悉尼dissertation代写

代写作业 美国:心肌预处理的影响

代写作业 美国:心肌预处理的影响

过去进行的研究是为了找出心血管机制和并发症背后的潜在原因。我将简要介绍我过去所从事的项目,以说明我的熟练程度和知识的熟练程度。在第一个项目的角色的角色caveolin-3腺苷导致增加线粒体PKCε探测。分析发现,腺苷受体的激活增加了细胞膜和线粒体PKC亚型的易位。已经证实,腺苷受体PKC和caveolin-3在缺血预处理的心脏保护中起着重要作用,它被认为与腺嘌呤诱导的PKC线粒体易位有关。

代写作业 美国:心肌预处理的影响

实验研究结果表明,在线粒体中调控PKC亚型的机制是新的。本分析探讨了心肌预处理的影响。本研究表明,PKC在激活时有选择性地针对小窝,并调节小窝定位蛋白以应对外部刺激。这种凹蛋白结构蛋白在信号转导通路中对下游效应因子的调控起着关键作用。在进行的第二个项目中,研究了Caveolin-3对两孔区钾离子通道Task1的调制。通过分析发现,重组Task1活性在HEK293T细胞中受到cav3的负调控,Task1与cav3相关。

代写作业 美国:心肌预处理的影响

The research that has been undertaken in the past is to find the underlying causes behind cardiovascular mechanisms and complications. I will explain briefly about the projects that I have undertaken in the past to explain about my proficiency and my adeptness of the knowledge. In the first project the role of Role of caveolin-3 in adenosine-induced increase in mitochondrial PKCε was probed. It was found from this analysis that the activation of the adenosine receptor had increased the translocation of PKC isoform in the caveolar plasma membrane and mitochondria. It has already been established that the adenosine receptors PKC and caveolin-3 play an important role in the cardio protection of ischemic preconditioning it was considered that this caveolin-3 or/and adenosine receptor signaling may be linked to adenosine-induced mitochondrial translocation of PKC.

代写作业 美国:心肌预处理的影响
The experimental empirical research results points out to a novel mechanism in regulating PKC isoforms in mitochondria. Impact of Myocardial preconditioning has been probed in this analysis. It has been shown in this research that PKC upon activation is selectively targets the caveola and regulates the caveolar-localized protein in response to the external stimula. This Caveolin structural protein was found to play a pivotal role in the regulation of the downstream effectors in the signal transduction pathways. In the second project that was undertaken there was determination of the modulation of the two-pore domain potassium channel Task1 by Caveolin-3 was probed. It was found from this analysis that recombinant Task1 activities were negatively regulated by Cav-3 and TASK1 associates with Cav-3 in HEK293T cells.