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Titlebook: Checkpoint Controls and Cancer; Volume 2: Activation Axel H. Schönthal Book 2004 Humana Press 2004

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发表于 2025-3-21 17:22:42 | 显示全部楼层 |阅读模式
书目名称Checkpoint Controls and Cancer
副标题Volume 2: Activation
编辑Axel H. Schönthal
视频video
概述Includes supplementary material:
丛书名称Methods in Molecular Biology
图书封面Titlebook: Checkpoint Controls and Cancer; Volume 2: Activation Axel H. Schönthal Book 2004 Humana Press 2004
描述Intracellular checkpoint controls constitute a network of signal transd- tion pathways that protect cells from external stresses and internal errors. Ext- nal stresses can be generated by the continuous assault of DNA-damaging agents, such as environmental mutagens, ultraviolet (UV) light, ionizing radiation, or the reactive oxygen species that can arise during normal cellular metabolism. In response to any of these assaults on the integrity of the genome, the activation of the network of checkpoint control pathways can lead to diverse cellular responses, such as cell cycle arrest, DNA repair, or elimination of the cell by cell death (apoptosis) if the damage cannot be repaired. Moreover, internal errors can occur during the highly orchestrated replication of the cellular genome and its distribution into daughter cells. Here, the temporal order of these cell cycle events must be strictly enforced—for example, to ensure that DNA replication is c- plete and occurs only once before cell division, or to monitor mitotic spindle assembly, and to prevent exit from mitosis until chromosome segregation has been completed. Thus, well functioning checkpoint mechanisms are central to the maint
出版日期Book 2004
版次1
doihttps://doi.org/10.1385/1592598110
isbn_softcover978-1-61737-603-0
isbn_ebook978-1-59259-811-3Series ISSN 1064-3745 Series E-ISSN 1940-6029
issn_series 1064-3745
copyrightHumana Press 2004
The information of publication is updating

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CHK1 Kinase Activity Assayortant checkpoint regulator that responds to DNA damage. Because CHK1 and CHK2 share some substrates such as CDC25C in vitro, this assay could also be used for CHK2 activity assay, except that the CHK2 antibody will replace the CHK1 antibody.
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Project Planning for Flex and Spring,; (2) induction of cell cycle arrest (Brd-U incorporation assay); and (3) inhibition of DNA double-strand break accumulation (phosphorylated-histone H2A.X detection). Together, this combination of techniques allows the evaluation of RB action in the coordinated checkpoint response to DNA damage.
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1064-3745 rom external stresses and internal errors. Ext- nal stresses can be generated by the continuous assault of DNA-damaging agents, such as environmental mutagens, ultraviolet (UV) light, ionizing radiation, or the reactive oxygen species that can arise during normal cellular metabolism. In response to
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Building the Flex User Interface,ecifically and efficiently down-regulates MDC1 expression, resulting in defective radiation-induced apoptosis in A549 cells. Transfection with siRNA-resistant MDC1 restores radiation-induced apoptosis. These findings suggest that siRNA can be a very useful tool for the exploration of gene function in mammalian checkpoint responses.
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Functional Analysis of the Spindle-Checkpoint Proteins Using an In Vitro Ubiquitination Assaylex (APC) or cyclosome. This chapter describes the detailed protocols of an in vitro ubiquitination assay reconstituted with purified APC, cofactors, other ubiquitination enzymes, and the spindle-checkpoint proteins. This assay is extremely useful in dissecting the biochemical functions of various spindle-checkpoint proteins.
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