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生物学论文翻译举例

发布者:鑫达医学翻译 发布时间:2012-09-11阅读:

泛素-蛋白酶体系统是真核细胞最大的胞内蛋白降解途径。泛素-蛋白酶体系统(UPS)参与许多细胞进程,包括细胞周期、细胞增殖、氧化应激等。UPS主要通过三种蛋白水解作用(糜蛋白酶样作用、胰岛素作用和半胱天冬酶样作用)来降解靶蛋白。肽醛(例如:MG132)和硼酸肽可以可逆地抑制蛋白水解作用,而β-内酯衍生物(例如:lactacystin)和环氧酮(例如:环氧霉素)可以不可逆地抑制蛋白水解作用。近年发现,UPS 在各种心血管疾病的发生发展中也发挥重要作用。有研究证明,蛋白酶体抑制可以通过降低NF-κB 的活性而减轻压力负荷导致的心肌重构,从一定程度上逆转心肌肥大。另外在原代新生大鼠心肌细胞也发现,部分抑制蛋白酶体活性可抑制心肌肥大。GSK-3 作为一种丝/苏氨酸蛋白激酶,参与调节许多细胞功能如代谢、转录、翻译、细胞生长和凋亡。以往研究证实,GSK-3β是一种内源性心肌肥大负调控因子。GSK-3β激活可磷酸化一些促心肌肥大因子如真核翻译起始因子(eIF) 2Bε, 活性T 细胞核因子(NFAT) 14, GATA4 15 和myocardin 16 而使它们失去活性,进而抑制心肌肥大。而本项目组曾在培养的人胚肾细胞(HEK293)发现,蛋白酶体抑制可以明显提高GSK-3 的活性。本文用原代培养的新生大鼠心肌细胞进行实验,第一部分主要探讨蛋白酶体抑制对心肌肥大的作用以及对GSK-3活性的影响;第二部分研究蛋白酶体抑制改善心肌肥大的机制,从而为心肌肥大的机制研究提高新的思路和探索。
Ubiquitin-proteasome system (UPS) is known as the largest protein degradation pathway in eukaryocytes. It has been reported to be involved in several biological processes, including cell cycle, cell proliferation and oxidative stress. For the protein degradation process, three activities including  were recruited for the degradation of target protein. Two compounds, peptide aldehyde (e.g. MG132) and peptide boronate, could prohibit the proteolysis reversibly, while beta-lactone derivates (e.g. lactacystin) and epoxyketone could prohibit the proteolysis irreversibly. Recent studies showed UPS played important roles in the occurrence and development of cardiovascular diseases (CVD). Proteasome inhibitor could reduce the myocardium remodeling caused bypressure load by inhibiting the activity of NF-κB, resulting in reverse of cardiomyocyte hypertrophy. Moreover, partial inhibition of proteasome activity could prohibit the cardiomyocyte hypertrophy in primary myocardial cells of neonatal rats.
Glycogen synthase kinase 3 (GSK-3) is a serine/threonine protein kinase that mediates cell functions including metabolism, transcription, translation, cell growth and apoptosis. According to the previous reports, GSK-3 beta was a negative regulatory factor (NRF) for endogenous cardiomyocyte hypertrophy. Activation of GSK-3 beta could deactivated the cardiomyocyte hypertrophy releasing factors, such as eukaryotic initiation factor (eIF) 2Bε, nuclear factor of activated T cells (NFAT) 14, GATA4 15 and myocardin 16 by phosphorylation, resulted in inhibition of cardiomyocyte hypertrophy. Our previous study indicated remarkable increase of GSK-3 activity after inhibition of proteasome function in human embryonic kidney (HEK) 293 cells. In this study, primary myocardial cells of neonatal rats were used to investigate the effects of proteasome inhibition on cardiomyocyte hypertrophy and GSK-3 activity, as well as the potential effects of proteasome inhibition on cardiomyocyte hypertrophy. All these could provide new methods for the mechanism of cardiomyocyte hypertrophy.
 


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