampal short- and long-term plasticity (paired-pulse depression, synaptic fatigue, long-term potentiation induction). These deficits were accompanied by a decreased basal level of the activated Ca21yCaM-dependent kinase II (CaMKII) ('60% of wild type). Furthermore, hippocampal slices of the mutant mice displayed a reduced ability to generate activated CaMKII after stimulation of protein phosphorylation and oxidation by treatments with okadaic acid and sodium nitroprusside, respectively. These results indicate a central role of Ng in the regulation of CaMKII activity with decisive influences on synaptic plasticity and spatial learning.

FUSE-binding protein (FBP) binds the single-stranded far upstream element of active c-myc genes, pos- sesses potent transcription activation and repression domains, and is necessary for c-myc expression. A novel 60 kDa protein, the FBP interacting repressor (FIR), blocked activator-dependent, but not basal, transcription through TFIIH. Recruited through FBP' s nucleic acid-binding domain, FIR formed a ternary complex with FBP and FUSE. FIR repressed a c-myc reporter via the FUSE. The amino terminus of FIR con-tained an activator-selective repression domain capable of acting in cis or even in trans in vivo and in vitro. The repression domain of FIR targeted only TFIIH' s p89/XPB helicase, required at several stages in tran-scription, but not factors required for promoter selection. Thus, FIR locks TFIIH in an activation-resistant configuration that still supports basal transcription.

探讨cPKCs特定亚型在脑低氧预适应形成过程中的作用，借助已建立的小鼠整体低氧预适应模型，应用SDS-PAGE和Western bolt等生化技术，并结合Gel Doc成像系统，半定量检测脑组织内cPKCα和γ的膜转位水平和蛋白表达量。结果发现，随低氧暴露次数（低氧2-4次）增加，在小鼠海马和皮层组织内cPKCγ膜转位水平增高显著（p<0.05，n=6）；然而，cPKCα的膜转位水平和cPKCα及γ的蛋白表达量的变化均不显著。提示，cPKCγ的激活可能参与了脑低氧预适应的形成过程。

目的：通过观察低氧刺激对培养SY5Y神经母细胞瘤细胞内nPKCε和nPKCθ膜转位激活的影响，以探讨两者是否参与细胞低氧预适应的发生。方法：利用本室建立的体外培养SY5Y细胞低氧刺激模型，并应用SDS-聚丙烯酰胺凝胶电泳（SDS-PAGE）、蛋白印记（Western-Blot）等方法，半定量分析SY5Y细胞内nPKCε、nPKCθ的膜转位水平。结果：SY5Y细胞经低氧刺激后，随刺激时间（0.5、2、4、6、8、12和24h）的延长，nPKCε在胞浆内的含量逐渐减少，而胞膜成分中的含量则明显增加，且于低氧刺激2h后的增高水平具有统计学显著意义（P<0.001）；然而nPKCθ在正常情况下只存在于胞膜成分内，且其含量不随低氧刺激时间的增加而改变（P>0.01）结论：nPKCε可能参与了细胞低氧耐受的发生。