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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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细胞的衰老与凋亡是机体发生在细胞水平的两个完全不同的分子事件.细胞衰老是指细胞增殖停止或不能维持原有的基本功能,细胞凋亡是指在基因控制下,细胞有序的自主的死亡.它们在机体的生长发育、创伤修复以及致病过程中起着重要的作用. 相似文献
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<正>1概述根据高考要求,本部分共有4个考点:细胞的分化,细胞的全能性,细胞的衰老和凋亡以及与人体健康的关系,癌细胞的主要特征及防治。每个知识点都是Ⅱ级要求,需要理解这些知识点与其他相关知识之间的联系和区别,能在较复杂的情景中综合运用这些知识点进行分析、判断、推理和评价。纵观近3年各地高考题,本部分所占分值不多,且都不是难题, 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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