乳腺癌PKCs表达与其分化程度的相关性

为了研究蛋白激酶C（PKC）和乳腺癌分化及转移的相关性，采用免疫组化SABC方法检测48例人乳腺癌的PKC蛋白表达，包括PKCα、βI、η和ξ等蛋白。结果表明，与分化低的乳腺癌对比，分化高的乳腺癌PKC蛋白表达水平提高。在临床I－II和III级的乳腺癌中，PKCη蛋白表达率分别为61．5％和9．1％，具有显著意义（P＜0．05），PKCξ蛋白表达率分别为92．3％和27．3％，具有极显著意义（P＜0．01）。另外，在乳腺癌未转移的病例中，PKCs蛋白表达水平普遍较高，其中PKCξ与肿转移相关性极显著（P＜0．01）。此外，PKCs蛋白表达水平与肿瘤患者年龄无关。以上结果提示，PKCη和PKCξ有可能作为评价临床乳腺癌分化和转移程度的指标之一。     

Functional interactions of protein kinase A and C in signalling networks: a recapitulation

On the basis of evidence collected from the literature, we propose a general model by which protein kinase (PK) A and the different PKC isoforms can inversely affect cell growth. Molecular switches, which are able to direct the signal towards antiproliferative or mitogenic pathways, are the different isoforms of Raf and PKC. Conflicting data are also reported and discussed in an attempt to reconcile them. Received 10 November 2005; received after revision 28 December 2005; accepted 3 January 2006     

非确定的公钥密码及其实现

首先引入非确定的公钥密码和解密成功率的概念, 并基于有限域上多变元问题的困难性, 给出其实现方案N-HFMS; 然后对F_q［M］中非奇异矩阵的数量进行分析, 利用Euler-φ_q函数推导出F_q［M］中非奇异矩阵的精确计数公式. 结果表明, 该方法不仅可对任意特定N-HFMS实例的解密成功率进行精确估算, 还可推导出N-HFMS方案的解密成功率下限, 从而在理论上证明N-HFMS的可行性. 利用N-HFMS方案, 可约定会话密钥, 进而实现保密通讯.     

基于身份的前向安全和可公开验证签密方案

针对具有前向安全性和可公开验证的签密方案进行研究,基于Liber 和Quisquater的签密方案,给出了一个新的签密方案,并对所提出方案的安全性和效率进行了分析.结果表明:文章给出的签密方案实现了同时提供前向安全性和可公开验证性;而基于身份公钥密码和双线性对技术,使该方案又具有密钥长度短和密钥管理简单的特点,使其具有与LQ签密方案相当的效率.这种高效性和高安全性签密方案的提出,不仅对相关公开问题的解决具有一定理论意义,同时文中签密方案能更好的满足电子商务等实际应用的高安全需求,因此也具有一定应用价值.     

PKA和PKC对HeLa细胞G2/M/G1进程的影响

为了研究ＰＫＡ和ＰＫＣ对ＨｅＬａ细胞Ｇ２→用Ｍ→Ｇ１期进程的影响,用ＰＫＡ和ＰＫＣ抑制剂分别处理同步的Ｇ２期和Ｍ期的ＨｅＬａ细胞后,测定了细胞有丝分裂指数和ＰＫＡ,ＰＫＣ与ＣＤＣ２激酶的活性。     

Regulation of muscle creatine kinase by phosphorylation in normal and diabetic hearts

Protein kinase C (PKC) is an important signaling molecule in the heart, but its targets remain unclear. Using a PKC substrate antibody, we detected a 40-kDa phosphorylated cardiac protein that was subsequently identified by tandem mass spectroscopy as muscle creatine kinase (M-CK) with phosphorylation at serine 128. The forward reaction using ATP to generate phosphocreatine was reduced, while the reverse reaction using phosphocreatine to generate ATP was increased following dephosphorylation of immunoprecipitated M-CK with protein phosphatase 2A (PP2A) or PP2C. Despite higher PKC levels in diabetic hearts, decreased phosphorylation of M-CK was more prominent than the reduction in its expression. Changes in CK activity in diabetic hearts were similar to those found following dephosphorylation of M-CK from control hearts. The decrease in phosphorylation may act as a compensatory mechanism to maintain CK activity at an appropriate level for cytosolic ATP regeneration in the diabetic heart. Received 15 September 2008; received after revision 30 September 2008; accepted 13 October 2008     

Regulation of mitochondrial aconitase by phosphorylation in diabetic rat heart

Mitochondrial dysfunction and protein kinase C (PKC) activation are consistently found in diabetic cardiomyopathy but their relationship remains unclear. This study identified mitochondrial aconitase as a downstream target of PKC activation using immunoblotting and mass spectrometry, and then characterized phosphorylation-induced changes in its activity in hearts from type 1 diabetic rats. PKCβ₂ co-immunoprecipitated with phosphorylated aconitase from mitochondria isolated from diabetic hearts. Augmented phosphorylation of mitochondrial aconitase in diabetic hearts was found to be associated with an increase in its reverse activity (isocitrate to aconitate), while the rate of the forward activity was unchanged. Similar results were obtained on phosphorylation of mitochondrial aconitase by PKCβ₂ in vitro. These results demonstrate the regulation of mitochondrial aconitase activity by PKC-dependent phosphorylation. This may influence the activity of the tricarboxylic acid cycle, and contribute to impaired mitochondrial function and energy metabolism in diabetic hearts. Received 31 October 2008; received after revision 17 December 2008; accepted 2 January 2009     

Regulation of membrane trafficking and endocytosis by protein kinase C: emerging role of the pericentrion,a novel protein kinase C-dependent subset of recycling endosomes

The protein kinase C (PKC) family of isoenzymes has been shown to regulate a variety of cellular processes, including receptor desensitization and internalization, and this has sparked interest in further delineation of the roles of specific isoforms of PKC in membrane trafficking and endocytosis. Recent studies have identified a novel translocation of PKC to a juxtanuclear compartment, the pericentrion, which is distinct from the Golgi complex but epicentered on the centrosome. Sustained activation of PKC (longer than 30 min) also results in sequestration of plasma membrane lipids and proteins to the same compartment, demonstrating a global effect on endocytic trafficking. This review summarizes these studies, particularly focusing on the characterization of the pericentrion as a distinct PKC-dependent subset of recycling endosomes. We also discuss emerging insights into a role for PKC as a central hub in regulating vesicular transport pathways throughout the cell, with implications for a wide range of pathobiologic processes, e.g. diabetes and abnormal neurotransmission or receptor desensitization. Received 11 August 2006; received after revision 20 September 2006; accepted 7 November 2006     

家兔在发育过程中外侧腓肠肌内MyHCs变化与诱发电位的关系

 为研究在生后不同年龄组家兔外侧腓肠肌各亚体肌纤维MyHCs变化与诱发电位的关系,探讨生后发育期间肌纤维MyHCs组成和作用差异与表型之间的相关联系,采用电生理记录仪结合十二烷基硫酸钠-聚丙烯酰胺凝胶电泳（SDS PAGE）检测外侧腓肠肌各亚体。结果表明中间亚体在刺激时各年龄组的峰值电压基本相同,而外侧亚体和内侧亚体分别有些变化。同时发现成年家兔的持续时间都较幼年的长,这可能与各亚体的肌纤维型构成比例有很大关系。外侧腓肠肌各亚体的肌球蛋白重链异构体（MyHCs）电泳条带分别显示MyHCsⅡa、Ⅱd（或Ⅱx）、Ⅱb、Ⅰ共4种,对应于骨骼肌纤维表型ⅡA型（FOG型）、ⅡX（FO型）、ⅡB型（FG型）及Ⅰ型（SO型）4类。