共查询到17条相似文献，搜索用时 453 毫秒
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端粒酶是位于真核细胞线性染色体ＤＮＡ的末端 ,由串联重复的ＤＮＡ序列与端粒结合蛋白组成的特殊结构。由于端粒能保证线性染色体ＤＮＡ完全复制 ,并防止染色体端—端融合 ,重组与降解 ,故它对稳定染色体的结构并保持基因完整有重要作用。在含有端粒酶的细胞中 ,由端粒酶维持端粒的长度。单细胞真核生物因含有端粒酶使其端粒的长度保持在一定范围内 ,且不受培养条件与培养时间的影响 ,这些细胞具有调节端粒酶活性的机制以保持端粒的长度。在正常的人体中 ,除了胚细胞、生殖细胞及骨髓造血干细胞等少数细胞外 ,其他的细胞缺乏端粒酶活性。这… 相似文献
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端粒是真核细胞染色体末端的特殊结构,主要功能是保护染色体不被核酸降解,防止染色体末端的丢失和融合,维持基因的稳定.端粒酶则是能合成端粒DNA的酶,使得端粒的长度和结构得以保持.端粒和端粒酶的发现激起了生命科学对衰老、肿瘤、干细胞等的研究热潮.从端粒和端粒酶与运动员科学选材、运动组织损伤的修复、对成体干细胞的修饰与应用、保护提高线粒体功能、调节胞浆Ca2＋和细胞因子、参与细胞周期调控等诸方面进行综述,旨在为端粒和端粒酶这一最新成果引进运动科学研究提供参考依据. 相似文献
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端粒和端粒酶是近年来生命科学研究的热点问题之一 .端粒是染色体末端独特的蛋白质—DNA结构 ,在保护染色体的完整性和维持细胞的复制能力方面起着重要的作用 .端粒酶则是由RNA和蛋白质亚基组成的 ,能够延长端粒的一种特殊反转录酶 .端粒长度和端粒酶活性的变化与细胞衰老和癌变密切相关 相似文献
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端粒、端粒酶与细胞衰老及肿瘤的关系 总被引：2，自引：0，他引：2
端粒是真核生物染色体末端的一种特殊结构，由富含G（鸟嘌呤）的DNA重复系列和蛋白质组成，端粒DNA不能为DNA聚合酶完全复制，随着细胞分裂的不断进行，端粒不断缩短，最终导致细胞衰亡，端粒酶是一种能合成染色体端粒DNA的核糖核蛋白酶，端粒酶活性的变化与肿瘤密切相关，端粒酶在治疗一些与老年有关的疾病及端粒酶抑制剂在肿瘤治疗方面都有着广阔的前景。 相似文献
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1．细胞衰老
阅读、分析下列材料，并结合你所学的知识回答问题：
细胞衰老是一种正常的生命现象。科学家提出的“端粒学说”阐述了细胞衰老的某些可能的机制。端粒是染色体末端的一种特殊结构，其DNA末端含有由简单的串联重复序列（如下图中的-TTAGGG-）组成的单链突出段，它们在细胞分裂时不能被完全复制，因而随分裂次数的增加而缩短，除非有端粒酶的存在。端粒酶由RNA和蛋白质组成，其RNA含有与端粒DNA重复序列互补的一个片段（如下图中的-AAUCCC-），是合成端粒DNA的模板；其蛋白质能催化端粒DNA的合成，催化的一种机制如下图。 相似文献
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端粒及端粒酶的研究 总被引：1，自引：0，他引：1
任亚红 《安徽教育学院学报》2004,22(6):84-85
端粒是真核生物染色体末端特有的结构,具有维持染色体结构的完整性、防止染色体末端降解、端-端融合等功能.端粒长度的维持主要依靠端粒酶的活性.端粒、端粒酶与细胞分裂、恶性肿瘤的发生有密切关系. 相似文献
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Immortalization of human umbilical vein endothelial cells with telomerase reverse transcriptase and simian virus 40 large T antigen 总被引：5，自引：0，他引：5
Objective: To establish normally conditionally-immortalized human umbilical vein endothelial cells (HUVECs) by ectopic expression of the human telomerase catalytic enzyme (hTERT) and simian virus 40 large T (SV40 LT) antigen. Methods: Primary HUVECs were transfected with recombinant retrovirus containing hTERT or SV40 LT respectively. Subsequently drug resistant cell clones were screened and expanded for further studies. Endothelial cell biomarkers were confirmed by examination. Results: The morphological phenotype of the transfected cells was similar to the non-transfected cells. Von Willebrand factor, hTERT and SV40 LT could be detected in transfected HUVECs. Moreover, higher telomerase activity in transfected cells was maintained for over 50 population doublings compared with only low level of endogenous telomerase transiently at early population doublings in primary HUVECs. When exposed to TNF-α(tumor necrosis factor-α), the expression of E-selectin in transfected cells was significantly up-regulated, but no alteration of endothelial lipase was found. Conclusion: Ectopic coexpression of hTERT and SV40 LT can effectively immortalize HUVECs without tumorigenicity in vitro. Immortalized HUVECs may be an ideal target of further molecular function studies. 相似文献
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DNA-damage response network at the crossroads of cell-cycle checkpoints,cellular senescence and apoptosis 总被引：2，自引：0，他引：2
Schmitt E Paquet C Beauchemin M Bertrand R 《Journal of Zhejiang University. Science. B》2007,8(6):377-397
Tissue homeostasis requires a carefully-orchestrated balance between cell proliferation, cellular senescence and cell death. Cells proliferate through a cell cycle that is tightly regulated by cyclin-dependent kinase activities. Cellular senescence is a safeguard program limiting the proliferative competence of cells in living organisms. Apoptosis eliminates unwanted cells by the coordinated activity of gene products that regulate and effect cell death. The intimate link between the cell cycle, cellular senescence, apoptosis regulation, cancer development and tumor responses to cancer treatment has become eminently apparent. Extensive research on tumor suppressor genes, oncogenes, the cell cycle and apoptosis regulatory genes has revealed how the DNA damage-sensing and -signaling pathways, referred to as the DNA-damage response network, are tied to cell proliferation, cell-cycle arrest, cellular senescence and apoptosis. DNA-damage responses are complex, involving ＂sensor＂ proteins that sense the damage, and transmit signals to ＂transducer＂ proteins, which, in turn, convey the signals to numerous ＂effector＂ proteins implicated in specific cellular pathways, including DNA repair mechanisms, cell-cycle checkpoints, cellular senescence and apoptosis. The Bcl-2 family of proteins stands among ＂the mos＂t crucial regula＂tors of apop＂tosis and performs vi＂tal func＂tions in deciding whether a cell will live or die after cancer chemotherapy and irradiation. In addition, several studies have now revealed that members of the Bcl-2 family also interface with the cell cycle, DNA repair/recombination and cellular senescence, effects that are generally distinct from their function in apoptosis. In this review, we report progress in understanding the molecular networks that regulate cell-cycle checkpoints, cellular senescence and apoptosis after DNA damage, and discuss the influence of some Bcl-2 family members on cell-cycle checkpoint regulation. 相似文献
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目的观察Epithalon多肽(Ala-Glu-Asp-Gly)延缓细胞衰老过程中细胞端粒长度及端粒酶活性的变化.方法体外采用三丁基过氧化氢(tert-butylhydroperoxide,t-BHP)诱导L-02细胞衰老,从细胞周期分析、端粒酶活性检测及端粒长度检测来观察Epithalon对细胞的影响.结果 t-BHP诱导建立的衰老模型,端粒长度明显缩短.Epithalon可明显减弱诱导导致细胞衰老的作用,减少t-BHP引起的端粒长度缩短,端粒酶活性呈阳性.结论 Epithalon具有一定的抗衰老作用,能延缓端粒的缩短,增长细胞寿命. 相似文献
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USP11通过去泛素化p53调控p53稳定性 总被引：2，自引：0，他引：2
Jia-ying KE ;Cong-jie DAI ;Wen-lin WU ;Jin-hua GAO ;Ai-juan XIA ;Guang-ping LIU ;Kao-sheng LV ;Chun-lin WU 《Journal of Zhejiang University. Science. B》2014,15(12):1032-1038
研究目的：深入研究p53的泛素化及稳定性的调控。创新要点：发现一个新的调控p53去泛素化的酶USPll,它可以通过与p53的结合去泛素化并稳定p53,从而揭示了一个新的p53去泛素化调控的机制。研究方法：通过免疫共沉淀发现p53可以与USP11结合（图1a）,通过泛素化检测试验发现USPI1可以去泛素化p53（图3a和3b）,最后通过逆转录．聚合酶链式反应（RT—PCR）试验发现在DNA损伤后,USP11对p53转录活性的提高是非常重要的。 相似文献
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核糖体是细胞生长所需的蛋白质合成的动力工厂,每一个核糖体的大小为4兆而顿,有18S、5．8S、28S和5S四种RNA及80S等蛋白质组成,细胞中约有50％的RNA是核糖体RNA,这些RNA直接或间接地参与形成数百万的核糖体,因此,核糖体RNA基因的转录调控机制一直是细胞生长和细胞周期调控研究的热点,细胞通过进化已经形成一套完整的配合RNA聚合酶共同完成的核糖体RNA转录调控机制。本文从核糖体RNA基因结构出发,就染色质重塑、组蛋白乙酰化及细胞周期三个方面探讨核糖体RNA转录调控机制。 相似文献
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DNA is the hereditary material in humans and almost all other organisms. It is essential for maintaining accurate transmission of genetic information. In the life cycle, DNA replication, cell division, or genome damage, including that caused by endogenous and exogenous agents, may cause DNA aberrations. Of all forms of DNA damage, DNA double-strand breaks(DSBs) are the most serious. If the repair function is defective, DNA damage may cause gene mutation, genome instability, and cell chromosome loss, which in turn can even lead to tumorigenesis. DNA damage can be repaired through multiple mechanisms. Homologous recombination(HR) and non-homologous end joining(NHEJ) are the two main repair mechanisms for DNA DSBs. Increasing amounts of evidence reveal that protein modifications play an essential role in DNA damage repair.Protein deubiquitination is a vital post-translational modification which removes ubiquitin molecules or polyubiquitinated chains from substrates in order to reverse the ubiquitination reaction. This review discusses the role of deubiquitinating enzymes(DUBs) in repairing DNA DSBs. Exploring the molecular mechanisms of DUB regulation in DSB repair will provide new insights to combat human diseases and develop novel therapeutic approaches. 相似文献
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Using the complete genome of Plasmodiumfalciparum 3D7 which has 14 chromosomes as an example, we have examined the distribution functions for the amount of C or G and A or T consecutively and non-overlapping blocks of m bases in this system. The function P(S) about the number of the consecutive C-G or A-T content cluster conforms to the relation P(S)oce-as;values of the scaling exponent αCG are much larger than αAT; and αAT of 14 chromosomes are hardly changed, whereas αCG of 14chromosomes have a number of fluctuations. We found maximum value of A-T cluster size is much larger than C-G, which implies the existence of large A-T cluster. Our study of the width function ξ(m) of cluster C-G content showed that follows good power law ξ(m)ocm-γ. The average γ for 14 chromosomes is 0.931. These investigations provide some insight into the nucleotide clusters of DNA sequences, and help us understand other properties of DNA sequences. 相似文献