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很多宿主细胞在病毒感染下通常会启动caspases通路凋亡途径导致细胞死亡,避免病毒的进一步扩增和传播.但最近的一些研究表明,病毒能利用激活的caspase蛋白酶对自身(非)结构蛋白进行特异性剪切,以利于病毒在细胞内的复制或参与病毒或宿主其他基因的转录调控等过程.作为一个病毒与宿主细胞相互作用关系的新的研究领域,论文对... 相似文献
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BCL-2家族蛋白对线粒体膜通透作用的调控和caspases的影响 总被引:6,自引:2,他引:4
线粒体通过释放凋亡蛋白来激活caspases和其它的细胞死亡受体,从而在转运细胞死亡信号中发挥重要作用。BCL-2家族蛋白位于线粒体膜上,对于凋亡因子来说,它具有调节线粒体膜通透性(MM P)的功能。最近的一些研究结果表明,BCL-2家族蛋白可能在释放线粒体凋亡因子中具有重要作用。 相似文献
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1 细胞凋亡的概念在多细胞生物中 ,细胞的死亡有两种不同的形式。一种是坏死性或意外性死亡 ( necrocis or acci-dental cell death) ,它是由于某些外界的因素 ,比如局部贫血、高热以及物理、化学损伤和生物的侵袭等 ,造成细胞急速死亡 ,即病理性细胞死亡 ,形态学上表现为细胞坏死。另一类为生理性细胞死亡 ,这是1972年 Kerr等在正常生理状态下观察到的 ,称为编程性细胞死亡 ( Programmed cell death PCD) ,形态学上表现为细胞凋亡 ( apoptosis) [1]。细胞凋亡是机体的正常细胞在受到生理性或病理性刺激后启动的自发的死亡过程 ,是一种主… 相似文献
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细胞凋亡检测技术的研究进展 总被引:5,自引:0,他引:5
细胞凋亡是一种不同于细胞坏死的细胞死亡方式,是在一定的生理或病理情况下,机体为维护内环境的稳定,通过基因调控,激活内源性核酸内切酶而发生的细胞自动消亡的过程,亦称为程序化细胞死亡(programmed cell death,PCD)。自1972年Kerr等根据细胞发生了与坏死完全不一样的死亡过程而提出细胞凋亡(apoptosis)的概念后,引起细胞生物工作者的注意,但由于当时检测技术的限制,这种细胞凋亡现象只停留于形态描述,缺乏定 相似文献
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细胞凋亡与哺乳动物配子发生 总被引:2,自引:0,他引:2
生物有机体内的细胞是必然要死亡的,这种死亡是一种不可抗拒的自然规律,其中一些死亡是生理性的,另一些则是病理性的。关于细胞死亡过程的研究,近年来已成为细胞生物学、分子生物学以及医学等领域研究的热点。目前认为细胞的死亡起码有两种方式,即细胞坏死(necrosis)与细胞凋亡(apoptosis)或程序性细胞死亡(programmed cell death,PCD)。细胞受到强烈的物理、化学或生物因子作用时引起细胞无序变化的死亡过程为细胞坏死;细胞凋亡是细胞在基因活动指导下发生的一系列分子、形态和生化改变所引起的细胞死亡,主要表现为细胞缩小,染色质浓缩,… 相似文献
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Apoptosis is a kind of cell death essential for normal functioning and survival of most multicellular organisms. Apoptosis plays an important role in physiological processes and in pathophysiology of some chronic diseases, including autoimmunity, cancer, lymphoma, AIDS, neurodegeneration and others. The present paper describes the interdisciplinary pathogenesis of programmed cell death, the mechanisms inducing apoptosis and the role of apoptosis in some physiological phenomena and in medical practice. 相似文献
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本研究旨在探究载脂蛋白CⅢ (ApoCⅢ)刺激猪主动脉血管内皮细胞前后的差异基因表达谱,从而揭示ApoCⅢ的功能。利用酶解法成功分离猪主动脉血管内皮细胞并进行体外培养,采用高通量测序技术筛选出ApoCⅢ刺激前后的差异表达基因。结果表明,ApoCⅢ刺激猪主动脉血管内皮细胞前后共有647个差异表达基因,包括390个上调表达基因和257个下调表达基因。实时荧光定量PCR (qRT-PCR)检测表明,高通量测序数据结果正确可靠。GO及Pathway分析结果显示,差异表达基因的功能涉及免疫应答、细胞凋亡及死亡等。这表明ApoCⅢ可通过炎症反应、细胞黏附、细胞凋亡等分子通路影响猪主动脉血管内皮细胞的生理功能,为进一步解析ApoCⅢ引发动脉粥样硬化发生的分子机制提供了理论基础。 相似文献
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YUE Yuan CHEN Hong-yan WANG Jia-wei XU Ming-qiang DING Yu JIANG Hao GAO Yan ZHANG Jia-bao YAN Shou-qing 《中国畜牧兽医》2016,43(3):585-591
The aim of this study was to investigate the differential expression genes induced by ApoCⅢ,and study the function of ApoCⅢ.Porcine aortic vascular endothelial cells were successfully isolated using enzyme digestion,and then screened the differential expression genes induced by ApoCⅢ using the Solexa high-throughput sequencing technology.The results showed 647 differential expression genes,including 390 up-regulated genes and 257 down-regulated genes.The qRT-PCR results verified that the gene expression results from Solexa sequencing data were reliable.GO and Pathway analysis showed that the function of differential expression genes were related to immune response,cell apoptosis and death.These findings suggested that ApoCⅢ affected the physiological function of porcine aortic endothelial cells by the molecular pathways of inflammation,cell adhesion and apoptosis,which provided a theoretical basis for further understanding the molecular mechanisms of atherosclerosis caused by ApoCⅢ. 相似文献
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Photodynamic agents, due to their selective uptake by tumor cells and photon-dependent selective activation, have immense implications for cancer treatment. The present study provided direct evidence that the photon activation of chloro-aluminum phthalocyanine sulphonate (A1PcS4) in the presence of extracellular Ca2+ caused a rapid increase followed by a sustained increase in intracellular concentration of calcium ion ([Ca2+]i) in a small cell lung carcinoma (SCLC) cell line, SBC-3. The [Ca2+]i increase by photodynamic stimulation was completely inhibited by the removal of extracellular Ca2+ and reintroduction of extracellular Ca2+ immediately led to a rapid elevation of [Ca2+]i. However, the increase was not inhibited by application of Ni2+, nifedipine, or SK&F 96365, a receptor-mediated and voltage-dependent Ca2+ entry blocker. The photosensitizer A1PcS4 alone or light alone (4 min) had no effect on [Ca2+]i. Cytotoxicity examination by trypan blue exclusion test, however, suggested photodynamic stimulation-induced cell injury which was observed in both the presence and the absence of extracellular Ca2+. These results indicate that [Ca2+]i increase may not be mandatory for photodynamic stimulation-induced cell injury. Whether [Ca2+]i increase can accelerate, at least in part, cell death under the physiological condition, whether the mechanism(s) of cell death can be different in the presence and the absence of extracellular Ca2+, and whether [Ca2+]i increase can be totally unrelated to cell death await further work. 相似文献
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Lossi L Cantile C Tamagno I Merighi A 《Veterinary journal (London, England : 1997)》2005,170(1):52-66
It is generally assumed that about half of the neurons produced during neurogenesis die before completion of maturation of the central nervous system (CNS). Neural cell death is also relevant in aging and several neurodegenerative diseases. Among the modalities by which neurons die, apoptosis has very much attracted the interest of investigators because in this type of cell death neurons are actively responsible for their own demise by switching on a number of genes and activating a series of specific intracellular pathways. This review focuses on the cellular and molecular mechanisms of apoptosis in normal and transgenic animal models related to naturally occurring neuronal death within the CNS. We will also consider some examples of apoptotic cell death in canine neuropathologies. A thorough analysis of naturally occurring neuronal death in vivo will offer a basis for parallel and future studies involving secondary neuronal loss such as those in neurodegenerative disorders, trauma or ischaemia. 相似文献