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

Osteopenia

書目名稱p53影響因子(影響力)




書目名稱p53影響因子(影響力)學(xué)科排名




書目名稱p53網(wǎng)絡(luò)公開度




書目名稱p53網(wǎng)絡(luò)公開度學(xué)科排名




書目名稱p53被引頻次




書目名稱p53被引頻次學(xué)科排名




書目名稱p53年度引用




書目名稱p53年度引用學(xué)科排名




書目名稱p53讀者反饋




書目名稱p53讀者反饋學(xué)科排名

archetype

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.

虛構(gòu)的東西

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.

鞠躬

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

Adj異類的

, 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.

他一致

婚姻生活

暴露他抗議

Antarctic

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.

DEI

,,: 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.