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Titlebook: p53; Ayeda Ayed,Theodore Hupp Book 2010 Landes Bioscience and Springer Science+Business Media, LLC 2010 Ayed.Cancer.Hupp.MDM2.p53.regulati

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發(fā)表于 2025-3-21 19:27:48 | 只看該作者 |倒序?yàn)g覽 |閱讀模式
書(shū)目名稱(chēng)p53
編輯Ayeda Ayed,Theodore Hupp
視頻videohttp://file.papertrans.cn/765/764610/764610.mp4
概述Discusses TP53 Mutations in Human Cancers Chapter on Regulation and Function of the Original p53-Inducible p21 Gene Presents key ideas in the field
叢書(shū)名稱(chēng)Molecular Biology Intelligence Unit
圖書(shū)封面Titlebook: p53;  Ayeda Ayed,Theodore Hupp Book 2010 Landes Bioscience and Springer Science+Business Media, LLC 2010 Ayed.Cancer.Hupp.MDM2.p53.regulati
描述Our understanding of human cancer in the past 40 years has been driven by linking innovative concepts and cutting edge technologies to key problems identified by clinical research. Some of the successes in cancer genetics identified from clinical work have been the identification of specific gene deletions in human chromosomes, the use of PCR-based cloning methodologies to identify and clone human cancer genes, the validation of the human cancer genes using transgenetic technologies in the mouse, and the ability to sequence whole genomes that has recently allowed a collation of all somatic and germline mutations in a human genome. In the same generation, entirely different disciplines involved in basic life science research have used model organisms like yeast, flies, worms, and cancer causing animal viruses as tools to develop windows to see into the machinery of the cell life cycle. The discoveries of pro-apoptotic genes, oncogenes, and covalent control mechanisms like phosphorylation and ubiquitination using the tools of science and technology have all been awarded Nobel prizes for their contribution to our understanding of how cells work. The discovery of p53 using the tumor ca
出版日期Book 2010
關(guān)鍵詞Ayed; Cancer; Hupp; MDM2; p53; regulation
版次1
doihttps://doi.org/10.1007/978-1-4419-8231-5
isbn_ebook978-1-4419-8231-5Series ISSN 1431-0414
issn_series 1431-0414
copyrightLandes Bioscience and Springer Science+Business Media, LLC 2010
The information of publication is updating

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發(fā)表于 2025-3-21 21:48:54 | 只看該作者
Cooperation between MDM2 and MDMX in the Regulation of p53,between p53 and its two negative regulators is maintained in proliferating cells, and is targeted by multiple signaling pathways to control the magnitude and duration of the p53-dependent transcriptional response to genotoxic stress.
板凳
發(fā)表于 2025-3-22 04:10:30 | 只看該作者
Regulation and Function of the Original p53- Inducible , Gene,nteractions, phosphorylation status, subcellular localization, and trafficking to the proteasome. Post-translational regulation of p21, particularly at its COOH terminus has a significant impact on p21 stability and abundance and therefore is an important determinant of intracellular p21 concentration.
地板
發(fā)表于 2025-3-22 05:30:20 | 只看該作者
Book 2010e discoveries of pro-apoptotic genes, oncogenes, and covalent control mechanisms like phosphorylation and ubiquitination using the tools of science and technology have all been awarded Nobel prizes for their contribution to our understanding of how cells work. The discovery of p53 using the tumor ca
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發(fā)表于 2025-3-22 12:32:30 | 只看該作者
, Mutations in Human Cancers: Selection versus Mutagenesis,, some mutants exert dominant-negative effects and/or acquire new pro-oncogenic activities. Our understanding of the behavior of mutant p53 functions is expanding and holds promises for applications to cancer risk assessment, early diagnosis, prediction of disease outcome, as well as for development of new therapeutic strategies.
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發(fā)表于 2025-3-23 05:17:06 | 只看該作者
p53 Localization,dria following stress where it interacts with pro- and anti-apoptotic members of the Bcl2 family, resulting in the release of factors from the mitochondria that drive apoptosis. This chapter will review studies of p53 localization control including its nuclear-cytoplasmic shuttling, movement to PML bodies and to the mitochondria.
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發(fā)表于 2025-3-23 05:40:12 | 只看該作者
,,: The Guardian’s Elder Brothers,n of . in squamous cancers results in overexpression of a ΔN protein that may counteract suppression by p63 as well as other family members. On the other hand, some mutant p53 can bind and inactivate p63 or p73, providing a mechanism for mutant p53 “gain-of-function” effect.
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